HomeMy WebLinkAboutNCD981927502_19920313_Geigy Chemical Corporation_SERB RISK_Baseline Risk Assessment-OCRBASELINE RISK ASSESSMENT
FOR THE GEIGY CHEMICAL CORPORATION SUPREFUND SITE
ABERDEEN, NORTH CAROLINA
Clement lntemational Corporation
Environmental and Health Science
March 13, 1992
Ms, Giezelle Bennett
Remedial Project Manager
~aste Management Division
USEPA Region IV
345 Courtland Street, N.!.
Atlanta, GA 3036S
Dear Ms. Bennett:
Clm&.t bite 1.aliollil eor,,cntlon
9300 Lee Higriway, Falr1u, VA 22031-1207
'70:1-934-3!00 Facalmllt. '703-9344278
Enllirorunmtal and Health Science
Please· find enclosed 4 bound copies and 1 unbound copy of the Baseline Risk Assessment for the Geigy <=}i$1111cal Corporation Superfund Sita. If you have any questions, please contact Ms. Lorraine M. Miller at (615) 336-4381.
Enclosure
BASELINE RISK ASSESSMENT
RECEIVED
'.1AR 1 ,,-· 1QU·) ....... ·1..,
0. L. CU/\'iir7JJ~GS
FOR THE GEIGY CHEMICAL CORPORATION SUPREFUND SITE
ABERDEEN, NORTH CAROLINA
Prepared for:
Olin Corporation
CIBA-GEIGY Corporation, and
Kaiser Alunimun & Chemical Corporation
· Lower River Road
Charleston, Tennessee 37310
Prepared by:
Clement International Corporation
9300 Lee Highway
Fairfax, Virginia 22031
March 13, 1992
I.
I I-\
TABLE OF CONTENTS
Section
EXECUTIVE SUMMARY
1.0
1.1
1. 2
1.3
2.0
2.1
2.2
2.3
2.4
2.5
2.6
3.0
3.1
3.2
INTRODUCTION
Site Background
Scope of Risk Assessment
Organization of Risk Assessment Report
IDENTIFICATION OF CHEMICALS OF POTENTIAL CONCERN
On-Site Surface Soils/Sediment ..
Off-Site Surface Soils/Sediment
On-Site Subsurface Soils/Sediment
2.3.1 Depth Interval 1.5 to 2.5 Feet
2.3.2 Depth Interval 3 to 10 Feet .
Off-Site Subsurface Soils/Sediment .
2.4.1 Depth Interval 1.5 to 3 Feet
2.4.2 Depth Invterval 3 to 10 Feet
Groundwater ........ .
2.5.1 Surficial Aquifer .. .
2.5.2 On-Site Second Uppermost Aquifer
2.5.3 Off-Site Second Uppermost Aquifer
Summary
TOXICITY ASSESSMENT
Health
3.1.1
3 .1. 2
Health
Effects Classification and Criteria Development
Health Effects Criteria for Potential Carcinogens
Health Effects Criteria for Noncarcinogens
Effects Criteria for Individual Chemicals of
Potential Concern .......... .
3.2.1 Aldrin ............. .
3.2.2 Alpha-, Beta-, and Delta-Isomers of
3.2.3
3.2.4
3.2.5
3.2.6
3.2.7
3.2.8
3.2.9
3.2.10
3.2.11
3.2.12
3.2:13
3.2.14
3.2.15
3.2.16
3.2.17
3.2.18
Hexachloride (BHC)
Gamma-BHC ........ .
Benzoic.Acid ...... .
Bis(2-ethylhexyl)phthalate
Chlordane
DDD, DDE, DDT
Dieldrin
Endrin Ketone
4-Methyl-2-Pentanone
Toxaphene ..... .
1,2,4-Trichlorobenzene
Trichloroethene
Barium
Manganese
Mercury.
Vanadium
Zinc
i
Benzene
E-1
1-1
1-1
1-2
1-3
2-1
2-4
2-8
2-8
2-8
2-8
2-10
2-10
2-10
2-12
2-12
2-15
2-18
2-19
3-1
3-1
3-2
3-4
3-6
3-9
3-10
3-11
3-12
3-13
3-14
3-15
3-16
3-17
3-18
3-19
3-20
3-21
3-22
3-24
3-25
3-26
3-27
TABLE OF CONTENTS (Continued)
Section
4.0
4.1
4.2
4.3
4.4
4.5
HUMAN EXPOSURE ASSESSMENT
Site Characterization
. . . . . . . . . . . . . . .
...............
Environmental Fate and Transport of Organochlorine Pesticides
Potential Exposure Pathways . . . . . . . . . ...
4.3.1 Potential Exposure Pathways Under Current Land and
Surrounding Land-Use Conditions ....
4.3.1.1 Surface Soil/Sediment Pathways .
4.3.1.2 Subsurface Soil/Sediment Pathways
4.3.1.3 Groundwater Pathways ...... .
4.3.1.4 Air Pathways .......... .
4.3.1.5 Summary of Current Land Use Pathways
4.3.2 Potential Exposure Pathways Under Future Land Use
Conditions .............. .
4.3.2.1 Surface Soil/Sediment Pathways ..
4.3.2.2 Subsurface.Soil/Sediment Pathways
4.3.2.3 Groundwater Pathways . . .. .
4.3.2.4 Air Pathways .... , ..... .
4.3.2.5 Summary of Future Land Use Pathways
Calculation of Exposure Point Concentrations ....
4.4.1 Exposure Point Concentrations in On-Site Surface
Soil/Sediment ................ .
4.4.2 Exposure Point Concentrations in Off-Site Surface
Soil/Sediment ............... .
4.4.3 Exposure Point Concentrations in Groundwater of the
Surficial Aquifer . . . . . . ....
4.4.4 Exposure Point Concentrations for Showering with
Groundwater ................. .
4.4.5 Exposure Point Concentrations in Ambient Air
4.4.6 Exposure Point Concentrations in Ambient Air Off-Site
4.4.7 Exposure Point Concentrations for Fugitive Dust Emissions
Quantification of Exposure .............. .
4.5.1 Exposure Estimates Under Current and Surrounding
4.5.2
Land-Use Conditions . . . . . . . . . . . . . .
4.5.1.1 Incidental Ingestion of Surface Soil/Sediment
4.5.1.2 D~rmal Absorption of Chemicals from Surface
Soils/Sediment ............. .
4.5.1.3 Inhalation of Dust Particulates and Volatilized
Exposure
4.5.2.1
4.5.2.2
4.5.2.3
4.5.2.4
4.5.2.5
4.5.2.6
Chemicals Released from Surface Soil/Sediment
Estimates Under Future Land-Use Conditions ...
Incidental Ingestion of Surface Soil/Sediment
Dermal Absorption of Chemicals from On-Site Surface
Soil/Sediment ................. .
Ingestion of Groundwater from the Surficial Aquifer
and MW-llD . . . . . . . . . . . . . . . ...
Chronic Inhalation Exposure to Chemicals
Volatilized During Showering . . ·. . . . . . .
Dermal Exposure to Chemicals During Showering
Inhalation of Volatilized Chemicals from Surface
Soil/Sediment ................
ii
4-1
4-1 •. I
4-5
4-7
4-8
4-8
4-9
4-9
4-12
4-12
4-13
4-14
4-14
4-18
4-18
4-19
4-20
4-21
4-23
4-23
4-23
4-26
4-29
4-30
4-34
4-34
4-34
4-36
4-42
4-58
4-58
4-64 ,,
4-66
4-72
4-86
4-87
I,
I
TABLE OF CONTENTS (Continued)
Section
5 .0
5.1
5.2
5.3
RISK CHARACTERIZATION 5-1
Risks Associated with Current Site and Surrounding Land-Use
Conditions . . . . . . . . . . . . . . . . . . . . . 5 -3
5.1.1 Risks Due to Surface Soil/Sediment Exposures 5-3
5.1.1.1 Risks Associated with Incidental Ingestion of
Off-Site Surface Soil/Sediment by Older
Children (8-13 years) . . . . . . . . .. 5-15
5.1.1.2 Risks Associated with Dermal Contact with Off-
Site Surface Soil/Sediment by Older Children
(8-13 years) . . . . . . . . . . . . 5-15
5.1.2 Risks Due to the Inhalation of Airborne Volatiles and
Dust Particulates ........... .
Summary of Cumulative Risks Under Current Land-Use Conditions
5.2.1 Cumulative Risks to an On-Site Trespasser
5.2.2 Cumulative Risks to a Off-Site Receptor ..
Risks Associated with Future Land-Use Conditions .
5.3.1 Risks Due to Surface Soil/Sediment Exposures
5.3.1.1 Risks Associated with Incidental Ingestion of
Surface Soil/Sediment by a Future Merchant
and a Child (1-6 years) and Adult Resident .
5.3.1.2 Risks Associated with Dermal Contact with Surface
Soil/Sediment by a Future Merchant and a Child
(1-6 years) and Adult Resident ...... .
5.3.1.3 Risks Associated with Incidental Ingestion and
Dermal Absorption of Off-Site Surface Soil/
Sediment by a Future Resident (Qualitative)
5.3.2 Risks Due to the Groundwater Exposures ....... .
5.3.2.1 Risks Associated with Ingestion of Untreated
Groundwater from the Sutficial Aquifer by a·
Future Merchant and a Child (1-6 years) and
5-16
5-16
5-17
5-17
5-19
5-19
. 5-19
. 5-23
5-23
5-27
Adult Resident ............. . . . . 5-27
5.3.2.2 Risks Associated with Ingestion of Untreated
Groundwater from MW-llD by a Future Child
(1-6 years) and Adult Resident ......... . 5-31
5.3.3
5.3.2.3
5.3.2.4
5.3.2.5
Risks Associated with Inhalation of Volatiles While
Showering with Surficial Groundwater by a Future
Child (1-6 years) and Adult Resident
Risks Associated with Dermal Exposures While
Showering with Surficial Groundwater by a
Future Child (1-6 years) and Adult Resident
Risks Associated with Inhalation of Volatiles
While Showering with Second Uppermost Aquifer
Groundwater by a Future Child (1-6 years)
5-31
5-34
and Adult Resident .......... . . . 5-34
5.3.2.6 Risks Associated with Dermal Exposures While
Showering with Surficial Groundwater by
a Future Child (1-6 years) and Adult Resident
Risks Due to the Inhalation of Airborne Volatiles ....
iii
5-41
5-41
TABLE OF CONTENTS (Continued)
Section
5.4 Summary of Cumulative Risks Under Future Land-Use Conditions
5.4.1 Cumulative Residential Risks
5.4.2 Cumulative Risks to Merchants
5.5 Summary of Potential Health Risks
6.0 ENVIRONMENTAL ASSESSMENT .....
6.1 Site Description and Potential Receptor Species
6.2 Potential Exposures and Impacts
6.2.1 Plants ...... .
6.2.2 Terrestrial Wildlife
6.2.3 Endangered Species
6.3 Summary and Conclusions
7.0
7.1
7.2
7.3
7 .4
UNCERTAINTIES
Environmental Sampling
Exposure Assessment
Toxicological Data.
Sensitivity Analysis
and Analysis
8.0 SUMMARY AND CONCLUSIONS
9 . 0 REFERENCES . . . . .
APPENDIX A
APPENDIX B
APPENDIX C
APPENDIX D
APPENDIX E
EPA REGION IV GUIDANCE FOR DATA SUMMARY
EQUATION USED FOR STATISTICAL ANALYSIS
SHOWER MODEL
-AIR EMISSIONS AND DISPERSION MODELING
RISK-BA~ED SOIL REMEDIATION GOALS
iv
5-47
5-47
5-47
5-49
6-1
6-1
6-3
6-3
6-3
6-7
6-8
7-1
7-1
7-3
·7_9
7-13
8-1
9-1
EXECUTIVE SUMMARY
Clement International Corporation evaluated the human·health and ecological
risks associated with past operations at the Geigy Chemical Corporation Site,
a former pesticide formulation facility. This Baseline Risk Assessment was
performed for the Potentially Responsible Parties under an Administrative
Order _on Consent with the United States Environmental Protection Agency Region
IV Administrator. The primary data used in this evaluation was collected
during the Remedial Investigation conducted by Environmental Resources
Management-Southeast, and the Feasibility Study conducted by Sirrine
Environmental.
The Geigy Chemical Corporation site is located in Aberdeen, North Carolina.
From 1947 until 1967 the site was used as a pesticide formulation facility.
Subsequent to 1968, the site had been used for retail distribution of
agricultural chemicals and fertilizers. Extensive remedial activities have
already occurred at the site; soil has been excavated and removed to ~azardous
waste treatment, storage and disposal facilities, and areas of the site have
been covered with geotextile, clean fill and an indigenous species of grass.
Thus, this Baseline RA addresses a no-further action alternative. The no-
further action alternative was evaluated in accordance with the National
Contingency Plan and USEPA guidance for risk assessments at Superfund sites.
Chemicals of potential concern were selected for quantitative evaluation in
the Baseline Risk Assessment. The quantitative evaluation consisted of the
estimation of the upperbound excess lifetime cancer risk associated with
exposure to chemicals from the site, as well as the potential for adverse
noncarcinogenic effects to occur. The predominant chemicals in on-site soil
are toxaphene and DDT and its metabolites ODE, and ODD, while in groundwater,
toxaphene and the BHC isomers are predominant.
A total of 11 exposure pathways were selected for de~Filed evaluation under
current and surrounding land-use conditions (a pathway describes how a
E-1
receptor may be exposed to. chemicals f+om the site). Incidental ingestion_ and
dermal absorption of chemicals in surface soil/sediment by an older child (8-
13 years) were evaluated for both on-site and off-site locations.
Additionally, the inhalation of chemicals volatilized from surface
soil/sediment was evaluated for an older child trespasser (8-13 years), a
merchant north of the site, and a nearby adult and young child resident (1-6
years) northeast of the site. The inhalation of wind blown dust particulates
by a merchant north of the site, and by a nearby adult and young child
resident (1-6 years) northeast of the site were evaluated.
Under future land-use conditions, a total of 22 exposure pathways were
selected for evaluation. Future on-site receptors evaluated include a
merchant, and an adult and young child (1-6 years) resident. For each of
these receptors incidental ingestion and dermal absorption of chemicals in
surface soil/sediment and inhalation of chemicals volatilized from surface
soil/sediment were evaluated. An additional seven pathways associated with
the domestic use of groundwater from the surficial aquifer at the site were
_evaluated. These include groundwater ingestion for a merchant, adult and
child resident, and inhalation and dermal absorption of chemicals while
showering for the adult and child resident. Ingestion of groundwater from an
off-site well screened in the second uppermost aquifer (MW-11D) was assessed
for both an adult and child resident due to the presence of pesticides.
Pesticides were not detected in the second uppermost aquifer directly beneath
the property boundaries. However, ingestion of groundwater from this aquifer
within the property boundary was evaluated for both an adult and child
resident.
Under current land-use conditions, risks ranged from to 8xlo-11 to 7xlo-6 for
the evaluated receptors: a trespassing older.child, young child and adult
residents northeast of the site, and merchants north of the site. The
cumulative risks for each receptor (risks combined across pathways) ranged
from 9xlo-8 to 9xlo-6. All of these risks are less than or within EPA's
remedial risk range of lxlo-4 to lxlo-6. In addition, potential adverse
E-2
, ..
noncarcinogenic effec_ts are not likely to occur under current land-use
conditions.
Under future land-use conditions, the risks associated with hypothetical
ingestion of surficial groundwater were of greatest concern, and ranged from
lxl□-3 to 4x10·3 for the evaluated receptors: a future on-site young child and
adult resident, and a future merchant. Risks associated with dermal and
inhalation exposure while showering to the pesticides in groundwater were much
lower than ingestion risks, and ranged from 2xl□-6 to 6x10·6 . Risks associated
with direct contact of on-site surface soil and inhalation of pesticides
released into ambient air from surface soil ranged from 9xl0"6 to 3x10·5, and
were dominated by the incidental ingestion of surface soil. Of the pesticides
present in surface soil, toxaphene was found to be the risk-limiting (risk-
driving) chemical. The cumulative risks under future land-use conditions
exceeded EPA's criterion of lxl0"4 and were dominated by the ingestion of
surficial groundwater. Potential adverse noncarc"inogenic effects were
predicted for all receptors ingesting pesticides in surficial groundwater.
Risks were also estimated for hypothetical future young child and adult
residents who might consume groundwater from the second uppermost aquifer in
the vicinity of monitoring well MW-11D. The risks associated with exposure to
pesticides in this groundwater ranged from 7xl0"4 to 2xl0"3 and were dominated
by ingestion. Potential adverse noncarcinogenic effects were also predicted
for these receptors from the ingestion of groundwater in the vicinity of MW-
11D.
Additionally, risks associated with domestic use of groundwater from the
second uppermost aquifer within property boundaries were evaluated for
hypothetical future adult and child residents. These risks ranged from
3xl0"6 to 2x1o·S and are attributed solely to the presence of trichloroethene.
Potential adverse noncarcinogenic effects were predicted for a hypothetical
future child resident.
E-3
Adverse ecological impacts_ associated with the site are not expected to occur.
No aquatic life impacts are expected, as _the two drainage ditches that occur
at the site do not contain enough water to sustain aquatic life. No impacts
on the vegetative. community are expected given the probable low phytotoxicity
of the insecticides of concern in ~oil. Adverse terrestrial Wildlife impacts
also are not expected. The site is not expected to support extensive wildlife
populations, given its small size, the limited diversity of the vegetative
community (which limits food and cover resources), and the availability of
higher quality habitat in adjacent areas. Some impacts are possible for soil
invertebrates living in limited areas of the site, although these impacts
could not be evaluated with any degree of certainty given the available
toxicological and exposure database. Even if toxic effects in soil
invertebrates are possible in localized areas, extensive impacts are
considered unlikely because the sandy and low-organic content soil present
naturally at the site is unlikely to support an abundant and diverse soil
invertebrate community.
A soil remediation goal for the risk-limiting chemical, toxaphene, was derived
in accordance with EPA guidance for the direct contact pathway of greatest
concern, i.e. the incidental ingestion of soil under future· residential
conditions (Appendix E). Not-to-exceed surface soil concentrations of 5 mg/kg
toxaphene, 50 mg/kg toxaphene, and 500 mg/kg toxaphene were found to represent
lx10·6, lxlo-5, and lx10·4 excess upperbound lifetime residual cancer risks
respectively, for site-wide exposure to all of the pesticides combined.
E-4
' .
1.0 INTRODUCTION
This Baseline Risk Assessment (Baseline RA) has been prepared by Clement
International Corporation to evaluate the magnitude and probability of an
adverse impact on human health and the environment associated with actual or
potential exposure to site-related chemicals at the Geigy Chemical Corporation
Site in Aberdeen, North Carolina. This assessment was performed pursuant to
an Administrative Order of Consent entered into by the United States
Environmental Protection Agency (USEPA), the Region IV Environmental
Protection Agency and the Potentially Responsible Parties for the Geigy
Chemical Corporation Site.
This Baseline RA satisfies the requirements under Subpart E, Section
300.430(d) of the revised National Contingency Plan (NCP) as promulgated on
March 8, 1990 (USEPA 1990a). Paragraph (d)(4) of this section directs that a
Baseline RA be conducted to characterize the current and potential threats to
public health and the environment that may be posed by contaminants migrating
to various environmental media.
This risk assessment is consistent with relevant guidance developed by the
United States Environmental Protection Agency (USEPA 1986a,b,c, 1989a,b,
1990b, 1991a) and USEPA Region IV (USEPA 1991b). The information used in this
risk assessment was obtained from data collected by ERM-Southeast as part of
the Remedial Investigation (RI) (ERM 1991), and from data collected by Sirrine
Environmental (Sirrine 1991) as part of the Feasibility Study.
1.1 SITE BACKGROUND
As previously described in the RI, the site is an approximately one-acre
parcel located on the Aberdeen and Rockfish Railroad right-of-way, just east
of the corporation city limits of Aberdeen, on Highway 211 in southeastern
Moore County. The property is in the form of an elongated triangle between
Highway 211 and the railroad, with the highway and railroad intersecting at
the apex of the triangle. A site location map was provided previously in
1-1
Figure 1-1 of the RI. The site is currently vacant and consists of partial
concrete foundations from. the two former warehouses, an office building, and a
concrete tank pad.
The Geigy Chemical Corporation Site has had several operators during the past
forty years. These include: Geigy Chemical Corporation (now CIBA-GEIGY
Corp.) from 1949-1955, Olin-Matheison Corporation (now Olin Corp.) from 1956-
1967, Columbia Nitrogen Corporation, 1968, Kaiser Aluminum and Chemical
Corporation 1969-1985, and Lebanon Chemical Corporation (now·Kaiser-Estech
Corp.) 1985-1989. From approximately 1946 to 1967, the site contained
formulating and distribution facilities for pesticides, including DDT,
toxaphene, and BHC. Technical grade pesticide was blended with clay or other
inert materials to form a usable product and repackaged for sale to local
cotton and tobacco growing markets. Since 1968, the site has been used by
retail distributors of agricultural chemicals, mainly fertilizers.
The east end of former Warehouse Building A was believed to have been used
primarily for the formulation and packaging of pesticides, and thus is
considered one of the primary sources of contamination. The remaining
portions of the former warehouse were used primarily for the storage of
fertilizers and other agricultural chemicals.
Extensive remedial activities have already occurred at the site; soil has been
excavated and removed to Hazardous Waste Treatment, Storage and Disposal (TSD)
Facilities, and certain areas have been covered with geotextile, clean fill
and an indigenous species of grass. Thus, this Baseline Risk Assessment
addresses a no further action alternative, evaluating potential human health
and environmental impacts associated with the site after extensive remedial
activity has taken place.
1.2 SCOPE OF RISK ASSESSMENT
This risk assessment evaluates exposure under current and future land-use
conditions. Exposure is conceptualized by the selection of exposure pathways,
1-2
--
which describe how a receptor may be exposed to the chemicals of potential
concern present in the environmental media investigated during the RI.
This risk assessment evaluates 11 current land-use exposure pathways, and 22
future land-use exposure pathways. A total of 17 pesticides were measured in
on-?ite surface soil and therefore were evaluated in this risk assessment.
Direct contact to on-site soil and sediment were evaluated di~ectly from
environmental measurements collected during the RI, as was exposure·to on-site
and off-site groundwater. Inhalation exposure to chemicals volatilizing from
groundwater during showering activities was evaluated through the use of the
peer-reviewed Foster and Chrostowski shower model (1987). Chemical migration
from on-site soil into ambient air was evaluated through the use of
volatilization and dust dispersion models. The soil volatilization model
synthesized from Bomberger et al. (1983), Millington and Quirk (1961) and
USEPA (1986), and the Industrial Source Complex Long Term (ISCLT) air
dispersion model were used to predict air concentrations of pesticides
volatilizing from surface soil. Dust emissions were determined using Cowherd
(1985), and these emissions were used with the ISCLT air dispersion model to
predict air-borne concentrations of dust originating from on-site surface
soil.
1.3 ORGANIZATION OF RISK ASSESSMENT REPORT
The risk assessment is organized as follows:
• Section 2, Identification of Chemicals of Potential Concern. The
chemicals detected in sampled environmental media during the
Remedial Investigation (RI) were identified and discussed. The RI
data were summarized by presenting the frequency of detection and
the range of detected concentrations in site-related samples and
in background samples. Based on an evaluation of the data and a
comparison to background and blank concentrations (as applicable),
chemicals of potential concern were selected for further
evaluation.
• Section 3, Toxicity Assessment. The methodology used to describe
the potential toxicity of chemicals to humans and the range of
toxic effects for each chemical of potential concern was
1-3
presented. Chemical-specific toxicity criteria to be used in the
quantitative r_isk assessment are presented.
• Section 4, Human Exposure Assessment. The potential pathways by
which populations may be exposed to chemicals of potential concern
were discussed and exposure pathways were selected for further
evaluation. For each pathway selected for quantitative
evaluation, the chemical concentrations at the point of potential
exposure were calculated followed by quantification of exposure
(intake).
• Section 5, Risk Characterization. The general principles of the
risk assessment process were described. For each exposure
pathway, quantitative risk calculations were performed by
combining the estimated intakes of potentially exposed populations
with toxicity criteria for each selected exposure pathway.
• Section 6, Ecological Risk Assessment. The potential risks to
aquatic life, terrestrial animals and plants were evaluated.
• Section 7, Discussion of Uncertainties. This discussion focused
on the major sources of uncertainty affecting the health risk
assessment: environmental parameter measurement, fate and
transport modeling, estimation of exposure parameters and
quantifications of exposures, and toxicological data.
• Section 8, Summary and Conclusions.
the findings of the human health and
This discussion
ecological risk
summarizes
assessment.
• Section 9, References. References are swnmarized by section.
• Appendix A, Data Summary based on Regional Guidance. Data summary
tables presenting arithmetic mean concentrations using detected
concentrations only (no nondetected values) are provided.
• Appendix B, Equation Used for Statistical Analysis. The equation
used to calculate the 95 percent upper confidence limit on the
arithmetic mean is provided.
• Appendix C, Shower Model .
shower model is presented
The Foster and Chrostowski (1987)
and discussed.
• Appendix D, Air Emissions and Dispersion Modeling. Details on
volatilization and dust dispersion models are presented and
discussed.
• Appendix E, Risk-Based Soil Remediation Goals. Not-to-exceed
concentrations of the risk-driving cheffiical in surface soil were
developed for the 10·6 , 10·5 and 10·4 risk levels.
1-4
C
2.0 IDENTIFICATION OF CHEMICALS OF POTENTIAL CONCERN
This section of the Baseline Risk Assessment d:iscusses the selection the
chemicals of potential concern for detailed evaluation. The purpose of
selecting chemicals of potential concern is to identify those chemicals
present at the site which are most likely to be of concern to human health and
the environment. In general, chemicals that are asso~iated with sampling or
laboratory artifacts, or naturally occurring chemicals that are within
background levels, are not selected as chemicals of potential concern.
This Section summarizes the data in the various media in accordance with USEPA
Guidance (1989a) for quantification of exposure in the human health risk
assessment. Using the USEPA (1989a) approach, the arithmetic mean was
calculated by averaging the detected concentrations with one-half the
detection limit of the non-detects. This method yields the most reliable
estimates of the upper confidence limit (UCL) for log-normally distributed
data sets. The arithmetic mean and 95% UCL on the population mean1
calculated using this method are presented in Section 4.4 of the Baseline RA
and are described below in further detail.
Additionally, the data were treated differently as per USEPA Region IV
Guidance (1991b). Region IV USEPA (1991b) recommends that the arithmetic mean
be calculated using detected values exclusively. These averages were
calculated with positive values only and are presented in Appendix A (Tables
A·l through A-6).
Prior to selecting chemicals of potential concern, the first step is to
summarize all available RI data ac_cording to the following procedures, which
are in general accordance with USEPA (1989a):
1Reference to the literature (Gilbert 1987) indicates that the confidence
interval is around the population mean rather than the arithmetic mean as
stated by USEPA (1989a).
2-1
• Remedial Investigation data collected and analyzed according to
USEPA' s Contra.ct Laboratory Program (CLP) procedures were used to
select chemicals for this assessment.
• The RI data were divided into groups which describe environmental
conditions relevant to exposure. For example, a group of
background data was used to determine if concentrations of
chemicals detected on or downgradient of the site ·are at naturally
occurring levels. Grouping data also helps in determining
exposure point concentrations for target populations. These data
groups are described in detail by environmental medium in Sections
2.1 through 2.5.
• Concentration data for surface soil and sediment were averaged
together. For duplicate samples at a given sampling point, the
average concentration for the sample location was calculated by
averaging the detected concentration(s) with one-half of the
detection limit of the non-detect(s). Groundwater sample results
were averaged across sampling events and across wells.
• Due to the fact that there are varying chemical-and sample-
specific detection limits, even within one medium, samples in
which a chemical was not detected were compared to the maximum
detected concentration for that chemical to determine if the non-
detects would be included in calculating the mean concentration.
If one-half the detection limit for a non-detect sample was
greater than the maximum detected concentration in the same medium
for that chemical, the sample was not included in the calculation
of the average for that chemical. This was done to prevent the
average from being artificially biased upwards by high detection
limits.
The results of this data compilation step are the arithmetic mean and 95%
upper confidence limit on the mean which are presented by environmental medium
in Section 4.4. This section presents tables that summarize the data by
frequency of detection, the arithmetic mean concentration and the range of
concentrations detected2 for each environmental medium.
It is important to recognize that the selection of a chemical as a chemical of
potential concern does not necessarily indicate that it poses a problem. The
selection of a chemical only indicates that there is a need to evaluate it in
2Exposure point concentrations that will be used to calculate risks
(e.g., the 95% upper confidence limit on the mean) will be presented in
Section 4.0.
2-2
the Baseline RA to determine if that chemical is associated with potential
health risks. This applies in particular to chlordane, heptachlor and
heptachlor epoxide which were infrequently detected and found in only one
media sampled at the site. Chlordane was detected only in surface soil while
heptachlor and heptachlor epoxide were detected only in subsurface soil.
Based on a review of the summarized data, chemicals were selected for further
evaluation in the risk assessment using the following methodology:
• According to USEPA (1989a), inorganic chemicals present at the
site at naturally occurring levels may be eliminated from the
quantitative risk assessment. According to this guidance, a
statistical method should be used to determine whether chemical
concentrations detected at the site are within, or elevated above,
background levels. This approach was used to evaluate background
concentrations for those sample groupings (sample groupings to be
discussed below) where at least three samples were available. The
statistical method that was used was considered to be appropriate
for the data under evaluation and accounted for data below the
limit of detection (USEPA 1988a). For this assessment, the
Cochran's approximation to the Behren's-Fisher (CABF) Students t-
test was used. Only three inorganic chemicals, copper, lead and
zinc were analyzed with a sufficient frequency to be evaluated
using this method.
• In cases where inorganic chemicals were not analyzed in designated
site-specific background samples, or were not analyzed in enough
samples to warrant statistical analysis, regional background
levels from counties adjacent to Moore County, North Carolina were
compiled from the U.S. Geological Survey and used for comparison
(Boerngen and Shacklette 1981). Using this approach, if the
maximum chemical concentration a medium was higher than two times
either the site-specific or the maximum concentration in the
regional background data, the chemical was selected for detailed
evaluation as recommended by USEPA Region IV guidance (USEPA
1991b).
• Site data were compared to available blank data (trip, field and
laboratory). If the detected concentration in a sample was less
than 10 times the blank concentration for common laboratory
contaminants (acetone, 2-butanone, methylene chloride, toluene,
and the phthalate esters), the chemical in that sample was not
included for evaluation in the risk assessment. For those organic
or inorganic chemicals that are not considered by USEPA to be
common laboratory contaminants (all other compounds), if the
detected concentration was less than 5 times the maximum detected
concentration in the blanks, the sample was not included in the
2-3
evaluation.
• All organic chemicals measured in various environmental media were
evaluated as per USEPA guidance (i.e., inorganic chemicals were
eliminated based on a background determination).
This remainder of Section 2 describes the data groupings for the site Baseline
RA and summarizes the selection of chemicals of concern within each of these
sampling groups.
2:1 ON-SITE SURFACE SOILS/SEDIMENT
Extensive remedial activities have occurred as part of the site investigation,
and large portions of surface soil/sediment were excavated and removed.to
Hazardous Waste Treatment, Storage and Disposal (TSD) Facilities, or were
covered with a minimum of six inches of clean soil (gray area depicted in
Figure 2-1). In several areas, as much as 11 feet of clean fill was added.
All samples characterizing depths within 0-1 foot were considered to be
surface soil, even if covered by clean fill (i.e., located in the gray area
depicted in Figure 2-1). A total of 89 surface soil/sediment samples describe
the remaining concentrations of chemicals at the site. Sediment samples (0-1
foot depth) were grouped with surface soil samples because on-site drainage
ditches are predominantly dry, and hence are more characteristic of surface
soil. Additionally, two background surface soil samples (one north of the
site, and the other east of the site), and one background sediment sample (1/4
mile west of the site along state Highway 211) were collected. The sampling
locations for these 89 samples and two of the background samples are shown on
Figure 2-1.
Table 2-1 presents the summary of chemicals in surface soil/sediment at the
site. A summary of the frequency of detection, the arithmetic mean, the
number of samples used to calculate the mean, the range of detected
concentrations and the range of background concentrations are also presented
in Table 2-1. The arithmetic mean was calculated using detected values in
addition to one-half the detection limit for non-detects, excluding high
detection limits, and is consistent with USEPA (1991a, 1989a) risk assessment
2-4
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2-5
TABLE 2-1
SUMMARY OF CHEMICALS IN SURFACE SOIL/SEDIMENT (Organics: ug/kg, Inorganics: mg/kg)
Mean Site-Specifc Range of Frequency of Sample Arithmetic Range of Detected Background Background Chemical Detection (c) Size (d) Mean (e) Concentrations Concentrations(f) Concentrations(g)
ON-SITE (a)
Organics: --------* Aldrin 2 I 89 33 4.4 5.9 ND (<8.5 to <9.2} * alpha-BHC 9 I 89 89 82 13 1,500 ND C <8.5 to <9.2) * beta-BHC 34 / 89 89 130 4.4 2,000 ND (<8.5 to <9.2) * delta-BHC 6 / 89 89 71 23 · 840 ND (<8.5 to <9.2) * galTIT!a-BHC 6 / 89 89 68 41 · 620 ND (<8.5 to <9.2) * Benzoic acid 3 I 3 3 1,400 200 -3,600 ND (<3,200) * alpha-Chlordane 1 / 89 28 41 45 ND (<85 to <92) * gaITma-Chlordane 1 / 89 32 75 49 NO (<85 to <92) * 4,4'-0DD 82 / B9 89 1,300 7.7 -15,000 9.2 · 32 * 4,4'-DDE 89 / B9 89 1,000 3.7 -11,000 11 · 76 * 4,4' -DDT 89 / 89 89 3,600 9.4 54,000 33 · 110 * Dieldrin 7 I 89 89 140 11 1,500 ND (<17 to <18) * Toxaphene 74 / 89 89 16,000 340 · 220,000 180 • 260
I norgani cs: ----------Alllllinllll 3 I 3 3 6,400 1,820 · 9,630 2,140 -2,660 50,000 100,000 Arsenic 3 I 3 3 1. 7 0.8 • 2.4 0.7 1.2 7.6 Barium 3 I 3 3 20 14.3 -22.7 8.9 300 700 Berylliun 1 / 3 3 0.1 0.1 ND 0.01 40 Cal ci llTI 3 I 3 3 2,200 687 -4,750 105 -907 4,000 8,500 Chromium 3 I 3 3 5. 1 2.8 -6.8 2.1 · 2.7 15 70 Copper 79 I 82 82 12 2.6 · 37.7 2.7 · 5.6 30 Iron 3 I 3 3 5,300 2,810 -7,080 1,380 · 1,640 20,000 · 70,000 Lead 89 / 89 89 51 1.4 -336 7.6 • 90.2 Magnesiun 2 I 2 2 1,100 208 · 2,000 158 5,000 7,000 Manganese 3 I 3 3 26 13.7 • 33.9 12.7 • 20.2 200 · 3,000 Potassiun 3 I 3 3 260 221 • 314 ND 5,000 · 26,000 Vanadillll 2 I 3 3 6.8 9.6 · 9.7 3.2 70 -150 Zinc 86 / 87 87 54 1.6 -732 15.3 · 26.4
OFF-SITE (b)
Organics: --------
* beta-BHC 1 / 9 7 270 540 ND (<8.5 to <9.2) * 4,4'-DDD 7 I 9 9 5,900 13 -25,000 9.2 -32 * 4,4'-DDE 8 / 9 8 1,400 29 -6,600 11 · 76 * 4,4'-DDT 9 I 9 9 13,000 73 · 52,000 33 · 110 * Dieldrin 1 / 9 3 9.8 12 ND (<17 to <18) * Toxaphene 8 / 9 9 51,000 200 · 190,000 180 · 260
Inorganics:
----------Copper 8 / 9 9 4.6 1.1 · 9.6 2.7 · 5.6 30 Lead 9 I 9 9 17 6.5 · 35.3 7.6 90.2 Zinc 7 I 7 7 21 6.8 -68.3 15.2 • 26.4
*=Chemical of potential concern.
ND= Not detected (range of detection limits reported in parentheses).
Ca) Sample results from SD-1-1 through SD-4-1 SD-6-1 to SD-8-1 SD-13·1 SD-18-1 to SD-21-1 SD-22-1
(duplicate of S0-6·1), SD-41, SS-01, SS-04, SS-09, SS-20-0 through SS-47-0, SS-49-0 thro~gh SS-63-0, SS-103·0
through SS-107-0, SS-110-0, SS-58-20S, SS·61-20S, SS·62·20S, SS-63-20S, SS·64·20S, SS-66·20S, SS-71-0,
ss-67-0 SS-68-0 SS-82-0 to SS-85-0 SS-87 to SS-90 SS·92-1DN SS-93·20E SS-92-0 through SS-97-0 SS-33
(duplic~te of ss:27>, SS-55 (duplicate of SS-44), ss!93-10N-o.s: and ss-168-0.s (duplicate of ss-93!10N-O.S).
Cb) Sample results from OSD-22-1 through OS0-28·1, OS0-30·1 (duplicate of OSD-22·1), OSD-42, and OSD-43. Cc) The nllllber of samples in which the chemical was detected divided by the total nllTiber of samples analyzed.
(d) Mean safll)le s·ize represents the m.mber of detected·values which were used to calculate the arithmetic mean.
(e) Arithmetic mean concentrations were calculated using only detected values according to USEPA Region IV
Guidance (1991b).
(~) Background consists of surface soil/sediment sa~les SS-121, SS-122 and OSD-21; in many cases, only 1 data point was available for a metal.
(g) Regional Background levels from Hoke, Chatham, and Randolf Col.D'lties, North Carolina (Boerngen and Shacklette
1981) and national background levels from Bod~k et al. (1988).
2-6
::
• I
,
'
guidance. The statistic entitled 11rnean sample size" presents the actual
number of samples used to calculate the arithmetic mean. This statistic is
helpful in evaluating the frequency of detection, since samples containing
elevated detection limits are not included in this number.
Phase 1 soil samples were analyzed for 23 target analyte list (TAL) metals,
cyanide, 20 pesticides, 7 Aroclors of PCBs, 34 volatile organic compounds, and
65 semivolatile compounds. Subsequent sampling efforts (Phase 2, 3, 4) were
focused on the analyses of three metals (copper, lead and zinc) and 20
pest_icides with USEPA consent which were suspected of being site-related.
The most prevalent chemicals were 4,4'-DDD, 4,4',DDE, 4,4'-DDT, and toxaphene
(82/89, 89/89, 89/89 and 74/89, respectively) and these chemicals were present
at the highest concentrations. Alpha-and gamma-chlordane and aldrin were
detected very infrequently (e.g., in 1/89, 1/89 and 2/89 samples,
respectively) at levels below the CLP detection limits. Delta-BHC, gamma-BHC
and dieldrin were also detected infrequently (6/89, 6/89 and 7/89 samples,
respectively). Benzoic acid was only analyzed in Phase 1 sampling as part of
the target compound list, and was detected in 3/3 samples at estimated
concentrations.
A background comparison was performed on all inorganics with available site-
specific background data in•surface soil/sediment and with regional data from
USGS for North Carolina. Only three metals were measured in all three
background samples, i.e. copper, lead and zinc. The CABF Student's t-test
indicated that lead and zinc were clearly within background concentrations,
while copper was borderline (statistical significance would change depending
on direction of rounding off of the calculations). Therefore, because the
concentration of copper was less than two times the regional background levels
in Chatham and Randolph Counties N.C. it was not selected as a chemical of
potential concern. Other inorganics with fewer than three data points were
evaluated by using USEPA 2X background rule. Aluminum, arsenic, barium,
beryllium, calcium, chromium, iron, lead, magnesium, manganese, potassium,
vanadium and zinc were within background concentrations and therefore were not
selected as chemicals of potential concern.
2-7
2.2 OFF-SITE SURFACE SOILS/SEDIMENT
Nine off-site surface soil/sediment samples we.re collected in the surrounding
site area, two of which were blind split samples. These sampling locations
are also depicted in Figure 2-1 and the resulting data are summarized in Table
2-1. A total of six chlorinated pesticides (beta-BHC, 4,4'-DDE, 4,4'-DDD,
4,4'-DDT, dieldrin, and toxaphene) and three inorganic chemicals (copper,
lead, and zinc) were detected in off-site surface soils/sediment. Toxaphene
was the pesticide present at the greatest concentrations as was the case for
the on-site surface soil/sediment.
Copper, lead and zinc were considered to be within site-specific background
levels based on a statistical comparison using CABF Students t-test, and thus
were not selected as chemicals of potential concern.
2.3 ON-SITE SUBSURFACE SOILS/SEDIMENT
2.3.1 Depth Interval 1.5 to 2.5 Feet
A total of 62 on-site subsurface soil/sediment samples were collected during
Phase 3 and 4 of the RI sampling efforts. The most prevalent chemicals were
4,4'-DDT, toxaphene, and beta-BHC (29/62, 35/62, and 22/62 samples,
respectively). Aldrin, endrin ketone, heptachlor and heptachlor epoxide were
detected infrequently in 1/58, 2/58, 2/62, and 1/48, respectively. Copper,
lead and zinc were the only three inorganics analyzed for, and were detected
in every sample. The data on subsurface soil/sediment at depths of 1.5 to 2.5
feet is presented in Table 2-2. This table summarizes the frequency of
detection, arithmetic mean, number of samples used to calculate the mean, and
range of detected concentrations.
2.3.2 Depth Interval 3 to 10 Feet
Seventy on-site subsurface soil/sediment samples were collected at depths of 3
to 10 feet. The data for these samples are presented in Table 2-3.
Toxaphene, beta-BHC and 4,4'-DDT were the most prevalent pesticides, and were
2-8
,..
,. '
Chemical
1 .5-2.5 FEET (d)
Organics:
Aldrin
alpha-BHC
beta-BHC
delta·BHC
ganma-BHC
4 41 -DDD
4:4'-DDE
4,41 -DDT
Oieldrin
Endrin ketone
Heptachlor
Heptachlor epoxide
Toxaphene
Inorganics:
Copper
Lead
Zinc
TABLE 2·2
SUMMARY OF CHEMICALS IN ON-SITE SUBSURFACE SOIL
. (Organics: ug/kg, Inorganics: mg/kg)
Frequency of
Detection (a)
1/62
9/62
22/62
8/52
9/62
9/62
17/62
29/62
9/62
2/62
2/62
1/62 35/62
57/57
52/52
49/49
Mean
Sample
Size (b)
58
62 62
62
62
62
62
62
62
58
62
48 62
57
52
49
Arithmetic
Mean (c)
14
86
100
45
38
130
130
990
90
28
30
4.7
8,200
7.7
13
27
Range of Detected
Concentrations
130
. 24 1,600
10 1,600
12 · 890
11 · 510
44 -1,400
27 2,500
23 14,000
32 1,600
29 280
48 470
15
180 130,000
1.5 17.7
2 202
3.2 269
(a) The nunber of samples in which the chemical was detected divided by the total number
of samples analyzed.
(b) The number of samples used to calculate the mean. This nllTiber may be less than the
denominator of the frequency of detection, because non-detect samples with high detection
limits were not included in calculating the mean.
(c) Arithmetic mean concentrat;ons were calculated us;ng detected values and one half the
detect;on L;m;t of non-detects.
(d) Sample results from SD-1-1.5, SD-1-2.5, SD-2·1.5, SD-2-2.5, S0-3·1.5, S0·3·2.5,
S0-6·1.5, SD-8·1.5, so-8-2.5, so-9-2.5, S0-10-1.5, SD-10-2.5, SD-11-1.5, S0-11·2.5, SD-12·1.5, S0-12·2.5, S0-13·1.5, SD-13-2.5, S0-19·1.5, S0-19·2.5, S0-21·1.5, SD-21·2.5,
S0-10-2, SD-11,2, SD-12-2, and SD-14-2.
Sample results also from SS-46·2, SS-48·2, SS-49·2, SS-51-2, SS-57-2 through
SS·59·2, SS-61·2 through SS-67·2, SS-69·2, SS-71·2, SS-82·2, SS-90-2 through SS-93·02,
SS-98·2 through SS-101·2, SS-103·2, SS-105·2, SS-106-2, SS-109-2, SS-110·2, SS-112-2,
SS-116-2 through SS-119·2, SS-132·2, SS-131·2 (blind split of SS-101·2), and SS-133-2
(blind split of SS-63·2).
2-9
detected in 19/70, 19/70 and 16/70 samples, respectively. Once .again
toxaphene was present at the greatest concentrations (up to 445 mg/kg in
SS-6). All other pesticides (aldrin, heptachl.or epoxide, alpha-, delta-,
gamma-BHC, dieldrin, and methoxychlor) were detected infrequently (in less
than 6/70 samples) at concentrations less than 13.5 mg/kg. Two semivolatile
chemicals, bis(2-ethylhexyl)phthalate and 1,2,4-trichlorobenzene were detected
at concentrations of 68 and 250 ug/kg, respectively. The most prevalent
inorganic chemicals were copper, lead and zinc (frequencies of detection of
64/65, 58/58 and 47/47, respectively). Lead and zinc were present at
concentrations substantially lower than those found in the subsurface 1.2-2.5
foot, and the surface soil/sediment samples.
2.4 OFF-SITE SUBSURFACE SOILS/SEDIMENT
2.4.1 Depth Interval·l.5 to 3 Feet
Seven off-site subsurface soil/sediment samples were collected during Phase 3
and 4 of the RI sampling efforts. The data for off-site subsurface
soil/sediment at depths of 1.5 to 3 feet are summarized in Table 2-4. The
depth interval is such because one sample included·in this grouping, OSD-29 is
a sediment composite of 1.5 to 3 feet. This table presents the frequency of
detection, the sample population, the arithmetic mean, and the range of
detected concentrations. A total of six pesticides and three inorganics were
detected. 4,4'-DDT and toxaphene were the predominant pesticides (detected in
5/7 and 7/7 samples, respectively). Copper, lead and zinc were each detected
in 7/7 samples. The chemical present at the greatest concentration was
toxaphene (up to 36 mg/kg), all other pesticides were at levels below 13
mg/kg.
2.4.2 Depth Interval 3 to 10 Feet
Two off-site subsurface soil/sediment samples were collected at depths of 3 to
10 feet. These data are also presented in Table 2-4. Six pesticides and two
inorganic chemicals (copper and lead) were present in these samples. All of
the chemicals except for alpha-BHC and 4,4'-DDE were detected in both samples.
2-10
r:
· I
TABLE 2-3
SUMMARY OF CHEMICALS IN ON-SITE SUBSURFACE SOIL
(Organics: ug/kg, Inorganics: mg/kg)
Mean
Frequency of Sarrple Arithmetic
Chemical Detection (a) Size Cb) Mean (c)
3 to 10 FEET Cd)
----------------Organics:
Aldrin 6/70 70 260
alpha·BHC 6/70 70 350
beta-BHC 19/70 70 200
del ta-BHC 5/70 69 49
ganma-BHC 4/70 69 47
Bis(2-ethylhexyl)phthalate 3/9 3 62
4,4' ·ODD 10/70 70 720
4.,4' -ODE 10/70 70 260
4,4'-0DT 16/70 70 1,600
Dieldrin 6/70 70 490
Heptachlor 1/70 66 8.3
Heptachlor epoxide 1/70 63 4.8
Methoxychlor 2/70 63 50
Toxaphene 19/70 70 14,000
1,2,4-Trichlorobenzene 1/12 10 190
Jnorganics:
Al uni nun 12/12 12 11,000
Arsenic 10/12 12 4.7
Barium 11 /12 12 6.2
Berylliun 4/12 12 0.19
Cadmillll 2/12 12 0.39
Calciun 5/5 5 4,500
Chromiun 12/12 12 11
Cobalt 1/12 12 1. 1
Copper 64/65 65 6.9
Iron 11/11 11 11,000
Lead 58/58 58 4.6
Magnesium 11 /11 11 950
Manganese 12/12 12 6.6
Nickel 5/12 11 2.0
Potassiun 3/7 7 130
Selenium 2/11 9 0.38
Silver 3/12 12 6.7
Sodi1.n1 2/2 2 180
Thall h.rn 1/12 12 0.5
Vanadil.rn 10/12 12 18
Zinc 47/47 47 14
Range of Detected
Concentrations
44 13,500
11 12,000 11 4,100
1B 1,900
21 1,500
59 68
92 27,500
27 • 8,750
42 · 54,000
32 • 9,700
190
16
110 • 180
175 · 445,000
250
3.4 27,700
0.53 22.6
2.7 14.9
0.24 0.48
0.67 0.92
140 11,200
0.5 35.6
4. 1
0.49 27.5 515 74,500
1.8 13. 7
51.9 74,500
0.22 18.5
1.8 3
193 327
0.46 · 1.5 1.1 · 69.5
173 · 186
3.3
4.8 63.4
1.2 · 82.6
Ca) The nt.rrber of sarrples in which the chemical was detected divided by the total nl.lTber
of samples analyzed.
Cb) The nt.rrber of sarrples used to calculate the mean. This nunber may be less than the
denominator of the frequency of detection, because non-detect sa~les with high detection
limits were not included in calculating the mean.
(c) Arithmetic mean concentrations were calculated using detected values and one half the
detection limit of non-detects.
Cd) Sample results from: surface soil • SS-46·5, SS-48·5, SS-48-10, ss-49·5, SS·51·5, ss-57·5,
SS-58·5, SS-59·5, SS-61·5 through SS-67·5, SS-63·10 through SS-66-10, SS-69-5, SS-69·10,
SS-71·5 through SS-73·5, SS-72·10, SS-73·10, SS-76·5 through SS-79-5, SS-76-10,
ss-81·5 SS-82·5 SS-90·5 through SS-93·5 SS-91·10 ss-98·5 through SS-101·5 SS-98·10 ss-103·5, ss-105'.5, ss-106-5, ss-108·5 th~ough ss-1io-5, ss-108-10, ss-110-10: '
SS-112·5, SS-113·10, SS-116·5 through SS-119·5, SS-130·5 (blind split of SS-109·5) and
SS-135·5 (blind split of SS-71·5); ss-3, ss-5, SS-6, SS-114, SS-115, SS-117, and SS-119
(covered by 3 to 4 feet of soil/gravel); sediment -SD-10-5, SD-10-10, SD-11-5, SD-12-5,
SD-14·10, and SD-14·5.
2-11
Toxaphene was the pesticide with the highest detected concentration (4.2
mg/kg).
All eight chlorinated pesticides (alpha-, beta-BHC, 4,4'-DDD, 4,4'-DDE, 4,4'-
DDT, dieldrin, endrin, and toxaphene) detected in off-site subsurface soil
(combined depth intervals of 1.5 to 10 feet) were considered to be chemicals
of potential concern. Again, because there were no background subsurface
soil/sediment samples available, the surface soil/sediment background levels
presented in Table 2-1 were used as a comparison for inorganic chemicals. The
inorganic chemicals copper, lead and zinc were detected at concentrations
below those present in the background surface soil/sediment samples, and
therefore were not considered to be chemicals of potential concern.
2.5 GROUNDWATER
Groundwater samples were collected during the RI from one existing on-site
water supply well, new monitoring wells, and private residential wells and are
shown in Figure 2-2. Four background wells were designated by their location
upgradient of the site, one for the surficial aquifer (MW-lS) and three for
the second uppermost aquifer (MW-1D, MW-14D, and MW-15D). Background data for
groundwater was used in order to select chemicals of potential concern.
2.5.1 Surficial Aquifer
Six wells (MW-lS through MW-6S) were screened in the surficial aquifer on-
site. Six off-site monitoring wells were screened in the surficial aquifer
(MW-7S through MW-lOS, 12S, and 13S). Well MW-lS is located upgradient of the
site and thus was considered background. The off-site monitoring wells were
not analyzed for inorganic chemicals (which are not of concern with respect to
the site). As shown in Table 2-5, ten pesticides, two other organic and 15
inorganic chemicals were detected in the surficial monitoring wells. Alpha-,
beta-, delta-and gamma-BHC were each detected in ·G/11 monitoring wells.
Aldrin and dieldrin were present in 2/11 and 3/11 monitoring wells,
respectively. Other pesticides or their metabolites were present with the
following frequencies of detection: toxaphene (3/11) and endrin ketone
2-12
C
TABLE 2-4
SUMMARY OF CHEMICALS IN OFF-SITE SUBSURFACE SOIL
(Organics: ug/kg, Inorganics: mg/kg)
Mean
Frequency of Sample Arithmetic Range of Detected
Chemical Detection Ca) Size Cb) Mean Cc) Concentrations
1.5-3 FEET Cd)
Organics:
4,4'-DDD 2/7 7 710 230 4,600 4,4'-DDE 3/7 7 280 45 1,700
4,4•-00T 5/7 7 2,600 140 13,000
Dieldrin 2/7 6 83 110 320
Endrin 1/7 6 42 140 Toxaphene 7/7 7 10,000 790 36,000
lnorganics:
Copper 7/7 7 5.1 1.6 8
Lead 7/7 7 6.9 1.6 31.8 Zinc 7/7 7 8. 1 3.8 12.2
3-10 FEET Ce)
Organics:
alpha-BHC 1/2 2 8.5 12 beta-BHC 2/2 2 21 15.3 -26 4,4'-D0D 2/2 2 86 75.S -97 4,4'-DDE 1/2 2 30 so
4,4'-DDT 2/2 2 450 330 -560 Toxaphene 2/2 2 2,900 1,610 -4,200
Jnorganics:
Copper 2/2 2 4.3 2.9 • 5.7
Lead 2/2 2 15 12.5 -17.8
(a) The nl.l'IDer of sarrples in which the chemical was detected divided by the
total nl.lmer of sarrples analyzed.
Cb) The nl.l'IDer of saq:,les used to calculate the mean. This nllllber may be less
than the denominator of the frequency of detection, because non-detect
saq:,les with high detection limits were not included in calculating the mean.
Cc) Arithmetic mean concentrations were calculated using detected values and one
half the detection limit of non·detects.
(d) S-les results fran OSD-24-1.5, OSD-24-2.5, OSD-27-1.5, OSD-27-2.5, OSD-30-1.5,
OS0-30-2.5, and OS0-29.
(el S-les results fran OSD-28-4, OSD-28·5 and OSD-45-3 (blind split of OSD-28·4).
2-13
"' ' I-' ..,.
GS-02-2
S-02-1
USGS-02-3
........ ........
Figure 2-2
Groundwater Well Locations at the
Geigy Chemlcal Corporetlon SHe
Aberdeen, North Cerolna
Adapled from ERM -Soulheast 1991
I I
........
MW-7S
I -MW-8S
•
........ ........ ........ . ·..: -:::.:,---=_..~ PZ-1 • ....._ .........
•
MW-9S/
-,....... ............ --. . ........
MW-6S --. • •
0
_:·.'I>· .... ·, . .
. ....... MW-55 • ....._ -........
MW-128 -
·····~
- --&..,__, PR,peny Urw
♦-w•
PUP p_,_M.W.Procl.ocllW.-
MW-4S • i MW-4D
MW-10S
~DECONPMI
EZZ::I°""'
~TriPlld
-
~Fam.r W•IINIIIN I (Cone:. Pad CW,)
o.mc.t Aulamoliv• c..nr,g Servin
and Hou&. ; ••••••
MW-15D/;
W-14D /
\ /
I, f·\
ALLRED
PMP
~[1:@[[n)@[nfil
Environmental and Health Science
119109·1,
ra
(5/11). Bis-2-(ethylhexyl)phthalate was measured at a low concentration and
frequency of occurrence; this chemical is often present as a result of
laboratory contamination. 1, 2 ,4-Trichlorobenz.ene was measured at low
estimated concentrations. Both bis(2-ethylhexyl)phthalate and 1,2,4-
trichlorobenzene will be evaluated together with all of the pesticides
measured in these wells.
No organic chemicals were detected in five of the six off-site monitoring
wells. A to_tal of eight pesticides were detected in MW-lOS, located south of
the site. Beta-BHC was present at the highest concentration (25 ug/L). No
pesticides were detected in upgradient monitoring well MW-lS.
Inorganics were also measured in the wells screened in the surficial aquifer,
but insufficient background analyses are available to determine if some of
these inorganics are elevated with respect to upgradient concentrations.
Since concentrations of inorganics in on-site surface and subsurface soil were
not elevated with respect to background concentrations, these inorganics in
· groundwater are not likely to be site-related. Several inorganic chemicals
were eliminated using USEPA Region !V's two times background rule. The
remaining inorganic chemicals will be quantitatively evaluated if USEPA-
approved toxicity criteria are available.
2.5.2 On-Site Second Uppermost Aquifer
Two on-site wells were screened in the second uppermost aquifer (MW-4D and MW-
6D). Table· 2-6 presents this data. At this time, it is not apparent whether
the second uppermost aquifer is hydraulically connected to the surficial
aquifer. A thick subsurface clay layer exists within property boundaries
which is a potential barrier against downward migration. The extent of this
barrier beyond property boundaries is not known. No pesticides were measured
in this aquifer on-site. One organic chemical (trichloroethene) , and seven ,
inorganfc chemicals were detected in the on-site second uppermost aquifer
monitoring wells. Trichloroethene (TCE) was detected in both MW-4D and MW-6D
in the Phase 1 sampling, at concentrations of 200 and 11 ug/L, respectively.
Subsequent sampling of these wells in Phase 4 revealed similar concentrations
2-15
TABLE 2-5
SUMMARY OF .CHEMICALS IN ~ATER FROM SURFICIAL AQUIFER (a)
(Organics: ug/L, Inorganics: ug/L)
Chemical
Organics: --------* Aldrin * alpha-BHC * beta-BHC * delta-BHC * ganma-BHC * 4,4 1 -ODE * Dieldrin
* Endrin ketone
Mean
Frequency of Sample
Detection (b) Size (c)
2 / 11 11
6 I 11 11
6 I 11 11
6 I 11 11
6 I 11 11
1 / 11 9
3 I 11 11
5 / 11 11 * bis(2-Ethylhexyl)phthalate 1 / 5 5 * Heptachlor epoxide 1 / 11 11
• Toxaphene 3 I 11 11 * 1,2,4-Trichlorobenzene 2 / 5 2
lnorganics:
----------* AlLlllinum 5 / 5 5 * BariLITI 3 I 3 3 Cadmillll 2 / 5 5 * Calcium 5 / 5 5 Chromium 2 / 5 5 Copper 1 / 5 5 * Iron 3 / 5 5 * Magnesium 5 / 5 5 * Manganese 3 / 3 3 * Mercury 1 / 5 5 * Potassil.111 5 / 5 5 Selenium 3 / 5 5 SodiLITI 5 / 5 5 * Vanadiln 2 / 5 5 * Zinc 5 / 5 5
*=Chemical of Potential Concern
Arithmetic
Mean (d)
0.1
4.4
5.2
4.8
3.6
0.1
0.3
0.6
5.4
0.1
3.6
4.5
5,600
172
3.8
23,000
3.4
9.6
690
7,700
70
0.3
52,000
1.2
8,900
15
220
ND= Not detected (range of detection limits reported in parentheses).
Site-Specific Range of Detected Background
Concentrations Concentrations (e)
0.1 0.4 ND (<0.1 to <0.5)
1.0 36 ND (<0.5)
0.7 25 NO (<0.5)
0.1 29 ND (<0.5)
0.4 30 NO (<0.5)
0.2 ND (<0.1)
0.2 -2.0 NO (<0.1)
0.2 -4.0 ND (<0.1)
7 NO (<10)
0.3 NO ( <O. 05)
0.8 9.6 NO (<10)
4.0 -5.0 ND (<10)
46.3 17,100 171 • 172
78.6 284 ND (f)
5.3 7.6 NO (<4)
918 49,800 438
4.3 6.5 ND (<4.8)
23.9 NO (<12)
36.7 -3,290 550 -955
745 -18,000 NO (f)
44 -104 ND (f)
1.0 NO (<0.2)
1,010 160,000 706 -744 1.2 2.4 4.7
4,270 12,900 7,560 -8,150
15.4 38 NO (<13)
11.9 579 15.8 -19.7
(a) Samples results from MW-2S through MW-6S and phase 4 samples M2-7S through MW-10S, MW-12S and MW-13S.
(b) The nllllher of samples in which the contaminant was detected divided by the total nlJTlber of sarrples analyzed.
(c) The nL.DTiber of samples used to calculate the mean. "This nL.DTiber may be less than the denominator of the
frequency of detection, because non-detect sarrples with high detection limits were not included in calculating the mean.
(d) Arithmetic mean concentrations were calculated using detected values and one half the detection limit of non-detects.
(e) Background consists of groundwater sarrples MW-1S and its duplicate designated MW-7S in phase 1.
(f) Data rejected by QA/QC because chemical was detected in a laboratory blank at a similar concentration.
\
2-16
\
I.
TABLE 2-6
SUMMARY Of CHEMICALS IN ~ATER FROM SECOND UPPERMOST AQUIFER
Frequency of
Chemical Detection (c)
ON-SITE (a)
Organics: --------* Trichloroethene 2 I 2
lnorganics:
----------Aluninum 2 I 2
Cactnium 1 / 2
Calcium 2 I 2
Iron 2 I 2
Lead 1 / 2
Magnesiun 2 / 2
Manganese 1 / 1
Potassilln 1 / 2
Sodi lln 1 / 2
Zinc 2 I 2
Off-SITE (b)
Organics:
* alpha-BHC * beta-BHC * delta-BHC * gamna-BHC
• Dieldrin
• Endrin ketone
• 4-Methyl-2-pentanone
1 / 3
1 / 3
1 / 3
1 / 3
1 / 3
1 / 3
1 / 3
(Organics: ug/L, Inorganics: ug/l)
Mean Sample
Size Cd)
2
2
2
2
2 2
2
1
2
1
2
Arithmetic
Mean Ce)
104.5
1,932
4
2,710
1, 128.5
5
1,015
118
5n
3,930
34.8
16
6.6
4.5
11 0.3
0.4
2
Range of Detected
Concentrations
29 -180
214 -3,650
5.9
1,010 -4,410
76.9 -2,180 9.2
620 -1,410
118
869
2,780 5,070
32.4 -37.1
16
6.6
4.5
11 0.3
0.4
2
Site-Specific
Background Concentrations (f)
ND (<10)
7,620
ND (<4)
3,370
4,280
10.2
1,540
91.2
875
4,620
69.3
ND (<0.05)
ND (<0.05)
ND (<0.05)
ND (<0.05)
ND (<0.1)
ND (<0.1)
ND (<0.1)
• It is not known whether these chemicals are site-related however,
evaluated at the request of USEPA Region IV.
these chemicals will be
ND= Not detected (detection limit reported in parentheses).
Ca)
Cb)
(C)
(d)
Ce)
Cf)
lnorganics include saffllles from phase 1 (MW-4D and MW-60). Organics include additional samples from
phase 4 (HW-4D and MW-60).
Samples results from MW-11D, MW-14D and MW-15D.
The nlll'Der of salll)les in which the chemical was detected divided by the total nl.llDer of samples
analyzed. However, for on-site wells phase I and phase 11 data were collected. Because phase I and phase II saq>les were averaged, this frequency for on-site groundwater represents the nUITDer of wells
in which the chemical was detected divided by the total nunber of wells sampled.
The nlllber of samples used to calculate the mean. This nlll'ber may be less than the denominator of the
frequency of detection, because non-detect s~les with high detection limits were not included in
calculating the mean.
Arithmetic mean concentrations were calculated using detected values and one half the detection limit of
non-detects.
Background consists of groundwater S8f11Jles MW-1D, MW-14D, and MW-15D.
2-17
of 160 and 47 ug/L TCE for MW-4D and MW-6D, respectively. The average
concentration of the two sampling events is presented in Table 2-6. Seven
inorganics were detected in MW-4D (aluminum, ~admium, iron, lead, manganese,
sodium, zinc) while only two inorganics were detected in MW-6D (zinc and
aluminum). Several inorganics were detected in tne laboratory blanks
(arsenic, barium, calcium, iron, magnesium, ffianganese, potassium, sodium, and
selenium).
Concentrations of inorganics in these on-site wells were compared to those in
the upgradient well MW-1D which was also screened in the second uppermost
aquifer. All inorganics with the exception of cadmium detected in MW-4D and
MW-6D were less than two times the concentrations in background (MW-1D).
Cadmium was measured in MW-4D at 5.9 ug/L which is very close to the
analytical detection limit of 4 ug/L in MW-1D and was not above background in
on-site soils. Thus, based on a comparison to upgradient wells none of the
chemicals measured in the second uppermost aquifer directly beneath the site
appear to be above background concentrations.
Samples from two upgradient private wells, the Allred and Powder Metal Product
(PMP) wells, contained TCE at concentrations of 72 and 360 ug/L, respectively.
The 360 ug/1 upgradient concentration is higher than the maximum measured
concentration in the second uppermost aquifer directly within property
boundaries. Further characterization will be conducted to determine the
source and extent of TCE in this groundwater.
2.5.3 Off-Site Second Uppermost Aquifer
Three off-site monitoring wells were screened in the second uppermost aquifer
(MW-11D, MW-14D, and MW-15D). Monitoring well MW-11D was the only well
screened in the second uppermost aquifer which contained pesticides. As shown
in Table 2-6, six pesticides were detected in MW-11D. The pesticides,
alpha-, beta-, delta-, and gamma-BHC were present at concentrations of 16,
6.6, 4.5, and 11 ug/L, respectively. Dieldrin and endrin ketone were also
detected at concentrations of 0.28 and 0.36 ug/L, respectively. The wells
screened in the second uppermost aquifer were not analyzed for inorganic
2-18
chemicals (which are not of concern with respect to the site). .Monitoring
well MW-15D contained a trace amount of 4-methyl-2-pentanone (2 ug/L), which
was also qualified with a "J", indicating an e.stimated concentration.
2.6 SUMMARY
Table 2-7 summarizes the chemicals of potential concern selected for each
medium. As the table and the previous discussions indicate, a total of 18
pesticides have been detected at the site which are considered to be chemicals
of potential concern. Additionally, three semivolatile organics (benzoic
acid, bis(2-ethylhexyl)phthalate, and 1,2,4-trichlorobenzene) and one volatile
organic (trichloroethene) were selected as a chemicals of potential for
further evaluation in this risk assessment. Toxaphene, 4,4'-DDT (and its
metabolites) and beta-BHC were the pesticides detected most frequently in
samples across all media. The chemicals presented in Table 2-7 with available
toxicity criteria will be quantitatively evaluated in this Baseline RA for the
media from which potential exposure could occur ..
2-19
TABLE 2-7
SUMMARY OF CHEMICALS OF POTENTIAL CONCERN (a)
Chemical
Organics:
Aldrin
alpha-BHC
beta-BHC
delta-BHC
garnna-BHC
Benzoic acid
Bis(2-ethylhexyl)phthalate alpha-Chlordane
ganma-Chlordane 4,4'-DDD
4 4' -DOE
4:4 1 -DOT
Dieldrin
Endrin Endrin ketone Heptachlor
Heptachlor epoxide Methoxychlor
4-Methyl-2-pentanone
Toxaphene
1,2,4-Trichlorobenzene
Tri ch l oroethene
Inorganics:
Al1i11inun
BarillTI
Calcillll
Iron
Magnesil.lJI
Manganese
Mercury
Potassiun
Vanadil.111
Zinc
On-Site
Surface
Soil/
Sediment
X
X
X
X
X
X
X
X
X
X
X
X
X
Off-Site
Surface
Soil/
Sediment
X
X
X
X
X
On-Site
Subsurface
Soil/
Sediment
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
Off-Site
Subsurface
Soil/
Sediment
X
X
X
X
X
X
X
X
Surficial
Aquifer
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
(a) Chemicals presented in this table are potentially related to former on-site activity and are above background concentration.
Second
Uppermost
Aquifer Cb)
X
X
X
X
X
X
X
X
(b) It is assuned that these chemicals are site-related in the absence of further field data.
Additional investigation will be done to elucidate the source of pesticides in the second uppermost aquifer.
X = Measured in this medil.lTI.
2-20
3.0 TOXICITY ASSESSMENT
The general methodology for the classification of health effects and the
development of health effects criteria is described in Section 3.1 to provide
the analytical framework for the characterization of hwnan health impacts in
Section 5.0. In Section 3.2, the health effects criteria that will be used to
derive estimates of risk are presented and the toxicity of the chemicals of
potential concern is briefly discussed.
3.1 HEALTH EFFECTS CLASSIFICATION AND CRITERIA DEVELOPMENT
For risk assessment purposes, indiVidual chemicals are separated into two
categories of chemical toxicity depending on whether they exhibit principally
noncarcinogenic or carcinogenic effects. This distinction relates to the
currently held scientific opinion that the mechanism of action for each
category is different (USEPA 1991). For the purpose of assessing risks
associated with potential carcinogens, USEPA has adopted the scientific policy
position that a small nwnber of molecular events can evoke changes in a single
cell, or a small nwnber of cells, that can lead to twnor formation. This is
described as a non-threshold initiator mechanism, because 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 (USEPA 1991). Another
asswnption stemming from USEPA's science policy is that the dose-response
curve is linear at low doses. In reality this curve can take many shapes
depending on the exact biological mechanisms of action of a chemical. The
dose-response curve will especially vary if the chemical is behaving as a
cancer promotor rather than as an initiator with the net effect that the most
accurate shape may be indicative of a threshold or quasi-threshold for
response. In the case of chemicals exhibiting noncarcinogenic effects
however, it is believed that organisms have repair and detoxification
capabilities that must be exceeded by some critica~ concentration (threshold)
before the health effect is manifested (USEPA 1991). ~For example, an organ
can have a large nwnber of cells performing the same or similar functions that
3-1
must be significantly depl.eted before the effect on .the organ is seen. This
threshold view holds that a range of exposures from just above zero to some
finite value can be tolerated by the organism without·appreciable risk of
causing the disease (USEPA 1991).
3.1.1 Health Effects Criteria for Potential Carcinogens
For chemicals exhibiting potential carcinogenic effects, USEPA's Carcinogen
Assessment Group has estimated the excess lifetime cancer risks associated
with various levels of exposure to potential human carcinogens by developing
cancer slope factors and unit risks. Cancer slope factors are expressed in
terms of reciprocal dose, as units of (mg/kg-day)-1 . Unit risks are expressed
as either a reciprocal air concentration in units of (µg/m3)-1, or as a
drinking water unit risk, in units of (µg/L)-1. Because regulatory efforts
are generally geared to ·protect public health, including even the most
sensitive members of the population, the cancer slope factors and unit risks
are derived using very conservative assumptions (USEPA 1991).
Slope factors and unit risks are derived from the results of human
epidemiological studies or chronic animal bioassays. The animal studies
usually must be conducted using relatively high doses to detect possible
adverse effects. Because humans are expected to be exposed to doses lower
than those used in the animal studies, the data are adjusted by using
mathematical models. The data from animal studies are typically fitted to the
linearized multistage model to obtain a dose-response curve. The 95% upper
confidence limit slope of the dose-response curve is subjected to various
adjustments and an interspecies scaling factor is applied to derive the slope
factor or unit risk 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 slope factors or
unit risks (USEPA 1986). 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
3-2
l
I
limits on lifetime risk. Slope factors and unit risks based on human
epidemiological data are also derived us~ng 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 slope factor or unit risk, they
could be considerably lower.
When the upper bound cancer slope factor is multiplied by the lifetime chronic
average daily intake (CDI) of a potential carcinogen (in mg/kg/day), or the
unit risk is multiplied by the inhalation exposure concentration (IEC) of a
potential carcinogen (in mg/m3), the product is the upper bound lifetime
individual cancer risk (or maximum probability of contracting, not dying from,
cancer) associated with exposure at that dose. Again, the upper bound means
that the risk estimate is unlikely to be underestimated but it may very well
be overestimated. This is because of the inherent conservativeness in the
cancer slope factors and unit risks (i.e., they are upper bound estimates) and
because exposure assumptions used in risk assessments (including this one) are
also conservative. An individual risk level of one in one million (lxl0"6),
for example, represents an upper bound probability of 0.0001% that an
individual will develop cancer over his or her lifetime as a result of
lifetime exposure to a potential carcinogen. By comparison, the average
American's background risk of developing cancer is approximately one in three
(American Cancer Society 1991), i.e., 33% or 330,000 times higher than a one
in one million risk level.
USEPA assigns weight-of-evidence classifications to potential carcinogens.
Under this system, chemicals are classified as either Group A, Group Bl, Group
B2, Group C, Group D, or Group E. The weight-of-evidence classification is an
attempt to determine the likelihood that an agent is a human carcinogen; the
classification thus affects the estimation of potential health risks although
it does not impact numerical potency. Three major factors are considered in
characterizing the overall weight of evidence for carcinogenicity: (1) the
quality of the evidence from human studies and (2) the quality of evidence
3-3
from animal studies, which. are combined into a characterization of the overall
weight of evidence for human carcinogenicity, and then (3) other supportive
information which is assessed to determine whether the overall weight of
evidence should be modified. USEPA's (1991) final classification of the
overall evidence has five categories:
Group A chemicals (human carcinogens) are agents for which there is
sufficient evidence to support the causal association between exposure
to the agents in humans and cancer.
Groups Bl and B2 chemicals (probable human carcinogens) are agents for
which there is limited (Bl) or inadequate (B2) evidence of
carcinogenicity from human studies. Group B2 agents also have
sufficient evidence of carcinogenicity from animal studies.
"Group C chemicals (possible human carcinogens) are agents for which
there is limited evidence of carcinogenicity in animals.
Group D chemicals (not classified 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-carcinogenicity in humans) are agents
for which there is no evidence of carcinogenicity in adequate human or
animal studies.
The cancer risks developed in this report are all accompanied by this weight-
of-evidence classification. The reader should keep in mind that regardless of
potency, there are important qualitative differences between chemicals which
have been demonstrated to be human carcinogens and those chemicals for which
the evidence is limited. For example, the risks estimated to be associated
with exposures to Group A chemicals are characterized by less uncertainty than
risks estimated for Group B2 chemicals.
3.1.2 Health Effects Criteria for Noncarcinogens
Health criteria for chemicals exhibiting noncarcinogenic effects are generally
developed using verified risk reference doses (RfDs) and reference
concentrations (RfCs). These are developed by USEPA's RfD/RfC Work Group
(USEPA 1991) or are obtained from USEPA's Health Effects Assessment Summary
3-4
Table (HEAST). The RfD is_ expressed in uni ts of dose, mg/kg-day, while the
RfC is expressed in concentration units, mg/m3. RfDs and RfCs are usually
derived either from human studies involving work-place exposures or from
animal studies, and are adjusted using uncertainty factors. The RfD or RfC is
·an estimate (with uncertainty spanning perhaps an order of magnitude) of the
daily exposure to the human population (including sensitive subpopulations)
that is likely to be without an appreciable risk of deleterious effects.during
a lifetime (USEPA 1991). The RfD/RfC is used as a reference.point for gauging
the potential effects of other exposures. Usually, exposures that are less
than the RfD/RfC are not likely to be associated with adverse health effects.
As the frequency and/or magnitude of the exposures exceeding the RfD/RfC
increase, the probability of adverse effects in a human population increases.
However, it should not be categorically concluded that all doses below the
· RfD/RfC are "acceptable" (or will be risk-free) and that all doses in excess
of the RfD/RfC are "unacceptable" (or will result in adverse effects).
Subchronic RfD's are developed by USEPA's Environmental Criteria and
Assessment Office (ECAO) and are used to characterize potential
noncarcinogenic effects associated with short-term exposures (2 weeks to 7
years as defined by USEPA (1989a). The subchronic RfD's and RfC's are
developed similar to chronic RfDs.
The RfDs/RfCs are derived using uncertainty factors which reflect scientific
judgement regarding the various types of data used to estimate the RfD/RfC.
Uncertainty factors, generally 10-fold factors, are intended to account for:
(1) the variation in sensitivity among members of the human population;
(2) the uncertainty in extrapolating animal data to the case of humans;
(3) the uncertainty in extrapolating from data obtained in a study that
is less-than-lifetime exposure;
(4) the uncertainty in using lowest-observable-adverse-effect level
(LOAEL) data rather than no-observable-adverse-effect level (NOAEL)
data; and
3-5
(5) the inability of any single study to adequately address all possible
adverse outcomes in humans (USEPA 1991).
When taken together, these uncertainty factors may confer an extra margin of
safety of up to a factor of 10,000.
3.2 HEALTH EFFECTS CRITERIA FOR INDIVIDUAL CHEMICALS OF POTENTIAL CONCERN
Tables 3-1 and 3-2 present chronic oral and inhalation health effects criteria
(RfDs/slope factors, and RfCs/unit risks), respectively, for the chemicals of
potential concern to be quantitatively evaluated in this_ assessment. The
toxicological properties of the chemicals of potential concern and the
toxicological basis of the health effects criteria listed in Tables 3.1 and
3.2 are discussed in below.
No health effects criteria were available for delta-BHC, therefore this
chemical could not be evaluated in the Baseline RA. In addition, no
inhalation health effects criteria have been developed for gamma-BHC, 4,4'-
DDD, 4,4'-DDE, and benzoic acid. Therefore, these chemicals could not be
quantitatively evaluated in the on-site trespasser, the off-site nearby
merchant, the off-site nearby resident, or the on-site hypothetical future
merchant scenarios of this risk assessment.
Qualitative toxicity summaries for these chemicals are presented below. The
data which are discussed below were derived from animal and occupational
health studies in which the doses of pesticides were very high and contact was
often long-term. An adverse effect under these conditions should not be
construed to occur at the trace levels found at the site.
There is substantial uncertainty surrounding the carcinogenicity of the
organochlorine pesticides and its extrapolation to humans. This uncertainty
is due to the preponderance of mouse liver tumors, lack of DNA reactivity,.
negative human epidemiologic evidence, contribution of benign tumors, and
conclusions related to mechanism of action.
3-6
...,
• -..J
11-Mar-92 -ORALTOX.WK1
.TABLE 3-1
ORAL TOXICITY CRITERIA FOR CHEMICALS OF POTENTIAL CONCERN (a)
Chronic RfD Subchronic RfD Target Organ/ Slope
(mg/kg-day) (mg/kg-day) Critical Factor (SF) Target
Chemical [Uncertainty Factor](b) [Uncertainty Factor](b) Effect (bl Source (mg/kg-day)-1 Organ(c)
Organic Chemicals:
-----------------Aldrin 3E-05 11000) 3E-05 11000) liver IRIS, HEAST 1. 7E+D1 Liver alpha-8HC 6.3E+OO Liver beta-BHC 1.BE+OO liver delta-BHC
ganma-BHC 3E-04 11000] 3E-03 1100) L iver/lddney IRIS, HEAST 1.3E+OO (e) liver Benzoic acid 4E+OO 11 I 4E+OO 11 l Malaise IRIS, HEAST BisC2-ethylhexyl) 2E-02 11000] 2E-02 11000) liver IRIS, HEAST 1.4E-02 Liver
phthalate
alpha-Chlordane 6E-05 11000] 6E-05 [1000) Liver IRIS, HEAST 1.3E+OO liver ganma-Chlordane 6E-05 [1000] 6E-05 11000) Liver IRIS, HEAST 1.3E+OO Liver 4,4' -DOD 2.4E-01 Liver 4,4'-DDE 3.4E-01 liver 4,4'-DDT SE-04 [100] SE-04 [100] liver IRIS, HEAST 3.4E-01 Liver
Dieldrin SE-05 [100] SE-05 [100] liver IRIS, HEAST 1.6E+01 Liver 4-Methyl-2-pentenone SE-02 11000) SE-01 11001 Liver/kidney HEAST, HEAST
Toxaphene 1.1E+OO Liver 1,2,4-Trichlorobenzene lE-03 11000] lE-02 1100) liver HEAST, HEAST
Trichloroethene 7.35E-03 11000] liver HA 1987 1.1E-02 liver
Inorganic" Chemicals:
-------------------Baril.In 7E-02 [3] SE-02 [100] Cardiovascular IRIS, HEAST Manganese 1E-01 [1 l 1 E-01 [1 l CNS IRIS, HEAST
Mercury 3E-04 11000] 3E-04 [1000] Kidney HEAST, HEAST
Vanadilln 7E 0 03 1100] 7E-03 1100] liver, kidney HEAST, HEAST
Zinc 2E-01 110] 2E-01 110] Anemia HEAST, HEAST ,__
(a) The following chemicals are not presented because they lack toxicity criteria: alllninlln, calcilln, endrin ketone, heptachlor
epoxide, iron, ·magnesil.111 and potassiun.
Cb) Uncertainty factors used to develop reference doses generally consist of m.iltiples of 10, with each factor
representing a specific area of uncertainty in the data available. The standard uncertainty factors include the following:
A 10-fold factor to account for the variation in sensitivity among the ment>ers of the hunan population; - A 10-fold factor to account for the uncertainty in extrapolation animal data to the case of hllll8ns; - A 10-fold factor to account for uncertainty in extrapolating from less than chronic NOAEls to chronic NOAELs; and
- A 10-fold factor to account for the uncertainty in extrapolating from LOAELs to NOAELs.
(c) A target organ is the organ most sensitive to a chemical's toxic effect. RfD's are based on toxic effects in
the target organ. If an RfD was based on a study in which a target organ was not identified, an organ or system known to
be affected by the chemical is listed. ·
(d) EPA Weight of Evidence for Carcinogenic Effects: [Al = Hunan carcinogen based on adequate evidence from hllll8n
studies; [821 = Probable hunan carcinogen based on inadequate evidence from hunan studies and adequate evidence
from animal studies; [C] = Possible hunan carcinogen based on limited evidence from animal studies in the
absence of hunan studies; [D] = Not classified as to hllll8n carcinogenicity; and CE] = Evidence of noncarcinogenicity.
(e) Under review by CRAVE workgroup.
NOTE: IRIS
HEAST
HA
= Integrated Risk Information System, January 1992.
Health Effects Assessment Sunnary Tables, Annual 1991.
Health Advisory
~ No information available.
\Jeight-
of-Evidence
Classification(d) Source
82 IRIS
82 IRIS
C IRIS
0
B2/C HEAST
82 IRIS
B2 IRIS
B2 IRIS
B2 IRIS
B2 IRIS
82 IRIS
B2 IRIS
B2 IRIS
0 IRIS
B2 IRIS
0 IRIS
0
0 IRIS 0 IRIS
0
w
' 00
11-Mar-92 -INHALTOX
TABLE 3-2
INHALATION TOXICITY CRITERIA FOR CHEMICALS Of POTENTIAL CONCERN (a)
Chemical
Chronic and
Subchronic
RfO
(mg/m3)
Chronic
Inhalation
RfO (mg/kg-day)
[Uncertainty
Factor] (b)
Subchronic
Inhalation
RfD (mg/kg-day)
[Uncertainty
Factor] (b) Target
Organ (c) Source
Unit Risk
(ug/m3)-1
Slope
Factor (d)
(mg/kg/day)-1
Organic Chemicals:
Aldrin
alpha-BHC
beta-BHC
delta-BHC
ganma-BHC
Benzoic acid
Bis(2-ethylhexyl)
phthlate
alpha Chlordane
ganma Chlordane
4,41 -D00 4 4'-DDE
4
1
4'-DDT
oietdrin
3E-03 [1000] 3E-02 [1001 Liver
4.90E-03
1.BOE-03
5.30E-04
IRIS
3.70E-04 3.70E-04
9. 70E-05
4.60E-03
3.20E-04
HEAST
1. 7E+01
6.3E+OO
1.8E+OO
1.3E+OO
1.3E+OO
3.4E-01 1.6E+01
1. 1E+OO Toxaphene
1,2,4-Trichlorobenzene
Trichloroethene IRIS 1. 70E-06 1.?0E-02 Cf)
Inorganic Chemicals:
Bariun
Managanese
Mercury
Venadiun
Zinc
4E-04· 4E-04
3E-04: 3E·04
1.1E-04 [9001
8.6E-05 [301 Respiratory
Neurotox.
HEAST
HEAST
(a) The following chemicals are not presented because they lack toxicity criteria: all111inl111, calcillJI, endrin ketone, heptachlor epoxide, iron, magnesillJI, and potassillJI.
(b) Uncertainty factors used to develop reference doses generally consist of multiples of 10, with each factor
representing a specific area of uncertainty in the data available. The standard uncertainty factors include the following:
A 10-fold factor to account for the variation in sensitivity among the members of the hllMn population;
A 10-fold factor to account for the uncertainty in extrapolation animal data to the case of hLmans;
- A 10-fold factor to account for uncertainty in extrapolating from less than chronic NOAELs to chronic NOAELs; and - A 10-fold factor to account for the uncertainty in extrapolating from LOAELs to NOAEls.
(c) A target organ is the organ most sensitive to a chemical's tOxic effect. RfD's are based on toxic effects in
the target organ. If an RfD was based on a study in which a target organ was not identified, an organ or system known to be affected by the chemical is listed.
(d) The slope factor was calculated from the cancer unit risk using standard default parameters of 70 kg body weight and a ventilation rate of 20 m3/day.
(e) EPA Weight of Evidence for Carcinogenic Effects: (A] = Hllllan carcinogen based on adequate evidence from hunan
studies; [82] = Probable hllllan carcinogen based on inadequate evidence from human studies and adequate evidence
from animal studies; (CJ = Possible hunan carcinogen based on limited evidence from animal studies in the
absence of human studies; (DJ = Not classified as to hunan carcinogenicity; and CE] = Evidence of noncarcinogenicity. Cf) Based on a metabolized dose.
NOTE: IRIS = Integrated Risk Information System, January 1992.
HEAST = Health Effects Assessment St.mnary Tables, Annual 1991.
= No information available,
We ght-
of-Ev dence (e)
Class fication
B2 82
C
0
82
B2
82
82
B2
82
82
0
82
0
0
Source
of Unit
Risk
IRIS
IRIS
IRIS
IRIS
IRIS
IRIS
IRIS
IRIS
IRIS
IRIS
IRIS
IRIS
IRIS
IRIS
IRIS
ORGANIC CHEMICALS OF POTEN.TIAL CONCERN
3.2.1 Aldrin
USEPA (1991) has classified aldrin as a group B2 agent (probable human
carcinogen) and has developed an oral cancer slope factor of l.70xlo•1
(mg/kg/day)-1 based on the increased incidence of liver carcinoma observed in
male and female C3H mice (Davis 1965, Epstein 1975) and in male B6C3Fl mice
(NCI 1978). USEPA (1991) has also derived an inhalation cancer unit risk of
4.9xl0-3 (ug/m3 )-1 , using the same critical studies and route to route
extrapolation. USEPA (1991) derived a chronic and subchronic oral reference
dose (RfD) for aldrin of 3.0xlo-s mg/kg/day based on a study in which rats
were fed aldrin for 2 years and displayed liver lesions at dose levels of
0.025 mg/kg/day (0.5 ppm) and greater (Fitzhugh et al. 1964). An uncertainty
factor of 1,000 was used to calculate the oral RfD.
Aldrin is absorbed following inhalation exposure; between 20-50% of the
inhaled vapor is absorbed and retained (Beyermann and Eckrich 1973, Shell
1984). Absorption of the aldrin in the pure state or dissolved in a suitable
vehicle also occurs following ingestion (Farb et al. 1973, Heath and Vandekar
1964, Hunter and Robinson 1967, 1969, Iatropoulos et al. 1975) and dermal
exposure (Feldmann and Maibach 1974, Sundaram et al. 1978a,b). It is
metabolically converted to dieldrin in fatty tissues (ACGIH 1986) and these
two insecticides are considered to have similar chemical and toxic effects
(USEPA 1988). Acute symptoms of aldrin intoxication in humans and animals
following ingestion or inhalation of high levels have included CNS stimulation
manifested primarily as hyperexcitability, muscle twitching, convulsions, and
depression (Borgmann et al. 1952a,b, Hayes 1982, Hodge et al. 1967, Hoogendam
et al. 1962, Jager 1970). Experimental studies indicate that dogs exposed for
longer periods of time to levels as low as 1 mg/kg aldrin developed hepa-tic
and renal toxicity (Fitzhugh et al. 1964, Treon and Cleveland 1955, Walker et
al. 1969). Rats fed aldrin for 2 years developed hepatic lesions and
nephritis at doses of 0.5 and 50 ppm, respectively (Fitzhugh et al. 1964).
3-9
Aldrin produced fetotoxic and/or teratogenic effects in hamsters fed a single
oral dose of 50 mg/kg (approximately 84 ppm) and in mice fed a single oral
dose of 25 mg/kg (approximately 6 ppm) (Ottolenghi et·al. 1974). Aldrin
produced marked effects on fertility, gestation, viability, and lactation in
mice given 25 mg/kg/day in a six-generation study (Deichmann 1972). Aldrin
produces chromosomal aberrations in mouse, rat, and human cells (Georgian
1974) and unscheduled DNA synthesis in rats (Probst et al. 1981) and humans
(Rocchi et al. 1980). Chronic oral exposure to aldrin has produced an
increase in hepatocellular tumors in mice (Davis 1965, Epstein 1975, NCI
1978). In contrast, chronic feeding studies with aldrin in rats indicate that
exposure was associated with nonneoplastic changes in the liver (NCI 1978,
Fitzhugh et al. 1964).
3.2.2 Alpha-, Beta-, and Delta-Isomers of Benzene Hexachloride (BHC)
USEPA (1991) has classified alpha-BHC as a Group B2--Probable Human
Carcinogen, beta-BHC as a Group C--Possible Human Carcinogen, and delta-BHC as
not classifiable as to human carcinogenicity. An oral cancer slope factor of
6.3 (mg/kg/day)·1 was derived for alpha-BHC based on an increased incidence of
liver tumors in mice exposed to alpha-BHC in the diet for 24 weeks (Ito et al.
1973, USEPA 1991). An oral cancer slope factor of 1.8 (mg/kg/day)·1 was
derived for beta-BHC based on increases in benign liver tumors in mice fed
beta-BHC in the diet (Thorpe and Walker 1973, USEPA 1991). The inhalation
cancer unit risks for these isomers were derived using the same critical oral
studies and route-to-route extrapolation [l.8xlo·3 and 5.3x10"4 (ug/m3)-1 for
alpha-and beta-BHC, respectively] (USEPA 1991).
The alpha-, beta-, and delta-isomers are three of the eight isomers of
hexachlorocyclohexane (HCCH) [also known as benzene hexachloride (BHC)] and
are constituents of technical-grade BHC, which is approximately 40-45% gamma,
20-22% delta, 18-22% alpha, 4% beta, 1% epsilon and inerts, and 10%
heptachlorocyclohexane by weight (Hooker Chemical Corporation 1969, IARC
1979). Human and animal data indicate that the alpha-, beta-, and gamma-
3-10
,
isomers are absorbed follo~ing oral and inhalation exposure (Baumann et al.
1980, Czegledi-Janko and Avar 1970; Kashyap 1986, Nigam et al. 1986, Saxena et
al. 1980, Saxena et al. 1981a, Saxena et al. 1981b, Albro and Thomas 1974).
Absorption following ingestion has been reported to be greater than 90% for
these isomers (Albro and Thomas 1974). In animals, acute oral exposure to
beta-BHC has caused renal effects (Srinivasan et al. 1984) while subchronic
oral exposure to beta-BHC has caused_hematological, neurological, and
reproductive effects and death (Van Velsen et al. 1986, Muller et al. 1981).
Cardiovascular, immunological, and neurological effects have been observed in
workers occupationally exposed to technical-grade BHC (Kashyap 1986). In
animals, long-term oral exposure to alpha-, beta-, and technical-grade BHC has
resulted in hepatic and renal effects (Ito et al. 1973, Ito et al. 1975,
Fitzhugh et al. 1950, Van Velsen et al. 1986). It appears that delta-BHC is
not as toxic to the liver as are other isomers. No liver effects were
observed in rats exposed to 50 mg/kg/day in the diet for 24 or 48 weeks (Ito
et al. 1975) or in mice fed 65 mg/kg/day in the diet for 24 weeks (Ito et al.
1973). No other studies regarding the toxicity of delta-BHC were located.
Oral exposure to technical-grade BHC and alpha-BHC has been reported to induce
dominant lethal mutations in mice and to produce mitotic disturbances in rats,
respectively (Lakkad et al. 1982, Hitachi et al. 1975). Hepatocellular
carcinomas have been observed in mice and rats orally exposed to alpha-and
beta-BHC (Ito et al. 1973, Ito et al. 1975, Thorpe and Walker 1973).
3.2.3 Gamma-BHC
USEPA (1991b) has classified gamma-BHC in group B2-C (Probable/Possible Human
Carcinogen), however this weight of evidence is currently under review
byUSEPA. USEPA (1991b) estimated an oral cancer slope factor for gamma-BHC of
1.3 (mg/kg/day)-1 based on the incidence of hepatocellular carcinomas observed
in mice administered gamma-BHC in their diet (Thorpe and Walker 1973).
Chronic and subchronic oral reference doses (RfD) of 3.0xlo-4 and 3.0xlo-3
mg/kg/day have been derived by USEPA (199la,b) based on an unpublished study
in which rats were administered gamma-BHC in their diet for 12 weeks (Zoecon
3-11
•
Corporation 1983). In this study liver and kidney toxicity were observed at
20 ppm (1.55 mg/kg/day) but not at 4 ppm (0.3 mg/kg/day). Uncertainty factors
of 1,000 and 100 were used to derive the chronic and subchronic RfD's,
respectively.
Gamma-Benzene Hexachloride (BHC), otherwise known as gamma-
hexachlorocyclohexane (HCCH) is readily absorbed by humans and animals
following oral and dermal exposures (USEPA 1985). Turner and Shanks (1980)
showed that in male rats approximately 48% of an oral dose of gamma-BHC
appeared in the blood 30 minutes following administration. Humans acutely
exposed to gamma-BHC via inhalation or topical application have exhibited
adverse hematological effects (Morgan et al. 1980, Vodopick 1975). Seizures
and convulsions have been observed in individuals who have acutely ingested or
applied high levels of gamma-BHC to their skin (Davies et al. 1983, Matsuoka
1981). In animals, the major toxic effects associated with acute and longer-
term oral exposures to gamma-BHC include immunosuppression (Desi et al. 1978,
Dewan et al. 1980), central nervous system effects (Tilson et al. 1987), and
adverse kidney and liver effects (Fitzhugh et al. 1950). Chronic occupational
exposures to gamma-BHC have resulted in hematological abnormalities (Samuels
and Milby 1971). Various reproductive effects from exposure to gamma-BHC have
been demonstrated in rodents (Shivanandappa and Krishnakumari 1982).
Hepatocellular carcinomas have been observed in mice exposed to gamma-BHC in
the diet (Thorpe and Walker 1973, Wolff et al. 1987).
3.2.4 Benzoic Acid
Benzoic acid has been approved for food use by the Food and Drug
Administration and is considered a "generally recognized as safe" (GRAS) food
additive (Opdyke 1979). The Joint FAO/WHO Expert Committee on Food Additives
(1974) has previously estimated an acceptable daily intake (ADI) for benzoic
acid by ingestion of up to 5 mg/kg. The USEPA has determined an oral RfD of
4 mg/kg/day for both chronic (USEPA 1991a) and subchronic (USEPA 1991b)
exposure to benzoic acid based on a no-observed-adverse-effect level (NOAEL)
3-12
of 312 mg/day for irritation and malaise in humans. An uncertainty factor of
1 was used in calculating the oral RfD. No inhalation health criteria have
been developed by USEPA.
Benzoic acid is absorbed following both oral and dermal exposure (Opdyke
1979). Large oral doses of benzoic acid produce gastric pain, nausea, and
vomiting in humans (Gosselin et al. 1984). The lowest reported oral lethal
dose in humans is 500 mg/kg body weight (Opdyke 1979). In experimental
studies with cats, oral benzoic acid doses of 0.13 to 0.30 g/kg body weight
given daily for 1 to 30 days induced central nervous system disturbances;
longer-term feeding of benzoic acid at daily doses of 0.2 g/kg body weight
induced liver damage (Opdyke 1979). One report indicated that benzoic acid
vapors are highly toxic by inhalation (Sax 1984); however, this report
provided no data relating to exposure conditions and doses. Although benzoic
acid itself has not been reported to be teratogenic, experimental animals
treated with benzoic acid have demonstrated increased sensitivity to the
teratogenic effects of salicylic acid and aspirin (Opdyke 1979). Benzoic acid
has tested negative for mutagenic activity in a number of assay systems. No
reports were available regarding the carcinogenic potential of this compound.
3.2.5 Bis(2-ethylhexyl)phthalate
DEHP has been classified in Group B2--Probable Human Carcinogen (USEPA 1991a).
USEPA (1991a) calculated an oral cancer slope factor for DEHP of l.4xlo·2
(mg/kg/day)"1 based on·data from the NTP (1982) study in which liver tumors
were noted in mice. USEPA has recommended an oral reference dose (RfD) for
DEHP of 2xl0"2 mg/kg/day for both chronic (USEPA 1991a) and subchronic (USEPA
1991b) exposures 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 the diet for 1 year; an uncertainty factor of 1,000 _was used to
develop both RfDs.
Bis(2-ethylhexyl)phthalate, also known as di-ethylhexyl phthalate (DEHP), is
3-13
readily absorbed following oral or inhalation exposure (USEPA 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,USEPA 1980, Carpenter et al. 1953). Reduced fetal weight
and increased number of resorptions have been observed in rats exposed orally
to DEHP (USEPA 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).
3.2.6 Chlordane
USEPA (1991) classified chlordane as a Group B2 agent (Probable Human
Carcinogen). This weight of evidence applies to those substances for which
there is sufficient evidence of carcinogenicity in animals and inadequate
evidence of carcinogenicity in humans. USEPA (1991) calculated an oral cancer
slope factor of 1.3 (mg/kg/day)·1 based on feeding studies conducted in mice
by NCI (1977) and Velsicol Chemical Corp (1973). In these studies, a·
significant increase in hepatocellular carcinomas was observed. An inhalation
unit risk of 3.7xl0"4 (ug/m3)·1 was also derived by USEPA (1991) using these
same studies and route-to-route extrapolation. USEPA (1991a) also reported a
chronic and subchronic (USEPA 1991b) oral reference dose (RfD) of
6x10-5 mg/kg/day based on a 30-month rat feeding study in which hepatic
effects were observed (Velsicol 1983). An uncertainty factor of 1,000 was
used to derive the RfD's.
Chlordane is absorbed following oral and inhalation exposures. The principal
toxic effects in humans following acute and chronic exposures to chlordane
include CNS excitation and blood dyscrasias (USEPA 1985). In animals exposed
acutely or chronically to chlordane, toxic effects include CNS excitation,
alteration of liver function, increased liver weight, and histopathologic.al
damage to the liver and other organs (USEPA 1985, Yelsicol 1983).
Intraperitoneal injection of female mice
their fertility. An NCI (1977) bioassay
3-14
with chlordan~ significantly reduced
~
revealed a highly significant dose-
-
I
'
I . ,
related increase in the incidence of hepatocellular carcinomas in male and
female B6C3Fl hybrid mice exposed to technical grade chlordane in their diet
for 80 weeks. Infante et al. (1978) reported on five ·cases of neuroblastoma
in chlordane with pre-and/or postnatal exposure to chlordane and heptachlor.
The authors also noted three cases of acute leukemia in individuals with a
prior history of exposure to technical grade chlordane. However, these
individuals had also been exposed to other chemical agents.
3.2.7 DDD, DDE, DDT
DDD, DDE, and DDT are classified _by USEPA's Carcinogen .Assessment Group in
Group B2 (Probable Human Carcinogen) based on inadequate evidence of
carcinogenicity from human studies and sufficient evidence of carcinogenicity
from animal studies (USEPA 1991). USEPA (1991) developed an oral cancer slope
factor for DDT of 0.34 (mg/kg/day)·1 based on the geometric mean of a number
of carcinogenicity studies. An inhalation cancer unit risk of 9.7xio·5
(ug/m3)·1 was also calculated from the oral data using route-to-route
extrapolation. USEPA (1991) also developed a chronic and subchronic oral RfD
for DDT of 5xl0"4 mg/kg/day based on a study in which liver lesions were
observed in rats fed 5 ppm but not in those fed 1 ppm (0.05 mg/kg/day) DDT for
27 weeks (Laug et al. 1950); an uncertainty factor of 100 was used to derive
the RfD. USEPA (1991) has reported an oral cancer slope factor of
0.24 (mg/kg/day)·1 for DDD based on a study in which an increased incidence of
lung tumors in males and lung and liver tumors in females was observed in mice
fed 250 ppm (TWA) DDD for 13 weeks (Tomatis et al. 1974). USEPA (1991) has
reported an oral cancer slope factor of 0.34 (mg/kg/day)·1 for DDE based on
feeding studies that reported increased incidences of hepatomas in hamsters
(Rossi et al. 1983) and in CF-1 mice (Tomatis et al. 1974), and an increased
incidence of hepatocellular carcinomas in B6C3F1 mice (NCI 1978).
DDT is absorbed by humans and experimental animals from the gastrointestinal
tract (USEPA 1984, 1980). Jenson et al. (1957) reported that 95% of ingested
DDT in rats is absorbed from the gastrointestinal tract. Absorption of DDT
3-15
through the skin is minima.l (USEPA 1980). In humans, DDT and its metabolites,
DOD and DOE are stored primarily in adipose tissue; storage of DDT in human
tissues can last up to 20 years (NIOSH 1978). Acute oral exposure to DDT in
humans and animals may cause dizziness, confusion, tremors, convulsions, and
paresthesia of the extremities. Allergic reactions in humans·following dermal
exposure to DDT have also been reported (USEPA 1980). Long-term occupational
exposure to DDT results in increased activity in hepatic _microsomal enzymes,
increased serum concentrations of LDH, SGOT and cholesterol, _decreased serum
concentrations of creatinine phosphokinase, increased blood pressure, and
increased frequency of miscarriages (NIOSH 1978). Liver effects, neurological
effects, immunosuppression, reduced fertility, embryotoxicity, and
fetotoxicity have also been reported in animals following subchronic and
chronic exposure to DDT (Laug et al. 1950, NIOSH 1978, McLachlan and
Dixon 1972, Schmidt 1973). DDT has been shown to be carcinogenic in mice and
rats at several dose levels or dosage regimens. The principal site of action
is the liver, but an increased incidence of tumors of the lung and lymphatic
system have also been reported in several investigations (NIOSH 1978, Tomatis
et al. 1974, NCI 1978). In animals, ODD. and ODE are typically less toxic and
than DDT. Exposure to ODD can produce lethargy and convulsions, although
studies reveal that this occurs less frequently than DDT exposure (Gosselin et
al. 1984). Exposure to DOD dust is irritating to the eyes, nose and throat;
ingestion causes vomiting and delayed symptoms similar to those caused
following ingestion of DDT (Weiss 1986). Symptoms of dermal exposure to DOD
include convulsions, excitement and reduced seizure threshold (RTECS 1987).
There is evidence to suggest that DOD is mutagenic and tumorigenic inducing
thorax, respiratory, liver and thyroid tumors in rodents (RTECS 1987). DDE
has been shown to cause DNA inhibition (RTECS 1987).
3.2.8 Dieldrin
USEPA has classified dieldrin in Group B2 (Probable Human Carcinogen) based on
inadequate evidence of carcinogenicity from human studies and sufficient
evidence of carcinogenicity from animal studies (USEPA 1991). USEPA (1991)
3-16
I.
reported an oral cancer sl.ope factor of 1. 6xl01 (mg/kg/day) "1 based on several
studies in which hepatocellular carcinomas were observed in mice administered
dieldrin in the diet (Walker et al. 1972, Thorpe and Walker 1973, NCI 1978,
Tennekes et al. 1981). An inhalation cancer unit risk of 4.6xlo·3 (ug/m3)·1,
has also been developed by USEPA (1991), based on route to route extrapolation
from the dietary studies used to derive the oral slope factor. USEPA
(199la,b) has established a chronic and subchronic oral reference dose (RfD)
of 5.0xl0"5 mg/kg/day for dieldrin based on liver lesions observed in rats
(Walker et al. 1969). The RfD's were derived using a no-observed-effect level
(NOEL) of 0.005 mg/kg/day and an uncertainty factor of 100.
Dieldrin can be absorbed by humans from the .gastrointestinal tract following
ingestion of the pesticide (NIOSH 1978), and absorbed through human skin
following percutaneous exposure (Feldmann and Maibach 1974). NIOSH (1978)
reported that another possible route of absorption by humans is through
inhalation (NIOSH 1978). Reported effects in humans following acute exposure
to dieldrin include malaise, incoordination, headache, dizziness,
gastrointestinal disturbances, and major motor convulsions (NRG 1982).
Dieldrin is acutely toxic to laboratory animals by the oral, dermal, and
inhalation routes. It is mildly irritating to the eye and skin. At high
doses, dieldrin affects the central nervous system, producing irritability,
tremors, and convulsions (Health and Vandekar 1964). In experimental animals
chronic oral administration of dieldrin is associated with liver and kidney
damage (Walker et al. 1969, Treon and Cleveland 1955, Murphy and Korschgen
1970). Oral administration of dieldrin is reported to result in reproductive
toxicity, fetotoxicity, and teratogenicity in mice and hamsters (Diechmann
1972, Ottolenghi et al. 1974). Dieldrin is reported to cause a significant
dose-related increase in the incidence of hepatocellular carcinoma in mice
exposed in the diet (NCI 1978, Davis and Fitzhugh 1962, Walker et al. 1972).
3.2.9 Endrin Ketone
Endrin ketone (also known as delta-ketoendrin) is an intermediate in the
3-17
metabolism of endrin in mammals. Acidification, sunlight and heat will
decompose endrin to endrin ketone (Apsimon et al. 1982, Whetstone 1964). No
information was available concerning the health effects of endrin ketone.
However, because endrin ketone is structurally similar to endrin, the ketone
intermediate is assumed to be as toxic as endrin. The physical and chemical
properties of ketones, e.g., elevated solubility in both water and organics,
suggests that the ketone may be more readily absorbed and more active than
endrin. No health based criteria have been established byUSEPA for endrin
ketone.
3.2.10 4-Methyl-2-Pentanone
4-Methyl-2-pentanone is also known as methyl isobutyl ketone. USEPA (1991a)
calculated an oral reference dose (RfD) of Sxlo-2 mg/kg/day for methyl
isobutyl ketone based on a study in which rats were administered 0, 50, 250,
and 1,000 mg/kg/day via oral gavage for 13 weeks. A no-observed-effect level
(NOEL) for increased liver and kidney weight and nephrotoxicity was noted at
50 mg/kg/day (Microbiological Associates 1986). A lowest observed adverse
effect level (LOAEL) of 250 mg/kg/day was established for increased liver and
kidney weight and nephrotoxicity. USEPA (1991b) calculated a subchronic RfD
of Sx10-1 mg/kg/day based on the same study and effect of concern. USEPA
(1991b) calculated chronic and subchronic inhalation RfDs of 2xlo-2 mg/kg/day
and 2xlo-1 mg/kg/day, respectively, based on a study in which rats exposed to
50 ppm (205 mg/m3) for 90 days developed no adverse liver or kidney effects
(Union Carbide 1983). An uncertainty factor of 1,000 was used to calculate
both the chronic oral and inhalation RfDs, while an uncertainty factor of 100
was used for subchronic RfDs.
Methyl isobutyl ketone is absorbed following both oral or inhalation exposure.
Workers exposed to 100 ppm of methyl isobutyl ketone in air reported
headaches, nausea, and respiratory irritation; however, these effects were not
noted at concentrations of 20 ppm (Elkins 1959). The most common symptom of
methyl isobutyl ketone exposure is narcosis; other symptoms include irritation
3-18
I .
of the eyes, nose and mucous membranes (ACGIH 1986). In animals, subchronic
inhalation exposure results in liver and.kidney toxicity (Union Carbide 1983).
Irreversible kidney damage was observed in rats exposed to 200 ppm of methyl
isobutyl ketone for 2 weeks followed by 100 ppm for 90 days. Reversible
kidney damage was seen in rats exposed to 100 ppm methyl isobutyl ketone for 2
weeks (MacEwen et al. 1971). Subchronic oral gavage exposure of rats to doses
of up to 1,000 mg methyl isobutyl ketone/kg/day resulted in disturbances of
conditioned reflexes and liver detoxification function, increased liver and
kidney weights, and nephrotoxicity .(USEPA 1986, Microbiological Associates
1986).
3.2.11 Toxaphene
USEPA (1991) has classified toxaphene as a Group B2--Probable Human
Carcinogen. An oral cancer slope factor of 1.1 (mg/kg/day)·1 was derived from
the results of the Litton Bionetics (1978) study that observed an increased
incidence of hepatocellular carcinomas and adenomas in mice administered
toxaphene in the diet. The inhalation cancer unit risk of 3.2x10-4 (ug/m3)·1
is also based on the oral data (USEPA 1991).
Toxaphene is a mixture of more than 670 compounds, most of which are
chlorinated camphenes (Paris and Lewis 1973). Human and animal data suggest
that toxaphene is absorbed following oral, inhalation, and dermal exposure
(Warraki 1963, McGee et al. 1952). Although dermal absorption of toxaphene is
believed to be extensive (DiPietro and Haliburton 1979), absorption following
oral or inhalation exposure is not (Chandurkar and Matsumara 1979, Crowder and
Dindal 1974). In both humans and animals, toxaphene is acutely toxic to the
central nervous system, while chronic exposure affects the central nervous
system to a lesser extent (Boots Hercules Agrochemicals Inc. n.d., USEPA
1980). Reversible respiratory toxicity including acute pulmonary
insufficiency has been observed in humans exposed to·toxaphene via inhalation
during pesticide spraying (Warraki 1963). In animals, acute and chronic
exposure to toxaphene also can cause adverse effects in.the liver and kidney
3-19
(Mehendale 1978, Trottman .and Desaiah 1980, Peakall 1976, Chu et al. 1986,
Boots Hercules Agrochemicals Inc. n.d., Fitzhugh and Nelson 1951, Boyd and
Taylor 1971). Subchronic oral administration has been reported to adversely
affect the adrenal gland, thyroid gland and immune system in animals (Mohammed
et al. 1985, Chu et al. 1986, Chu et al. 1988, Koller et al. 1983).
Behavioral effects and immunosuppression have been observed in offspring of
rats and mice, respectively, which received oral doses of toxaphene (Olson et
al. 1980, Allen et al. 1983). An increased incidence of chromosome
aberrations has been reported for cultured lymphocytes from women exposed to
unspecified levels of toxaphene via inhalation and/or dermal exposure (Samosh
1974). Bioassays have observed statistically significant increases in the
incidence of follicular-cell carcinomas or adenomas of the thyroid gland in
male rats and of hepatocellular adenomas and carcinomas in mice orally
administered toxaphene (NCI 1977, Litton Bionetics 1978).
3. 2. 12 1, 2, 4-.Triclorobenzene
USEPA (1991) developed a chronic and subchronic oral reference dose (RfD) for
1,2,4-trichlorobenzene of lxl0-3 and lxl0-2 mg/kg/day, respectively based on a
study by Carlson and Tardiff (1976) that.identified increased liver-to-body
weight ratios in male rats exposed at 40 mg/kg/day but not at 20 mg/kg/day; a
uncertainty factor of 1,000 and 100 were used to develop the chronic and
subchronic RfD's, respectively. USEPA (1991) developed an inhalation RfD of
3xlo-3 mg/kg/day based on increased uroporphyrin levels in rats exposed for 3
months (Watanabe et al. 1978); an uncertainty factor of 1,000 was used to
develop the RfD.
Information inferred from data describing the toxicity or excretion of
trichlorobenzenes suggests that they are absorbed following oral, dermal, and
inhalation exposure (USEPA 1985). Human exposure to 1,2,4-TCB in air can
result in eye and respiratory irritation. The effects in laboratory animals
of acute exposure 'to trichlorobenzenes include local irritations, convulsions, :•
and death. Liver, kidneys, adrenals, mucous membranes, and brain ganglion
3-20
.-
I .
cells appear to be target organs, with effects including edema, necrosis,
fatty infiltration of the liver, increased organ weights, porphyrin induction,
and microsomal enzyme induction (USEPA 1985). Studies on the toxic effects of
trichlorobenzenes following subchronic exposure indicate that, in general, the
liver and kidneys are target organs (Kociba et al. 1978, Coate et al. 1977,
Watanabe et al. 1978). Subchronic oral studies have found that 1,2,4-TCB
induces hepatic enzymes and liver porphyrins, increases liver weight, and
causes fatty infiltration of the liver (Carlson and Tardiff 1976,
Carlson 1977, Smith et al. 1978). Topical doses of 1,2,4-TCB have been
reported to result in extensor convulsions, necrotic foci in the liver, and
death in guinea pigs (Powers et al. 1975, Brown et al. 1969). Teratogenicity
studies after administration by the oral route in rats showed mild osteogenic
changes in pups and significantly retarded embryonic development as measured
by growth parameters (Black et al. 1983, Kitchin and Ebron 1983). Maternal
toxicity was observed at doses causing effects in the pups. Increased
incidences of non-neoplastic lesions were seen in multiple organs in both male
and female mice exposed to 1,2,4-TCB painted on the skin for 2 years (Yamamoto
et al. ·1957).
3.2.13 Trichloroethene
Absorption of trichloroethene (TCE) from the gastrointestinal tract is
virtually complete. Absorption following inhalation exposure is proportional
to concentration and duration of exposure (USEPA 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 (USEPA 1985). Hepatotoxicity has been reported in human and animal
studies following acute exposure to TCE (USEPA 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 increased liver weights (Kjellstrand et al. 1983). Industrial
3-21
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 following
exposure to TCE in dilute, aqueous solutions (USEPA 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, Maltoni et al. 1986). Trichloroethylene was
mutagenic in Salmonella typhimurium and in E. coli (strain K-12), utilizing
liver microsomes for activation (Greim et al. 1977).
USEPA (1991) classified TCE in Group B2--Probable Human Carcinogen based on
inadequate evidence in humans and sufficient evidence of carcinogenicity from
animal studies. An oral cancer potency factor of l.lxlo·2 (mg/kg/day)-1 has
been derived by USEPA (1991) based on two gavage studies conducted in mice in
which an increased incidence of liver tumors were observed (Maltoni et al.
1986, Fukuda et al. 1983). An inhalation cancer unit risk of
l.7x10-6 (µg/m3)-1, which is equivalent to a slope factor of l.7xlo-2
(mg/kg/day)-1 has been derived for TCE based on an increased incidence of lung
tumors in mice (USEPA 1991, NCI 1976). The slope factor is based upon a
metabolized dose. USEPA (1987) developed an oral reference dose (RfD) of
7.35xlo-3 mg/kg/day based on a subchronic inhalation study in rats in which
elevated liver weights were 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 USEPA.
INOGANIC CHEMICALS OF POTENTIAL CONCERN
3.2.14 Barium
USEPA (1991a) derived an oral reference dose (RfD) based on two human
epidemiologic studies which did not observe any adverse effects following
3-22
i. l
consumption of drinking water containing barium (Brenniman and Levy 1984,
Wones et al. 1990). Although no L0AEL was identified, the effect of concern
was high blood pressure. Using a NOAEL of 0.21 mg/kg/day and an uncertainty
factor of 3, an oral RfD of 7xl0"2 mg/kg/day was calculated. A subchronic RfD
of 5xl0"2 mg/kg/day has been established by USEPA (1991b) based on increased
blood pressure in rats chronically exposed to 5.1 mg barium/kg/day in their
drinking water (Perry et al. 1983). USEPA (1991b) has also developed chronic
and subchronic inhalation RfCs of 5xl0"4 and 5xl0"3 mg/m3 for .barium based on a
study by Tarasenko et al. (1977). These concentrations are equivalent to
l.0x10·4 mg/kg/day and l.0xlo·3 mg/kg/day, assuming a 70 kilogram individual
inhales 20 m3/day. In this study rats were exposed to barium carbonate dust
at airborne concentrations of up to 5.2 mg/m3 for 4-6 months. Adverse effects
noted at this concentration included decreased body weight, alterations in
liver function, and increased fetal mortality. Uncertainty factors of 1,000
and 100 were used in developing the chronic and subchronic RfCs. fCs,
respectively.
Adverse effects in humans following oral exposure to soluble barium compounds
include gastroenteritis, muscular paralysis, hypertension, ventricular
fibrillation, and central nervous system damage (USEPA 1984). Inhalation of
barium sulfate or barium carbonate in occupationally exposed workers has been
associated with baritosis, a benign pneumoconiosis (Goyer 1986). Human
epidemiologic studies have shown that chronic ingestion of drinking water
containing high levels of barium induces high blood pressure that results in a
prevalance of hypertension, stroke, heart and renal disease (Brenniman and
Levy 1984, Wones et al. 1990). Chronic oral exposure of experimental animals
to barium in drinking water also increases blood pressure (USEPA 1984, Perry
et al. 1983). Inhalation of barium carbonate dust by experimental animals has
been associated with reduced sperm count, increased fetal mortality, atresia
of the ovarian follicles, decreased body weight, and alterations in liver
function (USEPA 1984, Tarasenko et al. 1977).
3-23
3.2.15 Manganese
USEPA established a chronic (1991a) and a subchronic (1991b) oral reference
dose (RfD) of lx10·1 mg/kg/day for manganese based on a no-observed-adverse-
effects level (NOAEL) of 0.14 mg/kg/day in.humans chronically·exposed to
manganese in food (WHO 1973, Schroeder et al. 1966, NRG 1989). An uncertainty
factor of 1 was used to derive the reference doses. USEPA (1991b) calculated a
chronic and subchronic inhalation reference concentration (RfC) of 4xl0"4
mg/m3 based upon an occupational study conducted by Roels et al. (1987) in
which respiratory symptoms and psychomotor disturbances were observed. These
values are equivalent to a dose of lxl0"4 mg/kg/day, assuming a 70 kilogram
individual inhales 20 m3/day. An uncertainty factor of 900 was used to
derived both RfCs.
Manganese is absorbed at low levels following oral or inhalation exposure
(USEPA 1984a). The effects following acute exposure to manganese are unknown.
Chronic oral and inhalation exposure of humans to high levels of manganese
causes respiratory symptoms and pneumonitis in exposed workers and has been
associa't:'ed with a condition known as manganism, a progressive neurological
disease characterized by speech disturbances, tremors, and difficulties in
walking (Kawamura et al. 1941, Roels et al. 1987). Altered hematologic
parameters (hemoglobin concentrations, erythrocyte counts) have also been
observed in individuals exposed chronically. Chronic oral exposure of rats to
manganese chloride can result 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 (USEPA 1984a). Certain manganese compounds have been shown to be
mutagenic in a variety of bacterial tests. Manganese chloride and potassium
permanganate can cause chromosomal aberrations in mouse mammary carcinornal
cells. Manganese was moderately effective in enhancing viral transformation
of Syrian hamster embryo cells (USEPA 1984a,b).
3-24
_fl
I. I
3.2.16 Mercury
USEPA (1991) has reported an oral reference dose for both chronic and
subchronic exposures of 3xlo-4 mg/kg/day for inorganic mercury_ based on
several oral and parenteral studies conducted in the Brown Norway rat studies
which observed kidney effects (Fitzhugh et al. 1950, Druet et al. 1978,
Bernaudin et al. 1981). An uncertainty factor of 1,000 was used to derive the
RfDs. USEPA (1991) has also derived an inhalation reference ~oncentration
(RfC) for inorganic mercury of 3xlo-4 mg/m3 for both chronic and subchronic
exposures based on several human occupational studies in which neurotoxicity
was observed (Fawer et al. 1987, Piikivi and Tolonen 1989, Piikivi and
Hanninen 1989, Piikivi 1989). This is equivalent to a dose of 8.5x10·5
mg/kg/day assuming a 70 kilogram individual inhales 20 m3/day. An uncertainty
factor of 30 was used to derive both inhalation RfCs.
In humans, inorganic mercury is absorbed following inhalation and oral
exposure, however only 7% to 15X of administe~ed inorganic mercury is absorbed
following oral exposure (USEPA 1984, Rahola et al. 1971, Task Group on Metal
Accumulation 1973). In humans, organic mercury is almost completely absorbed
from the gastrointestinal tract and is assumed to be well absorbed via
inhalation in humans (USEPA 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 Beliles 1980). Chronic occupational exposure of
workers to elemental mercury vapors (0.1 to 0.2 mg/m3 ) has been associated
with mental disturbances, tremors, and gingivitis (USEPA 1984). Animals
exposed to inorganic mercury for 12 weeks have exhibited proteinuria,
nephrotic syndrome and renal disease (Druet et al. 1978). Rats chronically
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
3-25
included destruction of cortical cerebral ~eurons, damage to Purkinje cells,
and lesions of the cerebellum. Clinical .symptoms following exposure to
organic mercury compounds have included paresthesii, 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 (USEPA 1984). Both organic and inorganic compounds are
reported to be genotoxic in eukaryotic systems (Leonard et al. 1984).
3.2.17 Vanadium
USEPA (1991a) has derived a chronic and subchronic oral reference dose (RfD)
of 7xlo-3 mg/kg/day based on a chronic study in which rats received vanadium
in their drinking water (Schroeder et al. 1970). A no-observed-adverse-effect
level (NOAEL) of 0.77 mg/kg/day and an uncertainty factor of 100 were used to
develop the RfD. USEPA (1991a) has established an oral RfD for vanadium
pentoxide of 9xlo-3 mg/kg/day. This value is based on a chronic rat study in
which a NOAEL of 0.89 mg vanadium pentoxide/kg/day was noted. The only
reported effect was a decrease in the amount of cystine in the hair (Stokinger
et al. 1953). An uncertainty factor of 100 was used to calculate the vanadium
pentoxide RfD. USEPA has not developed inhalation criteria for vanadium.
Pentavalent vanadium compounds are generally considered to be more toxic than
other valence states. Many incidents of short-term and long-term occupational
exposures to vanadium, mainly vanadium pentoxide dust, have been reported.
Inhalation causes respiratory tract irritation, coughing, wheezing, labored
breathing, bronchitis, chest pains, eye and skin irritation and discoloration
of the tongue (NIOSH 1977, NAS 1974). Effects seen in experimental animals
following chronic inhalation exposure include fatty degeneration of the liver
and kidneys, hemorrhage, and bone marrow changes (Browning 1969).
3-26
_!l,
I.!
3.2.18 Zinc
USEPA (1991) has derived an oral reference do~e (RfD)·of 2xl0"1 mg/kg/day for
both chronic and subchronic exposures based on studies in which anemia and
reduced blood copper were observed in humans exposed to oral zinc doses of
2.14 mg/kg/day (Pories et al. 1967, Prasad et al. 1975). A safety factor of
10 was used to develop the RfDs. The RfD is currently under review by the
RfD/RfC workgroup.
Zinc is absorbed in humans following oral exposure; however, insufficient data
are available to evaluate absorption following inhalation exposure (USEPA
1984). Zinc is an essential trace element that is necessary for normal health
and metabolism and therefore is nontoxic in trace quantities (Hammond and
Beliles 1980). Exposure to zinc at concentrations that exceed recommended
levels has, however, been associ.ated with a variety of adverse effects. In
humans, chronic and subchronic inhalation exposure to zinc has been associated
with gastrointe.stinal disturbances, dermatitis, and metal fume fever,· a
condition characterized by fever, chills, coughing, dyspnea, and muscle pain
(USEPA 1984). Chronic oral exposure of humans to zinc may cause anemia and
altered hematological parameters (Pories et al. 19_67, Prasad et al. 1975).
Reduced body weights have been observed in studies in which rats were
administered zinc in the diet. There is no evidence that zinc is teratogenic
or carcinogenic (USEPA 1984).
3-27
I.
4.0 HUMAN EXPOSURE ASSESSMENT
The purpose of this section is to calculate the magnitude of potential
chemical exposures associated with the site under current and potential future
land-use conditions. As part of this evaluatio_n, information ·on the expos·ure
setting and the potentially exposed populations is presented (Section 4.1).
This is followed by a discussion of potential exposure pathways through which
populations could be exposed to chemicals at or originating from the site
(Section 4.2). For each pathway selected for quantitative evaluation, the
chemical concentrations at the points of exposure are estimated (Section 4.3),
followed by a calculation of potential chemical intakes (Section 4.4).
4.1 SITE CHARACTERIZATION
The Geigy Chemical Corporation Site is located on a railroad right-of-way on
Route 211 just east of the city limits of Aberdeen in eastern Moore County,
North Carolina. The site is bordered to the north by Route 211, to the south
by a wooded area and to the west by Route 211 and the Aberdeen and Rockfish
Railroad (ERM-Southeast 1991). The site is bordered by a residential property
to the east. A farm is located to the southeast of the site while the
property immediately north on the opposite side of Route 211 is used for
commercial purposes. A housing development is located 1/4 mile to the
northwest.
The site is well vegetated with grass, except for a gravel driveway, the
partial concrete foundation from former warehouses, a vacant office building,
and a concrete tank pad. The warehouses have been removed, chemical hOtspots
have been excavated and removed to a hazardous waste facility, and a large
portion of the site (approximately 58%) has been covered with clean soil and
an indigenous species of grass. The nearest human receptors to the site are
those residents living adjacent to the site to the east, other residents
northeast of the site along Route 211, residents of the farm to the south, the
4-1
residents northwest of th~ site, and merchants who are employed in the
businesses across Route 211 from the site. (see Figure 2-1).
Surface water runoff from the site only occurs after heavy precipitation and
is diverted to drainage ditches located south of the southeast corner of
former Warehouse A; west along the north side of the main railroad line; and
west along the south side of State Route 211.
The Aberdeen area is underlain by three main regional aquifer systems.
Vertical infiltration is commonly restricted by the occurrence of a clay layer
which serve as a confining unit. The confining unit which lies between the
surficial aquifer and the second uppermost aquifer is composed of clay, silty
clay, and sandy clay (ERM-Southeast 1991).
As described in the RI Report (ERM-Southeast 1991), potentiometric data from
the shallow monitoring wells indicate that groundwater flow from the eastern
and western portions of the site in the surficial aquifer meet in an elongated
zone of convergence which bisects the site. For the area east of the
convergence zone, groundwater in the surficial aquifer predominantly flows to
the west and northwest. For the area west of the convergence zone,
groundwater in the surficial aquifer predominantly flows to the east-southeast
(ERM-Southeast 1991). The groundwater flow within the second uppermost
aquifer is toward the west-northwest. The second uppermost aquifer serves as
the primary source of potable groundwater in the Aberdeen area. City
Municipal Supply Wells for the town of Aberdeen are screened in the second and
third uppermost aquifer (ERM-Southeast 1991). The closest municipal well to
the site is Municipal Well Number 4, located 1,000 feet directly to the west
of the site.
Tables 4-1 and 4-2 present the 1990 census population profile for residents
within a 0-1 mile and a 1-5 mile radius of the site. Within 0-1 miles, there
are 355 families, and a total of 1,208 people with a median age of 34 years
4-2
I.
TAllLE 4-1
POPULATION BY AGE AND SEX WITHIN ONE-MILE RADIUS
OF THE. GEIGY CHEMICAL CORPORATION SITE
GEIGY CHEMICAL
CORPORATION SITE
0-1 MILE
Population
Median Age
Families
1209
34.0
355
SITE: Circle
Latitudei 35,07,30
Longitude: 79,24,30
Households
Avg HH Size
Group Quarters
445
2.69
0.8%
Radius:
Degrees
Degrees
1.00
North:
miles
35.13
79.41 West:
Housing Units
Average Value
Average Rent
485
$ 83304
$ 276
POPULATION BY AGE AND SEX*
Male Female Total PoEulation
Number Percent Number Percent Number Percent
Total 590 100.0 618 100.0 1208 100.0
0 -4 4.4 7.5 45 7.3 89 7.4
5 -9 47 8.0 46 7. 4 93 7.7
10 -14 53 9.0 43 7.0 96 7 . 9
15 -19 51 8.6 44 7.1 95 7.9
20 -24 31 5.3 36 5.8 67 5.5
25 -29 39 6.6 38 6 . ]. 77 6.4
30 -34 52 8.8 56 9.1 108 8.9
35 -39 60 10.2 51 8.3 111 9. 2
40 -44 41 6.9 51 8.3 92 7.6
45 -49 38 6.4 33 5.3 71 5.9
50 -54 25 4.2 24 3.9 49 4. l
55 -59 25 4.2 35 5.7 60 5. 0
60 -64 24 4.1 29 4.7 53 4 . 4
65 -69 21 3.6 29 4.7 50 4. l
70 -74 21 3.6 23 3.7 44 3.6
75 -79 8 l. 4 19 3.1 27 2. 2
80 -84 7 1.2 10 1.6 17 1. 4
85+ 3 0.5 6 1.0 9 0.7
18+ years 413 70.0 456 73.8 869 71. 9
21+ years 390 66.1 433 70.1 823 68.1
65+ years 60 10.2 87 14.l 147 12.2
Median Age 32.9 35.l 34.0
NOTE: There was a tendency to report age on the date when the census
questionnaire was completed rather than on April 1, 1990. For
this reason, about 10% of persons in most age groups are probably
1 year younger, according to the Census.Bureau.
These population counts will not be adjusted, according to a Department
of Commerce announcement made on July 15, 1991.
Source: 1990 census of Population and Housing, Summary Tape File lA
copyright 1§§1 CACI Fairfax, VA
4-3
(800 ► 292-2224 8/23/91
TABLE 4-2
POPULATION BY AGE AND SEJ(WITHIN A ONE TO FIVE MILE RADIUS
OF THE GEIGY CHEMICAL CORPORATION SITE
GEIGY CHEMICAL
CORPORATION SITE
1-5 MILES
Population
Median Age
Families
19145
37.4
5349
SITE: Ring
Latitude: 35,07,3-0
Longitude: 79,24,30
Households
Avg HH Size
Group Quarters
7849
2.35
3.5%
Radius in miles:
Inner• 1-00
outer -s_oo
Housing Units
Average Value
Average Ren.t
8799
$102752
$ 311
POPULATION BY AGE AND SEX*
Male Female Total Population Number Percent Number Percent Number Percent
Total 8982 100.0 10161 100.0 19143 100.0
0 -4· 634 7.1 587 5.8 1221 6. 4 5 -9 627 7.0 644 6. 3 1271 6.6 10 -14 603 6.7 567 5.6 1170 6.1 15 -19 626 7. 0 576 5.7 1202 6.3 20 -24 630 7.0 . 591 5.8 1221 6.4 25 -29 696 7.7 719 7.1 1415 7 . 4 30 -34 683 7.6 761 7.5 1444 7. 5 35 -39 642 7.1 672 6.6 1314 6.9 40 -44 606 6.7 609 6.0 1215 6. 3 45 -49 500 5.6 526 5.2 1026 5 . 4 50 -54 356 4.0 437 4.3 793 4 . 1 55 59 413 4.6 507 5.0 920 4.8 60 -64 466 5.2 621 6.1 1087 5 . 7 65 -69 538 6.0 701 6.9 1239 6. 5 70 -74 440 4.9 588 5.8 1028 5. 4
75 -79 282 3.1 479 4.7 761 4.0 80 -84 144 1.6 301 3.0 445 2. 3 85+ 96 1.1 275 2.7 371 l. 9
18+ years 6753 75.2 8025 79.0 14778 77.2 21+ years 6344 70.6 7671 75.5 14015 73.2
65+ years 1500· 16.7 2344 23.1 3844 20.1
Median Age 34.9 39.7 37.4
NOTE: There was a tendency to report age on the date when the census
questionnaire was completed rather than on April 1, 1990~ For
this reason, about 10% of persons in most age groups are probably
1 year younger, according to the Census Bureau.
These population counts will not be adjusted, according to a Department
.of Commerce announcement made on July 15, 1991.
Source: 1990 Census of Population and Housing, Summary Tape File lA
Copyright 1991 CACI Fairfax, VA
4-4
(800) 292-2224 8/23/91
i
.. i
'·
(CACI 1991). Approximately 132 people or 11% of the population within the 0-1
mile radius are between the ages of 7 to 13 years.
4.2 ENVIRONMENTAL FATE AND TRANSPORT OF ORGANOCHLORINE PESTICIDES
The chemicals of concern at the site are primarily drawn from the class of
organochlorine pesticides. This class of pesticides was developed around the
time of World War II for its insecticidal activity. The members of the class
all poSsess some chemical structural similarities, however, it is convenient
to break them down into subgroups for ease of discussion. The BHC subgroup
(alpha-BHC, beta-BHC, gamma-BHC, and delta-BHC) was the first group to be
discovered and commercially utilized (Brooks 1977). This group is composed of
isomers of chlorine and hydrogen-saturated cyclohexane rings. The DDT
subgroup (4,4'-DDT and its metabolites/degradation products 4,4'-DDE and 4,4'-
DDD) was the next to be commercialized. The cyclodiene group was synthesized
in the early 1940's and commercialized rapidly thereafter. It includes
chlordane, heptachlor, aldrin, dieldrin, endrin, endosulfan, and numerous
other minor pesticides. Toxaphene is a mixture of over 175 chlorinated
camphenes which, at one time, was the most widely used of the organochlorine
insecticides. Overall, the class is character.ized by broad spectrum
insecticidal ability, low acute mammalian toxicity, a tendency to
bioaccumulate, and a high degree of persistence.
When found in soil, the BHC group can volatilize, leach to groundwater, sorb
to soil, or biologically degrade. ATSDR (1989) reports that the leaching
potential of gamma-BHC is extremely low and the sorption potential is high.
USEPA (1979) reported that biodegradation of the BHC group occurs through a
reductive dechlorination mechanism. When applied as a pesticide, gamma-BHC
and its analogs are likely to be rapidly volatilized (Glotfelty et al. 1984).
4-5
Four mechanisms have been _suggested for the loss of DDT residues from soils:
1) volatilization, 2) removal by harvest of organic matter, 3) water runoff
with sediment transport, and 4) chemical transformation (ATSDR 1989). Jury et
al. (1984) include DDT in the class of chemicals which is relatively immobile
with respect to infiltration but susceptible to volatilization. Biological
transformation of DDT to DDE and DDD occurs under a variety of conditions.
The half-life for the transformation ranges from 2 to >15 years depending on a
variety of environmental factors (ATSDR 1989). At the Geigy .Chemical
Corporation Site, the levels of DDT are expected to continue to decline,
however, levels of DDE and DDD may increase.
The cyclodienes exhibit environmental behavior which is similar to the other
chlorinated pesticides. Chlordane is a complex mixture of ·over 30 compounds
including heptachlor. In addition the term "chlordane" refers to isomers of a
specific chlorinated compound. ATSDR (1989) notes that chlordane is extremely
persistent in soils and can remain over 20 years. Chlordane is not readily
susceptible to mobilization by infiltration and biodegrades under a limited
set of circumstances. Volatilization is probably the most significant
transport route for chlordane (Jury 1984). The behavior of heptachlor is
similar, although heptachlor is more volatile and therefore less persistent
than actual chlordane isomers. Aldrin and dieldrin are related structurally.
Dieldrin is a natural epoxidation product of aldrin in addition to being
manufactured as a pesticide in its own right. ATSDR (1991) notes that
volatilization is the principle route of loss of dieldrin and aldrin from
soil, with the rate of volatilization being slower for dieldrin than aldrin.
Groundwater contamination through intact soils has a low potential of
occurring. Jury et al. (1987) note that, even with a high mobilization
potential scenario (soil with low organic carbon and high water content), it
would take an estimated 270 years for dieldrin to reach a soil depth of three
meters.
Toxaphene is also strongly sorbed to soil. Recent experimental results
(Jaquess et al. 1989) showed that toxaphene did not leach
4-6
--.
I. I
from intact soil columns when eluted with water. Leaching only.occurred if
other chemicals (organic .solvents, emulsifiers) were applied or if the soil
was allowed to fracture. There is some evide~ce that toxaphene components
undergo anaerobic dechlorination (ATSDR 1990) in soils, however, the dominant
process appears to be one of volatilization.
It has been long known that the natural removal of hydrophobic materials,
especially pesticides, from soils is a two-phase or bimodal process (Nash
1983, Edwards 1966). The first phase is one of relatively rapid disappearance
of the pesticide, followed by a slower second phase. It is hypothesized that
the difference is due to saturation of strong binding sites on the soil
matrix, which leaves a residue of loosely bound material to participate in
rapid volatilization. Once this has occurred, it is more difficult for the
strongly bound material to volatilize. The age of the pesticides at the Geigy
site indicates that the rapid phase has already occurred and the slow phase is
currently operational. In the interests of producing conservative health
protective inhalation exposure point concentrations, it was asswned that the
pesticides were newly applied.
In conclusion, the pesticides found at the Geigy site are likely to be
persistent. Their dominant environmental fate involves volatilization
followed by biological transformations. They are unlikely to be transported
to groundwater to a large extent which can be seen when considering the low
concentrations of pesticides measured in surficial groundwater in comparison
with the large amounts of pesticides which were removed from the site and
which were present in soil over a period of several years.
4.3 POTENTIAL EXPOSURE PATHWAYS
An exposure pathway describes the course a·chemical takes from the source to
the exposed individual. It is defined by four elements:
4-7
• a source and mechanism of chemical release to the environment;
• an environmental transport medium (e.g., air, soil) for the
released chemical;
• a point of potential contact with the contaminated medium
(referred to as the exposure point); and
• an exposure route ·(e.g. 1 ingestion, inhalation) at the contact
point.
An exposure pathway is considered complete only if all these·elements are
present. In a risk assessment, only complete exposure pathways are
quantitatively evaluated.
In this section, potential human exposure pathways are identified. Two
overall exposure conditions will be evaluated. The first is the current land-
use condition, which considers the site as it currently exists after extensive
remedial activities have occurred (i.e., the no-further action alternative).
The second is the future land-use condition, which evaluates potential risks
that may be associated with any probable change in site use assuming no
further remedial action occurs.
4.3.1 Potential Exposure Pathways Under Current and Surrounding Land-Use
Conditions
Table 4-3 summarizes the current land-use exposure pathway analysis,
indicating the exposure medium, release mechanism, exposure point, potential
receptor and route of exposure. This table also indicates whether each
pathway is potentially complete, and identifies those pathways that will be
quantitatively evaluated in the risk assessment.
4.3.1.1 Surface Soil/Sediment Pathways
Extensive remediation has already occurred at the site, resulting in low
concentrations of pesticides remaining in surface soil and ditch sediment.
Sediment in the ditches is generally dry since water flows in the ditches only
4-8
after storm events. As me~tioned in Section 2.0, the ditch sediment is
treated collectively with soil data at the site. Exposures to chemicals in
surface soil/sediment could occur by direct contact and subsequent dermal
absorption and/or incidental ingestion (as a result of hand-to-mouth contact).
An older child (8-13 years of age) trespassing on the site or off-site (south)
in the nearby vicinity is considered to be the most likely receptor who could
potentially be exposed to chemicals in surface soils/sediment (i.e., while
playing). Young children within 1-6 years of age are not expected to explore
these areas, since this age group spends most of its time in and near the
home. Thus, incidental ingestion and dermal absorption exposures to both on-
site and off-site surface soil/sediment by an older child will be
quantitatively evaluated.
4.3.1.2 Subsurface Soil/Sediment Pathways
Under current land-use conditions, it is highly unlikely that exposures to
chemicals in subsurface soil/sediment could occur by direct contact. An older
child trespassing on the site or in the ditches immediately south of the site
(off-site) is not anticipated to be digging or performing other activities
where they would contact subsurface soils. Additionally, the concentrations
of chemicals detected in subsurface soil/sediment were substantially lower
than those detected in surface soil/sediment (which will be evaluated for
direct contact). Since this exposure pathway is not complete, it will not be
evaluated.
4.3.1.3 Groundwater Pathways
Under current land-use conditions, groundwater from the surficial aquifer and
second uppermost aquifer at or near the site is not used for drinking water
purposes. Pesticides were measured in off-site well MW-11D. Under current
land-use conditions, there is no consumption of groundwater on-site or in the
vicinity of MW-11D and this pathway will be evaluated under future land-use
conditions.
4-9
~
' .....
0
Exposure
Medium
Surface Soil/
Sediment
Surface Soil/
Sediment
Subsurface
Soi !/Sediment
Subsurface
Soil/Sediment
Surface Water
Groundwater
(Surficie.l
Aquifer)
Groundwater
(Second
Uppermost
Aquifer)
Groundwater
(Second
Uppennost
Aquifer)
Mechanisms of Release
Direct contact .
Direct contact
Direct contact
Direct contact
Surface water runoff,
seepage
Percolation through
vadose zone into aquifer
Percolation through
vadose zone into aquifer
Percolation through
vadose zone into aquifer
TABLE 4-3
POTENTIAL EXPOSURE PATHWAYS UNDER CURRENT AND SURROUNDING LAND-USE CONDITIONS
Exposure Point
On-site
Off-site
On-site
Off-site
On-site and off-site
On-site wells and
off-site wells
Off-site wells
On-site
Potential Receptor
Older child (8-13
years) trespasser
Older child (8-13
years) trespasser
Older child (8-13
years) trespasser
Older child (8-13
years) trespasser
Older child (8-13
years) trespassers;
nearby adult and
child (1-6 years)
residents
None
Adult and child (1-
6 years) residents,
merchants
None
Route of Exposure
Incidental ingestion,
dermal absorption
Incidental ingestion,
dermal absorption
Incidental ingestion,
dermal absorption
Incidental ingestion,
dermal absorption
Incidental ingestion,
dermal absorption
Ingestion, inhalation
Ingestion, inhalation
Ingestion, dermal
absorption,
inhalation
Pathway Complete? Basis.
Yes. Chemicals are present
on on-site surface soil and
sediment in ditches.
Yes. Chemicals are present
on off-site surface soil/
sediment.
No. Ground intrusive
activities are not likely to
occur.
No. Ground intrusive
activities are not li~ely to
occur.
No. Ditches contain water
for a short time after storm
event -water readily
percolates.
No. Water from surficial
aquifer is not used due to
sanitation issues and the
area is tied to a municipal
water supply system.
No. Chemicals in off-site
well MW-llD of the second
uppermost aquifer may be
site-related. However,
groundwater in the vicinity
·of this well is not presently
used for domestic purposes,
No. No pesticides of
potential concern were
measured in on-site wells in
this aquifer. Groundwater
beneath the site is not
presently used.
Quan ti tati vely
Evaluated?
Yes.
Yes.
No.
No.
No.
No.
No.
No.
_n
Exposure
Medium
Air
Air
Air
Mechanisms of Release
Volatilization of
pesticides from surface
soil/sediment
Volatilization of
pesticides from surface
Soil/sediment
Dust dispersion
TABLE 4-3
POTENTIAL EXPOSURE PATHWAYS UNDER CURRENT AND SURROUNDING LAND-USE CONDITIONS
Exposure Point
On-site
Off-site
Off-site
Potential Receptor
Older child (8-13
years) trespasser
Nearby merchant,
nearby adult and
child (1-6 years)
residents
Nearby merchant,
nearby adult and
child (1-6 years)
residents
Route of Exposure
Inhalation
Inhalation
Inhalation
Pathway Complete? Basis.
Yes. Chemicals are present
in surface soil/sediment.
Yes. Low concentrations of
volatilized chemicals may
disperse off-site.
Yes. Chemicals in soil may
be transported off-site as
wind blown dust particles.
Quan ti tati vely
Evaluated?
Yes.
Yes.
Yes.
4.3.1.4 Air Pathways
Individuals in the vicinity of the site may be potentially exposed to
chemicals in the surface soil/sediment which are released to the air.
Airborne emissions of chemicals of potential concern could occur as a result
of volatilization of chemicals from surface soil/sediment and as a result of
transport of chemicals present on wind-entrained particulate ~atter. The
inhalation of chemicals adsorbed to wind-blown dust is not considered to be
likely because the surface of the site is well vegetated and often moist due
.to frequent precipitation (42 inches year) (NOAA 1989). However, the
inhalation of wind blown dust particulates by nearby merchants and residents
will be evaluated at the request of USEPA Region IV. Additionally, chemicals
of potential concern, may volatilize into ambient air. Thus, an older child
trespasser on-site may be exposed to pesticide vapors in ambient air by the
route of inhalation. In addition, nearby merchants (directly north of the
site) and residents in proximity to the site may also be exposed to chemicals
released from on-site surface soil/sediment through volatilization. Because
the predominant wind direction is towards the northeast, the residents
northeast of the site would be the receptors with the greatest potential for
exposure, and thus will be quantitatively evaluated.
4.3.1.5 Summary of Current Land Use Pathways
In summary, the exposure pathways that will be evaluated under current land-
use conditions are as follows:
• Incidental ingestion of chemicals in on-site surface soil/sediment
by an older child trespasser (8-13 years),
• Dermal absorption of chemicals in on-site surface soil/sediment by
an older child trespasser (8-13 years),
• Incidental ingestion of chemicals in off-~ite surface
·soil/sediment by an older child (8-13 y~afs),
4-12
,'
I :
• Dermal absorpt.ion of chemicals in off-site surface soil/sediment
by an older child (8-13 years),
• Inhalation of volatilized surface soil/sediment chemicals by
an older child trespasser (8-13 years),
• Inhalation of volatilized surface soil/sediment chemicals by a
merchant north of the site,
• Inhalation of volatilized surface soil/sediment chemicals by a
nearby child resident (1-6 years) northeast of the site,
• Inhalation of volatilized surface soil/sediment chemicals by a
nearby adult resident northeast of the site,
• Inhalation of chemicals in wind blown dust particles by a nearby
child resident (1-6 years) northeast of the site,
• Inhalation of chemicals in wind blown dust particles by a nearby
adult resident northeast of the site, and
• Inhalation of chemicals in wind blown dust particles by a nearby
merchants north of the site.
4.3.2 Potential Exposure Pathways Under Future Land Use Conditions
A no-further action alternative must address any changes of land-use
associated with the site which may result in exposure and risk to the
chemicals of potential'concern. The most likely land-use associated with the
site involves development for commercial use in the future, although the site
is currently owned by the Aberdeen and Rockfish Railroad, Because the site is
very small, is situated between a highway, and is bisected by a railroad
track, future residential development is not likely to occur. Figure 4-1
shows the existing right-of-ways associated with the railroad and highway 211.
Residential use of this site could only occur if the Aberdeen and Rockfish
railroad abandoned this property in the future. The railroad has been in
operation since 1892, and currently has no plans to abandon this railway.
Nonetheless, a future child (1-6 years) and adult resident will be evalu'ated.
Additionally, for the exposure pathway analysis, it has been assumed that a
hypothetical future business would be located directly on the site.
4-13
Table 4-4 summarizes the e.xposure pathway analysis for future land-use
conditions. This table indicates the exposure medium, release mechanism,
exposure point, potential receptor and route of exposure. Potentially
complete pathways are indicated, and those pathways that will be
quantitatively evaluated in the Baseline RA are noted.
4.3.2.1 Surface Soil/Sediment Pathways
Under future land-use conditions, it is possible that if the site is developed
for commercial purposes, a hypothetical on-site worker could be exposed
through direct contact with on-site surface soil/sediment. This contact could
occur from activities such as loading supplies, repairs, and general
maintenance of the grounds.·. Incidental ingestion and dermal absorption with
on-site surface soil/sediment by a hypothetical worker will, therefore, be
evaluated under future land-use conditions.
Additionally, if the property was no longer owned by the railroad, it is
possible (although unlikely) that the site could be developed for residential
use in the future. If this were the case, incidental ingestion and dermal
absorption of chemicals in on-site surface soil could potentially occur.
Therefore, these pathways will be quantitatively evaluated for residents under
future land-use conditions in accordance with guidance received from USEPA
Region IV.
Under future land-use conditions, it is improbable that the property
immediately south of the site would be developed for residential purposes due
to the proximity of the railroad tracks. However, potential future
residential use of the off-site area will be qualitatively discussed.
4.3.2.2 Subsurface Soil/Sediment Pathways
Under future land-use conditions, assuming the site is developed for
commercial purposes, a hypothetical future worker could potentially contact
4-14
TABLE 4-4
POTENTIAL EXPOSURE PATHWAYS UNDER FUTURE LAND-USE CONDITIONS
Exposure Potential Quantitatively
Medium Mechanisms of Release Exposure Point Receptor Route of Exposure Pathway Complete? Evaluated?
Surface Soil/ Direct contact On-site Merchant, adult Incidental ingestion, Yes, Low concentrations Yes.
Sediment and child C 1-6 dermal absorption of chemicals present in
years) residents surface soil/sediment.
Surface Soil/ Direct contact Off-site Adult and child Incidental ingestion, No. Proximity to No.
Sediment (1-6 years) dermal absorption railroad tracks makes
residents future development
unlikely.
Groundwater Percolation through On-site well Merchant, adult Ingestion Yes. Chemicals present Yes,
(Surficial vadose zone into and child (1-6 in on-site monitoring
Aquifer) aquifer years) residents wells.
Groundwater Percolation through On-site well Adult and child Inhalation Yes. Chemicals present Yes.
(Surficial vadose zone into (1-6 yaars) in on-site monitoring
Aquifer) aquifer residents wells may volatilize
during showering.
Groundwater Percolation through On-site well Adult and child Dermal absorption Yes.· Chemicals present Yes;
~
' (Surficial vadose zone into (1-6 years) in on-site monitoring ..... Aquifer) aquifer residents wells may be dermally
V, absorbed during
showering.
Groundwater Percolation through Off-site, residential Adult and child Ingestion Yes. Chemicals present Yes.
(Second vadose zone into well (1-6 years) in MW-11D may be site-
Uppennost aquifer residents related.
Aquifer)
Groundwater Percolation through On-site well Adult and child Ingestion, Inhalation Yes. TCE was present in Yes.
(Second vadose zone into (1-6 years) of volatiles the second uppermost
Uppermost aquifer residents aquifer within the
Aquifer) propertY boundaries,
although pesticides Were
not detected in this
aquifer.
l'-
' ....
"'
. Exposure
Medium
Subsurface
Soil/Sediment
Subsurface
Soil/Sediment
Air
Mechanisms of Release
Direct contact
Direct contact
Volatilization of
pesticides from surface
soil/sediment
TABLE 4-4
POTENTIAL EXPOSURE PATHWAYS UNDER FUTURE LAND-USE CONDITIONS
Exposure Point
On-site
Off-site
On-site
Potential
Receptor
Merchant
Adult and child
(1-6 years)
residents
Merchant, adlllt
and child (1-6
years) residents
Route of Exposure
Incidental ingestion,
dermal absorption
Incidental ingestion,
dermal absorption
Inhalation
Pathway Complete?
Yes. Potential
infrequent contact
during landscaping,
repairs, construction,
however, short duration
poses less of a risk
than surface soil
exposure.
No, Subsurface soil
will not be exposed.
Yes. Chemicals are
present in surface
soil/sediment.
Quantitatively
Evaluated?
No.
No.
Yes.
~
' t-' __,
WOODS
'\
' ~ )A /\ WOODS
\
W&!:il!
(%:?0',0?) HIGHWAY 211 RIGHT or WAY (50 rEET rROM CENTERLINE)
~"™1 RAILROAD RIGHT or WAY (80 rEET rROM CENTERLINE)
POWERUNE RIGHT or WAY (20 rEET rRCM CENTERLINE)
[•,•,•,•;•;1 PROPERTY NOT ENCUMBERED BY RIGHT OF WAYS (APPROXIMATELY 0.2 ACRES)
HIGHWAY CENTER UN[
.. .. "" 1ao n
D
WOODS
• FIGURE 4-1
RM.ROAD ANO HIGHWAY
RIGHT or WAYS
N
G[ICY CHEMICAL CORPORATION !;IT[
"B(lll)f[H, ~111 C~l!Ol 1""'
subsurface soil/sediment d~ring landscaping, maintenance or construction
activities. Direct contact with on-site subsurface soils or sediments could
result in the inadvertent ingestion of soils/sediment·and may also result in
absorption of chemicals through the skin. However, the risk resulting from
direct contact with subsurface soil is likely to be lower in comparison to
direct contact with surface soil/sediment due to the presence of much lower
chemical concentrations overall in the subsurface soils. Additionally,
subsurface soil will likely be contacted, if contacted at all, infrequently
and for a much shorter duration than surface soil/sediment. Although this
pathway was considered to be potentially complete in some situations, it was -
not quantitatively evaluated in this analysis for these reasons.
4.3.2.3 Groundwater Pathways
Ingestion of groundwater from the surficial aquifer by future workers and
residents is selected for evaluation in this assessment. Additional pathways
to be evaluated include inhalation of volatiles while showering and dermal
absorption of chemicals while showering for both adult and child residents.
With respect to the second uppermost aquifer, the only organic chemical
detected in the second uppermost aquifer within the property boundaries was
trichloroethene (TCE). Further characterization will be conducted to
determine the source and extent of TCE in this groundwater. Nonetheless,
ingestion of groundwater from this aquifer, in addition to inhalation of
volatiles while showering will be evaluated for both adult and child
residents. Additionally, ingestion of off-site groundwater from MW-11D in the
second uppermost aquifer will be quantitatively evaluated for both a child and
adult resident in this risk assessment.
4.3.2.4 Air Pathways
Under future land-use conditions, it is possible that the site could be
developed for commercial purposes. Thus, a hypothetical future on-site .,
merchant or resident could be exposed to airborne emissions of potential
4-18
1.
'
I
chemicals of concern via i~halation. Chemicals adsorbed to surface '
soil/sediment could potentially be released into the air through
volatilization or dust transport. Residential and merchant exposure to dust
was evaluated under current land-use conditions. Exposures to on-site
residents of chemicals which have volatilized from surface soil will be
evaluated under future land-use conditions.
4.3.2.5 Summary of Future Land Use Pathways
In summary, the exposure pathways that will be evaluated under future land-use
conditions are as follows:
• Incidental ingestion of on-site surface soils/sediment by
hypothetical future on-site adult and child (1-6 years) residents,
• Incidental ingestion of on-site surface soils/sediment by a
hypothetical future on-site merchant,
• Dermal absorption of chemicals adsorbed to surface soils/sediment
by hypothetical future on-site adult and child (1-6 years)
residents,
• Dermal absorption of chemicals adsorbed to surface soils/sediment
by a hypothetical future on-site merchant,.
• Ingestion of groundwater from the surficial aquifer by
hypothetical future on-site adult and child (1-6 years) residents,
• Ingestion of groundwater from the surficial aquifer by a
hypothetical future on-site merchant,
• Inhalation of volatile organic chemicals while showering with
groundwater from the surficial aquifer by hypothetical future on-
site adult and child (1-6 years) residents,
• Dermal absorption of chemicals while showering with groundwater
from the surficial aquifer by hypothetical future on-site adult
and child (1-6 years) residents,
4-19
• Ingestion of groundwater from the second uppermost aquifer by
hypothetical future on-site adult and child (1-6 years) residents,
• Inhalation of volatile organic chemicals while showering with
groundwater from the second uppermost aquifer within the property
boundaries by hypothetical future on-site adult and child (1-6
years) residents,
• Ingestion of groundwater from the off-site second uppermost
aquifer (MW-11D) by hypothetical future adult and child (1-6
years) residents,
• Inhalation of volatilized surface soil/sediment chemicals by
hypothetical future on-site adult and child (1-6 years) residents,
and
• Inhalation of volatilized surface soil/sediment chemicals by a
hypothetical future on-site merchant.
4.4 CALCULATION OF EXPOSURE POINT CONCENTRATIONS
The calculations of exposures to the chemicals of potential concern requires
the combination of exposure point concentrations with assumptions regarding
the frequency, duration and magnitude of receptor contact. Exposure point
soil concentrations were determined using the RI data where available, such as
for on-site and off-site soil exposure point concentrations. In other
instances, such as in the case of the air pathways, fate and transport models
were applied to calculate these concentrations.
According to USEPA guidance, the most appropriate measurement of central
tendency for environmental chemical concentrations is the arithmetic mean. In
order to account for uncertainty, USEPA guidance requires using the 95% upper
confidence limit (UCL) on the arithmetic mean concentration. The methodology
for calculating this statistic is discussed by Gilbert (1987) and Land
(1975).1 When the 95% UCL exceeds the maximum measured value, USEPA (1989a)
directs that the maximum measured value be used as the exposure point
1A review of the Land (1975) method presented in Gilbert (1987) shows
that the parameter recommended by USEPA (1989a) guidance is the 95% UCL on the
population mean.
4-20
\
1.:
\
concentration. This will,. however, result in an overestimation of exposure
and risks associated with the site, particularly for small sample sizes (e.g.,
off-site surface soil/sediment). There are other instances when the 95% UCL
is very close to the maximum detected concentration. For very large data sets
with small geometric deviations, the 95% UCL and the arithmetic mean
concentration differ very little.
For this risk assessment, exposure point concentrations were calculated for a
reasonable maximum exposure (RME) case and are presented below. The results
of the average case are presented in the Uncertainty Section (7.0). The RME
concentration is the 95% UCL on the mean concentration (or maximum as
necessary) as required by USEPA guidance. Maximum measured concentrations are
also presented in order to clearly indicate the instances when sample
variability and size required the use of the maximum concentration as a
default for the 95% UCL.
The following text summarizes the basis for the exposure point concentrations
for each pathway. In cases where mathematical modeling was performed to
estimate these concentrations, a description of the model is also provided.
4.4.1 Exposure Point Concentrations in On-Site Surface Soil/Sediment
RME on-site surface soil/sediment exposure point concentrations will be used
to evaluate direct contact exposure under both current and future land-use
conditions. Under current land-use conditions, the trespassing older children
are the receptors of potential concern, while under future land-use
conditions, hypothetical future workers and adult and child (1-6 years)
residents are the receptors which will be evaluated.
Table 4-5 presents the average, maximum and RME concentrations for chemicals
in on-site soil. In the case of benzoic acid, the RME concentration was set
equal to the maximum measured value because the 95% UCL was greater than the
maximum concentration (due to sample size and variability).
4-21
TABLE 4-5
EXPOSURE POINT CONCENTRATIONS FOR ON-SITE SURFACE SOIL/SEDIMENT
Chemical
Chemicals of
Potential Concern
Aldrin
alpha·BHC
beta-BHC
garrma-BHC
Benzoic acid
alpha-Chlordane
ganma-Chlordane
4,4'-000
4,4'-DDE
4,4' -DDT
Dieldrin
Toxaphene
Average
Exposure Point
Concentration
(ug/kg) (a)
4.4
82
130
71
1,400
41
75
1,300
1,000
3,600
140
16,000
RME
Exposure Point
Concentration
(ug/kg) Cb)
4.5
130
270
120
3,700
42
49
3,700
2,000
9,000
250
37,000
Maximum
Detected
Concentration
(ug/kg)
5.9
1,500
2,000
840
3,600
45
49
15,000
11 ,ODO
54,000 1,500
220,000
Ca) Average concentration (including one-half the detection limit for non-detected values).
Cb) RME concentration is the 95¾ upper confidence limit on the arithmetic mean,
or the maximum detected value, whichever is less.
4-22
I. :
' '
4.4.2 Exposure Point Concentrations in Off-Site Surface Soil/Sediment
Off-site surface soil/sediment concentrations were used to estimate exposure
point concentrations under current land-use conditions. The receptor of
concern is older children (8-13 years).
Table 4-6 presents the average, maximum and RME concentrations for chemicals
in off-site soil. For all of the chemicals of potential concern in off-site
soil/sediment, the RME concentrations were set equal to the maximum measured
values because the 95% UCL was greater than the maximum concentrations.
4.4.3 Exposure Point Concentrations in Groundwater
The RME exposure point concentrations will be used to evaluate ingestion of
chemicals in groundwater from both the surficial aquifer and the second
uppermost aquifer under future land-use conditions. Hypothetical future adult
and child (1-6 years) residents, and merchants are the receptors of potential
concern for the surficial aquifer which will be evaluated. Additionally, the
RME exposure point concentrations will be used to evaluate dermal absorption
of chemicals while showering during residential use of the surficial aquifer.
Table 4-7 presents the average, maximum and RME concentrations for chemicals
in the surficial aquifer at the site.
Hypothetical future adult and child (1-6 years) residents are the receptors of
potential concern for the second uppermost aquifer. The TCE concentration of
180 ug/L presented earlier in Table 2-6 will be used to evaluate ingestion of
groundwater in the second uppermost aquifer.
4.4.4 Exposure Point Concentrations for Showering with Groundwater
For inhalation exposure while showering, the groundwater concentrations for
volatile organic chemicals in the surficial aquifer presented in Tables 4-7,
and the maximum concentration for TCE presented earlier in Table 2-6 are input
4-23
TABLE 4-6
EXPOSURE POI NT CONCENTRATIONS FOR OFF-SITE SUR FACE S_OI L/SED IMENT
Chemical
Chemicals of
Potential Concern
beta-BHC
4 4' -DOD
4' 4' -DOE
4141 -DDT
oieldrin
Toxaphene
Average
Exposure Point
Concentration
(ug/kg) (a)
270
5,900
1,400
13,000
10
51,000
RME
Exposure Point
Concentration
(ug/kg) Cb)
540
25,000
6,600
52,000
12
190,000
Maximum
Detected
Concentration
(ug/kg)
540
25,000
6,600
52,000
12
190,000
(a) Average concentration (including one-half the detection limit for non-detected values).
(b) RME concentration is the 95% upper confidence limit on the arithmetic mean,
or the maximum detected value, whichever is less.
4-24
I ,
Chemicals of
Potential Concern
Surficial Aquifer
Organics:
Aldrin
alpha-BHC
beta-BHC
del ta-BHC
ga1TJT1a·BHC
Bis(2-ethylhexyl)phthalate
Dieldrin
4,4' ·DOE
Endr in ketone
Heptachlor epoxide
Toxaphene
1,2,4-Trichlorobenzene
Inorganics:
Aluminum
Bariun
Calcium
Iron
Magnesiun
Manganese
Mercury
Potassiun
Vanadium
Zinc
Second Uppermost Aquifer
Trichloroethene
TABLE 4-7
EXPOSURE POINT CONCENTRATIONS FOR GROUNDUATER
Average
Exposure Point
Concentration
(ug/L) (a)
1.DE·D1 4.4E+OO
5 .2E+OO
4.BE+OO
3.6E+OO
5 .4E+OO
1 .OE-01
1 .OE-01
6.0E-01
1.0E-01
3.6E+OO
4.SE+OO
5.6E+03
1. 7E+02
2.3E+04
6.9E+02 7.7E+03
7.0E+01
3.0E-01
5.2E+04
1. 5E+01 2.2E+02
1 .05E+02
RME
Exposure Point
Concentration
(ug/L) (b)
2.0E-01
3.6E+01
2.5E+01
2.9E+01
3.0E+01
6.4E+OO
1.2E+OO
1.0E-01
3. 7E+OO
3.0E-01
5.9E+OO
5.0E+OO
1. 7E+04
2.BE+02
5.0E+04
3.3E+03
1.BE+04
1.0E+02
1.0E+OO
1.6E+05
3.8E+01 5.8E+02
1.80E+02
(a) Average concentration (including one-half the detection limit for non-detected values).
Maximum
Detected
Concentration
(Ug/L)
4.0E-01 3.6E+01
2.5E+01
2.9E+01
3.0E+01
7.0E+OO 2.0E+OO
2.0E-01
4.0E+OO
3.0E-01
9.6E+OO
5.0E+OO
1. 7E+04
2.BE~02
5.0E+04
3.3E+03
1.BE+04
1.0E+02
1.0E+00
1.6E+05
3.8E+01
5.8E+02
1 .80E+02
(b) RME concentration is the 95¾ upper confidence limit on the arithmetic mean, or the maxi1T'l.1111 detected
value, whichever is less.
4-25
into a shower model (Foster and Chrostowski 1987). The outputs from the
shower model are in units of mg/m3 of the. organic chemicals released from
groundwater. These results are presented in Table 4-8. Exposure to chemicals
of potential concern that could volatilize from groundwater were estimated
using a shower model developed by Foster and Chrostowski (1986,1987). The
shower model estimates the rate of transfer of volatile organic chemicals
(VOCs) from shower droplets to the air and their subsequent inhalation. The
VOC concentrations in shower droplets input into the shower model are the
chemical concentrations in the groundwater. The shower model uses a
one-compartment indoor air model to estimate indoor air VOC levels which
assumed instantaneous and complete mixing in the room air and no chemical
decay of the VOCs once they are released into the room air. The model does
not estimate potential dermal absorption of contaminants while showering.
However, dermal absorption from short-term exposures to dilute water
concentrations is expected to be minimal in comparison to potential inhalation
exposures. Details of the shower model are given in Appendix C.
4.4.5 Exposure Point Concentrations in Ambient Air
The chemicals of potential concern in on-site surface soil will volatilize to
varying degrees into ambient air where inhalation by on-site receptors would
occur. Vnder current land-use conditions, the receptors of concern are old~r
trespassing children, while under future land-use conditions, hypothetical
merchants and future adult and child (1-6 years) residents are the receptors
of concern.
Table 4-9 summarizes the estimated average on-site exposure point air
concentrations over the periods of 6, 8.4, 9, 25 and 30 years; these time
periods correspond to average and RME durations for a trespassing older child,
a future child resident, a future merchant, and a future adult resident .. The
air concentrations were determined through the use of emission and air
dispersion models and take into account decreasing chemical releases over
time. Details of the modeling are presented in Appendix D.
4-26
I '
Chemicals of
Potential Concern
Surficial Aquifer
Aldrin
alpha·BHC
beta-BHC
ganma-BHC
BisC2-ethylhexyl)phthalate
Dieldrin
4,4'-DDE
Toxaphene
1,2,4-Trichlorobenzene
Second Uppermost Aquifer
Trichloroethene
TABLE 4-8
EXPOSURE POINT CONCENTRATIONS FOR CHEMICALS
VOLATILIZED WHILE SHOWERING
Average
Exposure Point
Concentration
(mg/m3) Ca)
3.11E·O7 1.32E·OB 5.37E-OB
6.31E·O7 4.73E·OB 6.35E·OB 1.14E·O7
2. 79E-O6
2.34E-O5
5.33E-O1
RME
Exposure Point
Concentration
(mg/m3) Cb)
6.21E·O7 4. 76E·D6 2.SBE-O7
5.79E·O3 5.61E·O8
2.54E-O7 1.14E-O7
4.57E-O6
2.6OE·OS
8.SOE·D1
(a) Average concentration (including one-half the detection limit for non-detected values).
Cb) RME concentration is the 95X upper confidence limit on the arithmetic mean.
4-27
TABLE 4-9
ON-SITE EXPOSURE POINT AIR CONCENTRATIONS Cal
Exposure Point
Air Concentration Chemicals of For 6 Year Period
Potential Concern (ug/m3) (b)
Aldrin 5.23E-06
alpha-BHC 5.06E-05
beta·BHC 2.81E-05
alpha-Chlordane 4. 74E-05
ganma-Chlordane 4.BSE-05
4,4'·DDT 4.31E-04
Dieldrin 1.SOE-04
Toxaphene 1.29E-02
Exposure Point
Air Concentration
For 8.4 Year Period
(Ug/m3) (C)
4.42E-06
4.27E-05
2.38E-05
4-01E-05
4.10E-05
3.65E-04
1.26E-04
1.09E-02
Exposure Point
Air Concentration
For 9 Year Period
Cug/m3l Cdl
4.27E-06
4. 13E-05
2.29E-05
3.65E-05
3.95E-05
3.52E-04
1.22E-04 • 1.0SE-02
Exposure Point
Air Concentration
For 25 Year Period
(ug/m3) Ce)
2.56E-06
2.48E-05
1 .38E-05
2.32E-05
2.38E-05
2.11E-04
7.33E-05
6.30E-03
Exposure Point Air Concentration
For 30 Year Period
Cug/m3l Cf)
2.34E-06
2.26E-05
1 .25E-05
2.12E-05
2.17E-05
1.93E-04
6.71E-05
5.77E-03
(a) Represents an estimated or modeled spatial average air concentration within property boundaries over the designated exposure period.
(b) Modeled on-site average air concentration for a 6 year period which will be used to estimate exposure to an older child trespasser (average and RME cases).
Cc) Modeled on-site average air concentration for a 8.4 year period which will be used to estimate exposure to a merchant (average case).
(d) Modeled on-site average air concentraion for a 9 year period which will be used to estimate exposure to a future resident (average case).
(e) Modeled on•site average air concentration for a 25 year period which will be used to estimate exposure to a merchant (RME case).
Cf) Modeled on-site average air concentration for a 30 year period which will be used to estimate
exposure to a future resident CRME case).
4-28
I .
I
I
I -.
Emissions from surface soi~ were estimated using a soil volatilization model
synthesized from Bomberger et al. (1983), Millington and Quirk (1961) and
USEPA (1~86). USEPA's model was originally developed·for estimating air
exposures in USEPA's development of PCB clean-up levels. Because of the high
soil affinity of PCBs, the model assumes that transport of a chemical in soil
is primarily by passive diffusion in the soil and ignores all other forms of
transport. The pesticides in the site soil are similar to PCBs in terms of
their high affinities for soil, low volatility and general persistence, and
therefore the USEPA model is considered appropriate for this assessment when
used with site-specific chemical and soil parameters. In addition, the model
was used with conservative initial and boundary conditions (e.g., a uniform
initial concentration and infinite depth of contamination) which tend to
overpredict average flux rates over the period of·exposure.
The average flux rates calculated over the various periods of exposure for the
chemicals of potential concern were used with the Industrial Source Complex
Long Term (ISCLT) air dispersion model to predict air concentrations. The
ISCLT model is a USEPA-developed guidance model, which means that it is
approved and recommended for air dispersion modeling (USEPA 1987).
Meteorological data from the National Weather Service (NWS) station at Fort
Bragg, North Carolina were input into the model. This station is 25 miles to
the east and is the nearest NWS station to the site. A 50-by-50 foot receptor
grid was established over the site. Average on-site air concentrations were
determined as the mean of the modeled concentrations at the nodes of the
receptor grid which were within the site boundary.
4.4.6 Exposure Point Concentrations in Ambient Air Off-Site
The chemicals of potential concern which have volatilized will disperse off-
site where other receptors may be located. Under current land-use conditions,
exposure point concentrations in the commercial area to the north and the
residential area to the northeast of the site were modeled. An additional
off-site location was not designated under future land-use conditions since
4-29
the predominant wind direc.tion is to the north and northeast and thus,
exposure point concentrations in areas of potential future development would
not be greater than those already modeled to the north and northeast of the
site.
Table 4-10 summarizes the estimated average exposure point air concentrations
in the commercial area north of the site, while Table 4-11 presents the
estimated average exposure point air concentrations in the·residential area
northeast of the site. The air concentrations are presented for various
periods which correspond to exposure durations for the off-site receptors of
concern. Air concentrations were estimated in this manner in order to take
into account decreasing chemical emissions over time. Emission and air
dispersion calculations were conducted using the same methodology as presented
above. Details of the modeling are presented in Appendix D.
4.4.7 Exposure Point Concentrations for Fugitive Dust Emissions
The chemicals of potential concern adsorbed to on-site surface soil particles
can be entrained into ambient air through the action of wind erosion.
However, most of the site is vegetated so the potential for wind erosion at
the site is considered low. Exposure point concentrations for wind blown dust
were determined by first estimating an emission rate for respirable particles
as a result of wind erosion, then the emission source information was input to
an air di~persion model to calculate ambient air concentrations for off-site
receptors. Emissions of respirable dust were calculated using the Cowherd et
al. (1985) emission factor as recommended by the USEPA (1988) for evaluating
the potential degree of particulate emission via wind erosion. Ambient air
concentrations associated with the dust emissions were calculated for the
nearest off-site resident and commercial establishment using the USEPA's ISCLT
air dispersion model. Table 4-12 presents the ambient air concentrations for
both exposure points. Details of the emissions and air dispersion modeling
are presented in Appendix D.
4-30
\
I. '
I
Chemicals of
Potential Concern
Aldrin
alpha·BHC
beta·BHC
alpha-Chlordane
gamna-Chlordane
4,4'-DDT
Dieldrin
Toxaphene
TABLE 4-10
OFF-SITE EXPOSURE POINT AIR CONCENTRAHONS NORTH OF THE SITE (a)
Exposure Point Exposure Point Air Concentration Air Concentration
For 8.4 Year Period For 25 Year Period
(ug/m3) (b) ( ug/n,3) ( C)
4.32E·D6 2.SOE-06
4.17E-05 ?,42E·OS
2.32E·OS 1.35E-D5
3.91E·OS 2.27E·OS
4.01E·D5 2.32E·OS
3.56E·04 2.06E·04
1.24E·04 7.16E-05
1.06E·02 6.15E-03
(a)
(b)
(C)
Represents an estimated or modeled average air concentration at the location of the nearest
downwind corTmercial area over the designated exposure period.
Modeled off-site average air concentration for a 8.4 year period, which will be used to
estimate exposure to a merchant north of the site (average case).
Modeled off-site average air concentration for a 25 year period, which will be used to
estimate exposure to a merchant north of the site (RME case),
4-31
TABLE 4-11
OFF-SITE EXPOSURE POINT AIR CONCENTRATIONS TO THE NORTHEAST OF THE SITE (a)
Exposure Point Exposure Pciint Exposure Point Air Concentration Air Concentration Air Concentration Chemicals of For 6 Year Period For 9 Year Period For 30 Year Period Potential Concern (ug/m3J (bl (ug/m3) Ccl (ug/m3J Cd)
Aldrin 5.15E·07 4.20E-07 2.30E-07
alpha-BHC 4.98E·06 4.06E·06 2.23E·06
beta-BHC 2. TTE-06 2.26E·06 1.24E·06
alpha-Chlordane 4.67E-06 3.81E·06 2.09E·06
ganma-Chlordane 4.78E-06 3.90E·06 2.14E-06
4,4'-DDT 4.25E-05 3.47E-05 1.90E·OS
Dieldrin 1.47E-05 1.20E·OS 6.59E·06
Toxaphene 1.27E-03 1.03E-03 5.66E·04
(a) Represents an estimated or modeled average air concentration at the location of the nearest
downwind residential area over the designated exposure period.
Cb) Modeled off-site average air concentration for a 6 year period which will be used to estimate
exposure to a young child resident northeast of the site (average and RME cases).
Cc) Modeled off-site average air concentration for a 9 year period which will be used to estimate
exposure to an adult resident northeast of the site (average case).
Cd) Modeled off-site average air concentration for a 30 year period which will be used to
estimate exposure to an adult resident notheast of the site (RME case).
4-32
\
I.
TABLE 4-12
EXPOSURE POINT CONCENTRATIONS FOR OUST PARTICULATES.
Merchant Resident
Exposure Point Exposure Point
Concentration Concentration
Chemical (ug/m3) (a) (ug/m3) Cb)
Chemicals of
Potential Concern
-----------------
Aldrin 1.84E-O9 1.BSE-1O
alphe-BHC 3.46E-O8 3.49E-O9
beta-BHC 5.O1E-O8 5.OSE-O9
delta-BHC 3.O1E-O8 3.O3E-O9
ganma-BHC 2.BBE-O8 2.9OE-O9
Benzoi c acid 5.84E-O7 5.89E-O8
alpha-Chlordane 1. 71E-O8 1. 73E-O9
ganma-Chlordane 1.75E-O8 1.ffi-O9
Dieldrin 6.29E-O9 6.31E-O9
4,4 1-000 5.43E-O7 5.47E-O8
4,4 1-DDE 4.59E-O7 4.63E-O8
4,4 1-DDT 1.54E-O6 1.56E-O7
Toxaphene 6.68E-O6 6.73E-O7
(a) Modeled off-site dust particulate concentration which will
be used to estimate exposure to merchants north of the site.
(b) Modeled off-site dust particulate concentration which will
be used to estimate exposure to residents northeast
of the site.
4-33
4.5 QUANTIFICATION OF EXPOSURE
To quantitatively assess exposure associated with the ·selected pathways, the
chronic daily intake (CDI) of each chemical of potential concern was
estimated. CDls are expressed as the amount of a substance ingested or
dermally-absorbed per unit body weight per unit time, or mg/kg-day. The CDI
is averaged over a lifetime of 70 years for carcinogens and over the exposure
period for noncarcinogens. CDis are estimated using concentrations of
chemicals together with other exposure parameters that specifically describe
the exposure pathway.
4.5.1 Exposure Estimates Under Current and Surrounding Land-Use Conditions
Under current land-use conditions, intakes associated with inhalation of
chemicals volatilized and wind blown from on-site surface soil/sediment to
both on-site and off-site receptors, and incidental ingestion and dermal
contact with both on-site and off-site surface soil/sediment were estimated.
The assumptions associated with calculating these exposures and the equations
used to estimate CDis are provided below. It should be noted that despite the
fact that pesticide concentrations in soils are expected to decline due to
volatilization and/or biological degradation, it was assumed for direct
contact exposures that the chemicals would remain constant over the exposure
period.
4.5.1.1 Incidental Ingestion of Surface Soil/Sediment
Older child trespassers who may occasionally explore the site or the ditch
areas off-site may come in direct contact with the chemicals of potential
concern through the incidental ingestion of surface soil/sediment. Exposures
for this pathway are calculated using the following equation:
4-34
\
I. .'
where
CDI
c.
IR
CF
FI
ED
EF
BW
Days
AT
CDI = C5 •IR•FI•EF•ED•CF
BW•AT•Days
chronic daily chemical intake (mg/kg-day),
chemical concentration in soil (ug/kg),
soil ingestion rate (mg/day),
conversion factor (1 kg/109 ug),
fraction ingested from source or a probability of exposure
( uni tless) ,
duration of exposure (years),
frequency of exposure (days/year),
average body weight (kg),
conversion factor (365 days/year), and
averaging time (70 years for carcinogens, duration of
exposure for noncarcinogens).
The assumptions used to estimate CDls for the older child trespasser by this
exposure pathway are listed in Table 4-13 and are briefly described below. The
RME exposure point soil concentrations (C5) presented in Tables 4-5 and 4-6
were used in the above equation for on-site and off-site exposure scenarios,
respectively.
For the older child trespasser, a reasonable maximum exposure (RME) case was
evaluated. The frequency of exposure (EF) was derived by assuming a child
will trespass on the site one day a week, 50 weeks per year. In order to
estimate the CDI for a trespassing older child contacting both on-site and
off-site surface soil/sediment, a probability of contact with each of these
areas was developed. This probability factor defined here as (Fl) takes into
account the probability of ingestion of the chemicals of potential concern
based on the fraction of the site covered with clean fill, or not containing
pesticides. It was estimated that approximately 42% of ·the site contains
chemical residuals in surface soil/sediment, while 58% of the site has been
covered with clean soil.
4-35
For both on-site and off-site scenarios, a soil ingestion rate (IR) of 100
mg/kg was used for the RME exposure conditions. This value is taken from
USEPA guidance (1989a, 1991a). A time-weighted average body weight (BW) value
of 37 kg for older children was based on data provided in USEPA (1989b).
The exposure point concentrations and resulting CDis for chemicals exhibiting
carcinogenic effects and chemicals exhibiting noncarcinogenic effects due to
the ingestion of site surface soil/sediment are summarized i~ Table 4-14 for
an on-site older child trespasser. Table 4-15 presents the exposure point
concentrations and the resulting CDis for exposure to off-site soil/sediment
by an older child trespasser.
4.5.1.2 Dermal Absorption of Chemicals from Surface Soils/Sediment
Potential exposures through dermal contact with chemicals of potential concern
in soil may occur by an older child trespasser on the site, or in a nearby
impacted area. CDI estimates for dermal contact with chemicals in
soil/sediment were calculated using the equation below:
where
CDI
c.
SA
AF
Ab
EF
ED
CF
BW
Days
AT
chronic daily chemical intake (mg/kg-day),
chemical concentration in soil (ug/kg),
skin surface area available for contact (cm2),
soil-to-skin adherence factor (mg/cm2),
dermal absorption fraction (unitless),
frequency of exposure events (days/year),
duration of exposure (years),
conversion factor (1 kg/109 ug),
average body weight (kg),
conversion factor (365 days/year), and
averaging time (70 years for carcinogens, duration of
exposure for noncarcinogens).
4-36
I. :
TABLE 4·13
EXPOSURE PARAMETERS FOR THE INCIDENTAL INGESTION
OF SURFACE SOIL/SEDIMENT
BY OLDER CHILDREN
CURRENT LAND-USE CONDITIONS.
Parameters
Age Period
Exposure Frequency (days/year) (a)
Exposure Duration (years) (b)
Soil Ingestion Rate (mg/day) (c)
Fraction Ingested (dimensionless) (d)
Body Weight (kg) (e)
Period Over Which Risk is Being Estimated
(years)
Carcinogenic (f)
Noncarcinogenic
Reasonable
Maximum Exposure
(RME) Case
[8-13 Years of Age]
50
6
100
0.42
37
70
6
(a) Assumes an individual will trespass on the site one day a week, 50
weeks a year.
(b) Assumes children and teenagers from ages 8 to 13 play on the site.
(c) Based on USEPA (1991a, 1989a).
(d) A probability of contact factor which is the ratio of the area
containing chemical residues in surface soil/sediment to the total
property area (0.42 of the property).
(e) Calculated from USEPA (1989b).
(f) Based on USEPA (1991a, 1989a) standard assumption for lifetime. This
value is used in calculating exposures for potential carcinogens.
4-37
11-Mar-92 --cf-icct
TABLE 4-14
EXPOSURE POINT CONCENTRATIONS AND CHRONIC DAILY INTAKES FOR INCIDENTAL INGESTION Of ON-SITE SOIL/SEDIMENT BY AN OLDER CHILD TRESPASSER UNDER CURRENT LAND-USE CONDITIONS (a)
Chemical
Chemicals Exhibiting
Carcinogenic Effects
Organics:
Aldrin
alpha-BHC
beta-BHC
garrrna-BHC
alpha-Chlordane
garrrna-Chlordane
4 4' -DOD
4;4'-DDE
4 4'-DDT
oieldrin
Toxaphene
Chemicals Exhibiting
Noncarcinogenic Effects
Organics:
Aldrin
ganma-BHC
Benzoic acid
alpha-Chlordane
garrrna-Ch l ordane
4 4'-DOT
oieldrin
RME
Exposure Point
Concentration
(ug/kg) (cJ ·
4.SOE+DO
1.30E+02 2.70E+02
1.20E+02
4.20E+01
4.90E+01
3.70E+03
2.00E+03
9.00E+03 2.50E+02
3.70E+04
4.SOE+OO
1.20E+02
3.60E+03
4.20E+01
4.90E+01
9.00E+03
2.50E+02
RME Chronic Daily
Intake
(mg/kg-day) (d)
6.00E-11
1. 73E-09
3.60E-09
1.60E-09
5.60E-10
6.53E·10
4.93E-08
2.67E-08
1.20E-07
3.33E-09
4.93E-07
7.00E-10
1.87E-08
5.60E-07
6.53E·09
7.62E-09
1.40E-06 3.89E-08
Ca) COis have been calculated for those chemicals of potential concern with toxicity criteria. The following chemicals of potential concern are not presented due to lack of toxicity criteria: delta-BHC.
(b) Average concentration (including one-half the detection limit for non-detected values). (c) RME concentration is the 95¾ upper confidence limit on the arithmetic mean. (d) See text for exposure assl.lTptions.
4-38
;
TABLE 4-15
EXPOSURE POINT CONCENTRATIONS AND CHRONIC DAILY INTAKES FOR INCIDENTAL
INGESTION OF OFF-SITE SOIL/SEDIMENT BY AN OLDER CHILD
Chemical
Chemicals Exhibiting
Carcinogenic Effects
Organics:
beta·BHC
4 41 -DDD
4141 -DDE
414'·0DT
oieldrin
Toxaphene
Chemicals Exhibiting
Noncarcinogenic Effects
Organics:
4 4'-DDT
oieldrin
UNDER CURRENT LAND-USE CONDITIONS (a)
RME
· Exposure Point
Concentration
(ug/kg) (c)
5.4OE+O2
2.5OE+O4
6.6OE+O3
5 .2OE+04
1.2OE+O1
1.9OE+O5
5.2OE+O4
1.2OE+O1
RME
Chronic Daily
Intake
(mg/kg-day) (d)
7.2OE-O9
3.33E-O7
8.8OE-O8
6.93E-O7
1.6OE·1O
2.53E-O6
8.O9E·O6 1.87E-O9
(a) COis have been calculated for those chemicals of potential concern with toxicity criteria.
Cb) Average concentration (including one-half the detection limit for non-detected values).
(c) RME concentration is the 95% upper confidence limit on the arithmetic mean.
Cd) See text for exposure ass~tions.
4-39
In general, the parameters_ describing frequency and duration of exposure ( EF,
ED), and body weight (BW), were identical to those used for estimating
ingestion of soil by an on-site and off-site child trespasser and are
presented in Table 4-16. Additionally, the exposure point concentrations used
in the dermal absorption pathway are the same as presented in·Tables 4-5 and
4-6 for the on-site and off-site surface soil/sediment ingestion pathways,
respectively.
Parameter values that differ between the two scenarios include the amount of
chemical absorption, the amount of soil accumulation, and the area of exposed
skin. For this pathway, it was assumed that the skin surface area (SA)
available for contact for an older child was 3,086 cm2/day. This value is the
age-weighted 50th percentile values from USEPA (1985, 1989a) for 8-13 year
olds, assuming the surface area of the hands, one-half of the arms, and for
one-half of the legs (27% of the total surface area) is uncovered and exposed.
A soil-to-skin adherence factor (AF) of 1.0 mg/cm2 was used. This value was
calculated based on data provided by Driver et al. (1989) for soil types most
characteristic of the Candor series soil present at the site [gravely sands,
and silty sands containing low (0.43%) total organic carbon]. The expected
lifetime used in calculating CDis for carcinogens was assumed to be 70 years
(USEPA 1991a, 1989a).
The amount of chemical absorbed through the skin into the body from contacting
soil is also needed to estimate dermal exposures. Intensive investigation
into the amount of chemicals that may be absorbed through the skin under
conditions normally encountered in the environment (and assumed to occur for
this assessment) are, however, almost completely lacking. For a chemical to
be absorbed through the skin from soil, it must be released from the soil
matrix, pass through the stratum corneum., the· epidermis, the dermis I and into
the systemic circulation. In contrast, chemicals absorbed by the lung or
gastrointestinal tract may pass through only two cell layers (Klaassen et al.
1986).
4-40
TABLE 4-16
EXPOSURE PARAMETERS FOR DERMAL CONTACT
WITH SURFACE SOIL/SEDIMENT
BY OLDER CHILDREN
CURRENT LAND-USE CONDITIONS.
Parameters
Age Period
Exposure Frequency (days/year) (a)
Exposure Duration (years) (b)
Skin Surface Area available for Contact
(cm2) (c)
Soil to Skin Adherence Factor (mg/m2) (d)
Dermal Absorption Factor (dimensionless) (e)
Chlorinated Pesticides
Benzoic Acid
Body Weight (kg) (f)
Period Over Which Risk is Being Estimated
(years)
Carcinogenic (g)
Noncarcinogenic
Reasonable
Maximum Exposure
(RME) Case
[8-13 Years of Age]
so
6
3,086
1.0
0.01
0.01
37
70
6
(a) Assumes an individual will trespass on the site one day a week, SO
weeks a year.
(b) Assumes children and teenagers from ages 8 to 13 play on the site.
(c) Surface area based on SOth percentile values from USEPA (1989a) and
USEPA (1985). Based on skin surface area of hands, one-half arms,
and one-half legs for a child 8-13 years of age.
(d) Based on Driver et al. (1989) and Clement (1988).
(e) Based on USEPA Region IV guidance.
(f) Calculated from USEPA (1989b).
(g) Based on USEPA (1991a, 1989a) standard assumption for lifetime.
This value is used in calculating exposures for potential
carcinogens.
4-41
For the purposes of this a~sessment, the amount of exposure due to dermal
absorption is evaluated by estimating the. fraction of absorption from
contacted soil that may occur for the selected chemicals of potential concern.
When a chemical is found in soil which has become deposited onto the skin,
there are two competing processes which dictate the direction and rate of
pesticide removal --absorption and volatilization. Even for chemicals with
relatively low volatility, the presence of a thin film and elevated
temperature of the skin can make volatilization an important process. In this
assessment, the effects of volatilization are ignored which can lead to an
over-estimate of risk. There are a number of factors which can affect the
dermal absorption of a compound including the concentration in the applied
dose, the site of exposure, inter-individual variability, and the vehicle in
which the chemical is delivered to the skin (e.g., in a solvent or soil
matrix). Because of the paucity of experimental data on dermal absorption
from soil, not all of these parameters can be taken into account in estimating
dermal absorption factors. In general, the extent of absorption appears to be
related to the hydrophobicity of a compound whereas the rate of absorption is
probably related to mass transfer parameters such as molecular volume. A
dermal absorption factor of 1% was used for all organic chemicals.·
CDis representing absorption from soil were estimated using the exposure
parameters discussed above and are summarized in Tables 4-17 and 4-.18 for on-
site and off-site older child trespassers, respectively. The CDI's are
calculated differently for chemicals exhibiting carcinogenic and
noncarcinogenic effects (with respect to averaging time).
4.5.1.3 Inhalation of Dust Particulates and Volatilized Chemicals Released
from Surface Soil/Sediment
Inhalation exposures to vapor emissions in ambient air were estimated for
several receptors, an on-site older child (8-13 year-old) trespasser,
merchants across Route 211 directly north of the site, and a child (1-6 years)
and adult resident to the northeast of the site. Exposure point air
concentrations were estimated through the use of mathematical emission and air
4-42
'
TABLE 4·17
EXPOSURE POINT CONCENTRATIONS AND CHRONIC DAILY INTAKES FOR DERMAL CONTACT
OF ON-SITE SOIL/SEDIMENT BY AN OLDER CHILD TRESPASSER
Chemical
Chemicals Exhibiting
Carcinogenic Effects
Organics:
Aldrin
alpha-BHC
beta-BHC
ganma-BHC
alpha-Chlordane
ganma-Chlordane
4 4'-000
4' 4'-DDE
41 4'-DDT
oieldrin
Toxaphene
Chemicals Exhibiting
Noncarcinogenic Effects
Organics:
Aldrin ganma-BHC
Benzoic acid
alpha-Chlordane
ganma-Chlordane
4 4' -DDT
oieldrin
UNDER CURRENT LAND-USE CONDITIONS. (a)
RME
Exposure Point
Concentration
(ug/kg) (c)
4.SDE+OO
1.3OE+O2
2. 7OE+O2
1.2OE+O2
4.2OE+O1
4.9OE+O1
3.7OE+O3
2.OOE+O3
9.OOE+O3
2.5OE+O2
3.7OE+O4
4.SOE+OO
1.2OE+O2
3.6OE+O3
4.2OE+O1
4.9OE+O1
9.OOE+O3
2.5OE+O2
RME
Chronic Dai Ly
Intake
(mg/kg-day) Cd)
4.41E·11
1.27E·O9
2.64E·O9
1.18E·O9
4.11E·1O
4.BOE-1O
3.62E·O8
1.96E·O8
8.81E·O8
2.45E·O9
3.62E·O7
5.14E·1O
1.37E·O8
4.11E-O7
4.BOE-O9
5.6OE-O9
1.O3E·O6
2.86E·O8
(a) COis have been calculated for those chemicals of potential concern with toxicity criteria.
The following chemicals of potential concern are not presented due to lack of toxicity
criteria: delta-BHC.
(b) Average concentration (including one-half the detection limit for non-detected values).
(c) RME concentration is the 95% upper confidence limit on the arithmetic mean.
Cd) See text for exposure assllllptions.
4-43
TABLE 4-18
EXPOSURE POINT CONCENTRATIONS AND CHRONIC DAILY INTAKES
Of Off-SITE SOIL/SEDIMENT BY AN OLDER CHILD UNDER CURRENT LAND-USE CONDITIDNS (a)
RME
Exposure POint
Concentration
Chemical (ug/k.g) (c)
Off-site Chemicals Exhibiting
Carcinogenic Effects
Organics:
beta-BHC
4 4'-000
4' 4'-DDE
4 1 4'-DDT
oieldrin
Toxaphene
Off-site Chemicals Exhibiting
Noncarcinogenic Effects
Organics:
4 41 -DDT
oieldrin
5.40E+02
2.50E+04 6.60E+03
5 .20E+04
1.20E+01
1.90E+05
5.20E+04
1.20E+01
FOR DERMAL CONTACT
RME
Chronic Daily
Intake
(mg/kg-day) Cd)
5.29E-09
2.45E-07
6.46E-OB
5.09E-07
1.18E-10
1.86E-06
5.94E-06
1 .37E-09
Ca) COis have been calculated for those chemicals of potential concern with toxicity criteria.
(b) Average concentration (including one-half the detection limit for non-detected values).
(c) RME concentration is the 95¾ upper confidence limit on the arithmetic mean.
(d) See text for exposure asslillptions.
4-44
dispersion models previously described in Sections 4.4.5 and 4.4.6 and
presented in Tables 4-9 through 4-11. Additionally, inhalation exposures to
dust particulates by merchants north of the site and a child and adult
resident to the northeast of the site were estimated. Exposure point
concentrations for the dust emissions were previously described in Section
4.4.7 and presented in Table 4-12.
Exposures associated with inhalation of volatilized chemicals released from
surface soil/sediment are calculated using the following equation:
where
CDI
c.
IR
ET
EF
ED
BW
AT
Days
C • IR • ET • EF • ED CDI = --'''-=~~=-~---BW. AT. Days
chronic daily intake (mg/kg-day),
exposure point concentration in air
(mg/m3);
inhalation rate (m3fhour),
exposure time (hours/day),
frequency of exposure (days/year),
duration of exposure (years),
body weight over the period of exposure (70 kg; EPA 1989a),
averaging time (70 years for carcinogens, duration of
exposure for noncarcinogens),
conversion factor (365 days/year).
Note that CDis are calculated differently for chemicals exhibiting
carcinogenic versus noncarcinogenic effects. In the former case, exposure is
extrapolated over a lifetime of 70 years while in the latter case, CDis are
estimated over the actual duration of exposure.
For the on-site older child trespasser, the exposure parameters describing
frequency and duration of exposure, body weight, lifetime were identical to
those used for estimating incidental ingestion of chemicals from on-site
surface soil/sediment as shown in Table 4-19. It was further assumed that
4-45
TABLE 4-19
EXPOSURE PARAMETERS FOR INHALATION OF VOLATILIZED CHEMICALS
BY OLDER CHILD TRESPASSERS
CURRENT LAND-USE CONDITIONS
Parameter
Age Period
Exposure Frequency (days/year) (a)
Inhalation rate (m3/bour)(b)
Exposure Duration (years) (c)
Exposure Time (hours/day) (d)
Body Weight (kg) (e)
Period Over Which Risk is Being
Estimated (years)
Carcinogenic (f)
Noncarcinogenic
Reasonable Maximum
Exposure (RME) Case
[8-13 Years of Age]
50
1.1
6
4
37
70
6
(a) Assumes an individual will trespass on the site one day a week, 50
weeks a year.
(b) Based on age-weighted ventilation rates for light activity (USEPA 1989b).
(c) Assumes children and teenagers from ages 8 to 13 play on the site. (d) Assumes children play on the site a maximum of 4 hours per day. (e) This value is the time-weighted average body weight for 8-13 year olds and was calculated using data provided in USEPA (1989b). (f) Based on USEPA (1991a, 1989a) standard assumption for lifetime.
This value is used in calculating exposures for potential
carcinogens.
4-46
I '
older children would play .on the site a maximum of 4 hours/day (ET), 50
days/year (EF) for 6 years (ED).
For an off'.site merchant north of the site, the RME parameter values used to
estimate CDis are shown in Table 4-20. Merchants were assumed to work 241
days/year, which is based on 5 days/week, 50 weeks/year, (with 2 weeks
subtracted for vacation), and an additional 9 days subtracted for federal
holidays. A standard default value of 25 years employment dµration (ED) was
used (USEPA 1991a). Standard default assumptions were made regarding body
weight (BW) (70 kg), and lifetime (AT) (70 years) (USEPA 1989a).
For off-site residents, the exposure parameters are presented in Tables 4-21
and 4-22 for a child (1-6 years) and an adult, respectively. Children were
assumed to breath at a rate of 15 m3/day (NCRP 1985), to weigh (BW) 15 kg
(USEPA 1989b) and to be exposed 350 days/year (EF) for 6 years (ED). The
ventilation rate is age-weighted and assumes 10 hours at rest and 14 hours of
active play (NCRP 1985). Adult residents were assumed to have an inhalation
rate of 20 m3/day (USEPA 1991a), to be at home 350 days/year (EF) for a
duration of 30 years (ED). Both values are based upon USEPA (1991a, 1989a),
and represent the upper-bound durations at one residence. Again, standard
default assumptions were made regarding body weight (BW) (70 kg), and lifetime
(AT) (70 years) (USEPA 1989a).
The resulting CDis for chemicals exhibiting carcinogenic effects and chemicals
exhibiting noncarcinogenic effects due to the inhalation of volatile chemicals
are summarized in Tables 4-23 through 4-26 for each of the scenarios,
respectively. The resulting CDis for inhalation of fugitive dust emissions
are presented in Tables 4-27 through 4-29, for the nearby merchants, child
residents and adult residents, respectively.
4-47
(a)
(b)
(c)
(d)
(e)
TABLE 4-20
EXPOSURE PARAMETERS FOR INHALATION OF DUST PARTICULATES
AND VOLATILIZED CHEMICALS BY NEARBY ADULT MERCHANTS
SURROUNDING LAND-USE CONDITIONS
Parameter
Exposure Frequency (days/year) (a)
Inhalation rate (m3/day) (b)
Exposure Duration (years) (c)
Body Weight (kg) (d)
Period Over Which Risk is Being
Estimated (years)
Carcinogenic (e)
Noncarcinogenic
Reasonable Maximum
Exposure (RME)· Case
241
20
25
70
70
25
A merchant is assumed to work 5 days/week, 50 weeks/year (2 weeks
subtracted for vacation), minus 9 days for federal holidays.
Based on USEPA (1991a).
Based upon USEPA (1991a).
Standard default value (USEPA 1989a, 1991a).
Based on USEPA (1991a, 1989a) standard assumption for lifetime.
This value is used in calculating exposures for potential
carcinogens.
4-48
I.\
TABLE 4·21 ·
EXPOSURE PARAMETERS FOR INHALATION OF DUST PARTICULATES AND VOLATILIZED
CHEMICALS BY NEARBY CHILD RESIDENTS
SURROUNDING LAND-USE CONDITIONS
Parameter
Age Period
Exposure Frequency (days/year) (a)
Inhalation rate (m3/day) (b)
Exposure Duration (years) (c)
Body Weight (kg) (d)
Period Over Which Risks is Being
Estimated (years)
Carcinogenic (e)
Noncarcinogenic
Reasonable
Maximum Exposure
(RME) Case
[l - 6 Years of Age]
350
15
6
15
70
6
(a) Standard default value provided by USEPA (1991a).
(b) Based on age weighted ventilation rates for a 1-6 year old
assuming 10 hours at rest and 14 hours of active play (NGRP
1985).
(c) Assumes a residential exposure for a 1-6 year old.
(d) Value based on USEPA (1991a).
(e) Based on USEPA (1991a, 1989a) standard assumption for
lifetime. This value is used in calculating exposures for
potential Carcinogens.
4-49
TABLE 4-22
EXPOSURE PARAMETERS FOR INHALATION OF DUST PARTICULATES AND
VOLATILIZED CHEMICALS BY NEARBY ADULT RESIDENTS
SURROUNDING LAND-USE CONDITIONS
Parameter
Exposure Frequency (days/year) (a)
Inhalation rate (m3/day) (b)
Exposure Duration (years) (c)
Body Weight (kg) (d)
Period Over Which Risk is Being
Estimated (years)
Carcinogenic (e)
Noncarcinogenic
Reasonable Maximum
Exposure (RME)· Case
350
20
30
70
70
30
(a) Standard default value provided by USEPA (1991a).
(b) Based on USEPA (1989a, 1991a).
(c) Based on the national upper-bound time at one residence (USEPA 1991a, 1989a).
(d) Standard default value provided by USEPA (1991a, 1989a). (e) Based on USEPA (1991a, 1989a) standard assumption for
lifetime. This value is used in calculating exposures for
potential carcinogens.
4-50
I.
TABLE 4-23
EXPOSURE POINT CONCENTRATIONS AND CHRONIC DAILY ·INTAKES FOR INHALATION
OF VOLATILIZED CHEMICALS BY AN ON-SITE OLDER CHILD TRESPASSER UNDER CURRENT LAND-USE CONDITIONS Cal
Chemical
Chemicals Exhibiting
Carcinogenic Effects
Organics:
Aldrin
alpha·BHC
beta-BHC
alpha-Chlordane
garrrna-Chlordane
4 4'-DDT
oieldrin
Toxaphene
RME
Exposure Point
Concentration
(ug/m3) Cc)
5.23E·O6
5.O6E-O5
2.81E-O5
4. 74E·O5
4.BSE-O5
4.31E-O4
1.SOE-O4
1 .29E·O2
RME Chronic Daily
Intake (COi)
Cmg/kg·dayJ Cd)
7.3OE·12
7.O7E-11 3.92E-11
6.62E-11
6.TTE-11
6.O2E·1O 2.O9E-1O
1.BOE-O8
(a) COis have been calculated for those chemicals of potential concern with inhalation
toxicity criteria. The following chemicals of potential concern are not presented
due to lack of inhalation toxicity criteria: delta-BHC, garrma-BHC, 4,4'-DDD, and 4,4'-DDE.
Cb) Average concentration (including one-half the detection limit for non-detected values).
(c) RME concentration is the 95¾ upper confidence limit on the arithmetic mean.
(d) See text for exposure asslll'ptions.
4-51
TABLE 4·24
EXPOSURE POINT CONCENTRATIONS AND CHRONIC OAILY INTAKES FOR INHALATION OF
VOLATILIZED CHEMICALS BY A NEARBY ADULT MERCHANT TO THE NORTH
Chemical
Chemicals Exhibiting
Carcinogenic Effects
Organics:
Aldrin
alpha·BHC
beta-BHC
alpha-Chlordane
gal11'!la-Chlordane
4 41 -DDT
oieldrin
Toxaphene
UNDER CURRENT LAND-USE CONDITIONS (a)
RME
Exposure Point
Concentration
(Ug/m3) (C)
2.50E·06
2.42E·05
1.35E·05
2.27E·05
2.32E·05
2.06E·04
7.16E·05
6.15E·03
RME
Chronic Daily
Intake (CDI)
(mg/kg-day) (d)
1.68E·10
1.63E·09
9.10E·10
1.53E·09
1.56E·09
1.39E·08
4.82E·09
4.14E·07
(a) COis have been calculated for those chemicals of potential concern with inhalation toxicity
criteria. The following chemicals of potential concern are not presented due to lack of
inhalation toxicity criteria: delta-BHC, garrma-BHC, 4,4'-DDD and 4,4'-DOE.
(b) Average concentration (including one-half the detection limit for non-detected values).
(c) RME concentration is the 95% upper confidence limit on the arithmetic mean. Cd) See text for exposure essurptions.
4-52
TABLE 4-25
EXPOSURE POINT CONCENTRATIONS AND CHRONIC DAILY INTAKES
FOR INHALATION OF VOLATILIZED CHEMICALS BY A CHILD (1-6 YRS) RESIDENT TO THE NORTHEAST UNDER CURRENT LAND-USE CONDITIONS Ca)
Chemical
Chemicals Exhibiting
Carcinogenic Effects
Organics:
Aldrin alpha-BHC beta-BHC
alpha-Chlordane
garrrna-Chlordane
4 4' -DOT
oieldrin
Toxaphene
RME
Exposure Point
Concentration
(ug/m3) Cb)
5.lSE-07
4.98E-06 2. TTE-06
4.67E-06
4. 78E-06
4.25E-05
1 .47E-05
1.27E-03
RME
Chronic Daily
Intake (CDI)
(mg/kg-day) (C)
4.23E-11
4.09E-10
2.28E-10 3.84E-10
3.93E-10
3.49E-09 1.21E-09
1.04E-07
Ca) COis have been calculated for those chemicals of potential concern with toxicity
criteria. The following chemicals of potential concern are not presented due to
lack of inhalation toxicity criteria: delta-BHC, ganma-BHC, 4,4'·00D and 4,4'-DDE.
Cb) RME concentration is the 95X upper confidence limit on the arithmetic mean
(which includes one-half the detection limit for non-detected values).
Cc) See text for exposure assllll)tions.
4-53
TABLE 4·26
EXPOSURE POINT CONCENTRATIONS AND CHRONIC DAILY ·INTAKES FOR INHALATION OF
VOLATILIZED CHEMICALS BY AN ADULT RESIDENT TO THE NORTHEAST
Chemical
Chemicals Exhibiting
Carcinogenic Effects
Organics:
Aldrin
alpha·BHC
beta-BHC
alpha-Chlordane
ganma-Chlordane
4 41 -DDT
oieldrin
Toxaphene
UNDER CURRENT LAND-USE CONDITIONS (a)
RME
Exposure Point
Concentration
(ug/m3) (c)
2.3DE-07
2.23E·06
1.24E·06
2.09E·06
2.14E·06 1.90E·05
6.59E·06
5.66E·04
RME
Chronic Dai Ly
Intake (CDI}
(mg/kg-day) Cd)
2.70E·11
2.62E·10
1.46E· 10
2.45E·10
2.51E·10
2.23E·09
7.74E·10
6.65E·08
(a) CDis have been calculated for those chemicals of potential concern with inhalation toxicity criteria.
The following chemicals of potential concern are not presented due to lack of inhalation toxicity criteria: delta-BHC, ganma-BHC, 4,4'-DDD and 4,4'-DDE.
(b) Average concentration (including one-half the detection limit for non-detected values).
Cc) RME concentration is the 95% upper confidence limit on the arithmetic mean.
Cd) See text for exposure ass1.1T1ptions.
4-54
I
TABLE 4-27
EXPOSURE POINT CONCENTRATIONS AND CHRONIC DAILY INTAKES FOR INHAL·ATION OF
DUST PARTICULATES BY A NEARBY AOULT MERCHANT TO THE NORTH
Chemical
Cheniicals Exhibiting
Carcinogenic Effects
Organics:
Aldrin
alpha·BHC
beta-BHC
alpha-Chlordane
ganma-Chlordane
4,4'-D0T
Dieldrin
Toxaphene
UNDER CURRENT LAND-USE CONDITIONS (a)
RME
Exposure Point
Concentration
(ug/m3) (b)
1.84E·09
3.46E·08
5.0lE-08
1. 71E-08
1.75E-08
1.54E-06
6.26E·08
6.68E-06
RME
Chronic Daily
Intake (CDI)
(mg/kg-day) (c)
1.24E-13
2.33E-12
3.38E-12
1.15E-12
1.18E·12
1.04E-10
4.22E·12
4.SOE-10
(a) COis have been calculated for those chemicals of potential concern with inhalation toxicity
criteria. The following chemicals of potential concern are not presented due to lack of
inhalation toxicity criteria: delta·BHC, ganma-BHC, 4,4'-000 and 4,4'-DDE.
Cb) RME concentration is the 95¾ upper confidence limit on the arithmetic mean
(which includes one-half the detection limits of non-detected values).
(c) See text for exposure ass~tions.
4-55
TABLE 4-28
EXPOSURE POINT CONCENTRATIONS AND CHRONIC DAILY INTAKES FOR INHALATION OF DUST PARTICULATES BY A CHILD (1·6 YRS) RESIDENT TO THE NORTHEAST UNDER CURRENT LAND-USE CONDITIONS (a)
Chemical
Chemicals Exhibiting Carcinogenic Effects
Organics:
Aldrin
atpha-BHC
beta-BHC
alpha-Chlordane
ganma-Chlordane
4,4'-00T
Dieldrin
Toxaphene
RME
Exposure Point
Concentration
(ug/m3) Cb)
1.BSE-10
3.49E-09 5.DSE-09
1.73E·D9
1. 77E-09
1.56E·07
6.31E·09
6.73E-07
RME
Chronic Daily Intake (CDI)
(mg/kg-day) (c)
1.52E·14
2.87E·13
4.15E-13
1.42E·13
1.45E·13
1.28E·11
5.19E·13
5.53E·11
(a) COis have been calculated for those chemicals of potential concern with toxicity criteria. The following chemicals of potential concern are not presented due to tack of inhalation toxicity criteria: delta-BHC, ganma-BHC, 4,4'-DDD and 4,4'-DDE. (b) RME concentration is the 95¾ upper confidence limit on the arithmetic mean (which includes one-half the detection limit for non-detected values). (c) See text for exposure assllllptions.
4-56
TABLE 4-29
EXPOSURE POINT CONCENTRATIONS AND CHRONIC DAILY INTAKES FOR INHALATION OF DUST PARTICULATES BY AN ADULT RESIDENT TO THE NORTHEAST .
Chemical
Chemicals Exhibiting
Carcinogenic Effects
Organics:
Aldrin
alpha-BHC
beta-BHC
alpha-Chlordane
ganma-Chlordane
4 4'-DDT
oieldrin
Toxaphene
UNDER CURRENT LAND-USE CONDITIONS (a)
RME
Exposure Point
Concentration
(ug/m3) Cb)
1.BSE-1O
3.49E-O9
5.OSE·O9
1.73E-O9
1. TTE-O9
1 .56E-O7
6.31E-O9
6.73E-O7
RME
Chronic Daily
Intake (CDI)
(mg/kg-day) (c)
2.17E-14
4.1OE-13
5.93E-13
2.O3E-13
2.OBE-13
1.83E-11
7.41E-13
7.9OE·11
(a)
CbJ
(c)
COis have been calculated for those chemicals of potential concern with inhalation toxicity criteria.
The following chemicals of potential concern are not presented due to lack of inhalation toxicity
criteria: delta-SHC, ganma-BHC, 4,4'-00D and 4,4'-DDE.
RME concentration is the 95¾ upper confidence limit on the arithmetic mean
(which includes one-half the detection limits of non-detected values).
See text for exposure assllnptions.
4-57
4.5.2 Exposure Estimates Under Future Land-Use Conditions
This section presents the chronic daily intakes estimated for the future land
use exposure pathways. Intakes associated with inhalation of volatilized
chemicals from surface soil/sediment, incidental ingestion and dermal contact
with surface soil/sediment and ingestion of groundwater are estimated.
Additionally, exposure associated with inhalation of volatiles and dermal
absorption while showering are estimated. The assumptions for estimating
exposures and the equations used to calculate CDis are presented below.
4.5.2.1 Incidental Ingestion of Surface Soil/Sediment
Under future land use conditions, it will be assumed that both a hypothetical
on-site merchant and a future adult and child (1-6 year) resident could be
exposed to the chemicals of concern through the incidental ingestion of
surface soil. Exposure parameter values for this scenario are summarized in
Table·4-30, and exposure point concentrations were presented in Table 4-5.
Exposures associated with incidental ingestion of soil/sediment are calculated
using the following equation:
where
CDI
c.
IR
FI
EF
ED
CF
BW
Days
chronic daily chemical intake (mg/kg-day),
chemical concentration in soil (ug/kg),
soil ingestion rate (mg/day),
fraction ingested from source or probability of exposure
(unitless),
frequency of exposure (days/year),
duration of exposure (years),
conversion factor (1 kg/109 ug),
average body weight (kg),
conversion factor (365 days/year), and
4-58
TABLE 4-30
EXPOSURE PARAMETERS FOR INCIDENTAL INGESTION
OF ON-SITE SURFACE SOIL/SEDIMENT
FUTURE LAND-USE CONDITIONS
Residents
Parameters Child Adult
(1-6 yrs)
Adult
Merchant
Exposure Frequency (days/year) (a)
Exposure Duration (years) (b)
Soil Ingestion Rate (mg/day) (c)
Fraction Ingested (dimensionless) (d)
Body Weight (kg) (e)
Period Over Which Risk is Being
Estimated (years)
Carcinogenic (f)
Noncarcinoge~ic
170
6
200
1
15
70
6
170
30
100
1
70
70
30
120
25
so
1
70
70
25
(a) A merchant is assumed to work 5 days/week, 50 weeks/year (2 weeks
subtracted for vacation), minus 9 days for federal holidays and is
to spend half of that time outside. Values for adult and child
residents are based on 5 days/week during the warmer months, April
through October, and 1 day/week during November through March
(USEPA Region IV).
(b) All three values based upon USEPA (1991a). Adult duration is the
national upper-bound time at one residence (USEPA 1991a).
(c) Based on USEPA (1989a, 1991a).
(d) A probability of contact factor (FI) of 1 was conservatively used
based upon USEPA Region IV direction.
(e) Standard default value provided by USEPA (1991a, 1989a).
(f) Based on USEPA (1991a, 1989a) standard assumption for lifetime.
This value is used in calculating exposures for potential
carcinogens.
4-59
AT averaging time (70 years for carcinogens, duration of
exposure for noncarcinogens).
For future adult and child residents, an exposure frequency (EF) of 170
days/year is used based on the recommendation of USEPA Region .IV. The
exposure frequency assumes residents will be outside in their yards 5
days/week during the warmer months of the year (April through October), and 1
day/week during November through March. For an adult resident, an exposure
duration (ED) of 30 years, the national upper-bound time at one residence is
used (EPA 1991a, 1989a). Soil ingestion rates of 100 mg/day and 200 mg/day
are used (USEPA 1991a, 1989a) for an adult and 1-6 year old child,
respectively. The standard default parameters for body weight (BW) of 15
kilograms and 70 kilograms for a child (1-6 years) and an adult, respectively
and lifetime (AT) of 70 years are used (USEPA 1991a).
Merchants were assumed to come into contact with soil/sediment for 120
days/year (EF). It is assumed that merchants work 50 weeks/year (2 weeks
subtracted for vacation), with 9 days subtracted for federal holidays and is
to spend half of that time outside. A soil ingestion rate (IR) of 50 mg/kg
was used (USEPA 1991a). Standard default assumptions were made regarding
employment duration (ED) (25 years) (USEPA 1991a), body weight (BW) (70 kg),
and lifetime (AT) (70 years) (USEPA 1989a). A fraction ingested from the
source area (FI) of 1.0 was used.
Using these exposure parameter values and the equation provided above, CDis
were estimated for the selected chemicals of concern. The resulting CDis for
chemicals exhibiting carcinogenic effects and chemicals exhibiting
noncarcinogenic effects due to incidental ingestion of site surface
soil/sediment are summarized in Tables 4-31, 4-32 and 4-33 for a hypothetical
future child resident, adult resident and merchant, respectively.
4-60
i.
TABLE 4-31
EXPOSURE POINT CONCENTRATIONS AND CHRONIC DAILY INTAKES FOR INCIDENTAL INGESTION
OF ON-SITE SOIL/SEDIMENT BY A CHILD RESIDENT (1-6 YRS)
Chemical
Chemicals Exhibiting
Carcinogenic Effects
Organics:
Aldrin
alpha-BHC
beta·BHC
ganrna-BHC
alpha-Chlordane
ga1T1T1a-Chlordane
4 4' -DOD
4:41 ·DOE
4,4' -DDT
"' Dieldrin
Toxaphene
Chemicals Exhibiting
Noncarcinogenic Effects
Organics:
Aldrin
gamna-BHC
Benzoic acid
alpha-Chlordane
ga1TJT1a·Chlordane
4 41 -DDT
oieldrin
UNDER FUTURE LAND USE CONDITIONS (a)
RME
Exposure Point
Concentration
(ug/kg) (c)
4.SOE+OO
1.3OE+O2
2. 7OE+O2
1.2OE+O2
4.2OE+O1
4.9OE+O1
3.7OE+O3
2.OOE+O3
9.OOE+O3
2.SOE+O2
3.7OE+O4
4.SOE+OO
1.2OE+O2
3.6OE+O3
4.2OE+O1
4.9OE+O1
9.OOE+O3
2.SOE+O2
USEPA RME
Chronic Dai Ly
Intake
(mg/kg-day) Cd)
2.4OE-O9
6.92E·O8
1.44E-O7
6.39E·O8
2.24E-O8
2.61E-O8
1.97E·O6
1.O6E·O6
4.79E-O6
1.33E-O7
1.97E-O5
2. 79E·O8
7.45E·O7
2.24E·OS
2.61E·O7
3.O4E·O7
5.59E·OS
1.SSE-O6
Ca) COis have been calculated for those chemicals of potential concern with toxicity
criteria. The following chemicals of potential concern are not presented due
to lack of toxicity criteria: delta-BHC.
(b) Average concentration (including one-half the detection limit for non-detected
values).
Cc) RME concentration is the 95% upper confidence limit on the arithmetic mean.
Cd) See text for exposure assllTlptions.
4-61
TABLE 4-32
EXPOSURE POINT CONCENTRATIONS AND CHRONIC DAILY ·INTAKES FOR
INCIDENTAL INGESTION OF ON-SITE SOIL/SEDIMENT BY ADULT .
RESIDENTS UNDER FUTURE LAND-USE CONDITIONS (a)
Cherni cal
Chemicals Exhibiting
Carcinogenic Effects
Organics:
Aldrin alpha-BHC
beta-BHC
garrma-BHC
alpha-Chlordane
ganrna-Chlordane
4 4'-DDD
41 4'·DDE
4
1
4'-DDT
oieldrin
Toxaphene
Chemicals Exhibiting
Noncarcinogenic Effects
Organics:
Aldrin
garrma-BHC
Benzoic acid
alpha-Chlordane
garrma•Chlordane
4 4' ·DDT
oieldrin
RME
Exposure Point
Concentration
(Ug{Kg) (C)
4.SOE+OO
1.30E+02
2.70E+D2
1.2DE+02
4.20E+01
4.90E+01
3. 70E+03
2.00E+03
9.00E+03
2.50E+02
3.70E+04
4.SOE+OD
1 .20E+02
3.60E+03
4.20E+01
4.90E+01
9.00E+03
2.50E+02
USEPA RME
Chronic Daily
Intake
(mg/kg-day) Cd)
1.28E-09
3.71E-08
7.70E-08
3.42E-08
1.20E-08
1.40E-08
1.06E-06
5.?0E-07
2.57E-06
7.13E-08
1.06E-05
2.99E-09
7.98E-08 2.40E-06
2.79E-08
3.26E-08
5.99E-06
1.66E-07
(a) COis have been calculated for those chemicals of potential concern with toxicity criteria.
The following chemical of potential concern is not presented due to lack of toxicity
criteria: delta·BHC.
Cb) Average concentration (including one-half the detection limit for non-detected values).
(c) RME concentration is the 95X upper confidence limit on the arithmetic mean.
Cd) See text for exposure ass1.1Tptions.
4-62
I.
TABLE 4·33
EXPOSURE POINT CONCENTRATIONS AND CHRONIC DAILY INTAKES FOR
INCIDENTAL INGESTION OF ON-SITE SOIL/SEDIMENT BY ADULT MERCHANT UNDER FUTURE LAND·USE CONDITIONS Ca)
Chemical
Chemicals Exhibiting
Carcinogenic Effects
Organics:
Aldrin
alpha-BHC
beta-BHC
ganma-BHC
alpha-Chlordane
ganma-Chlordane
4,4' -DDD
4 41 -DDE
41 41 -DDT
oietdrin
Toxaphene
Chemicals Exhibiting
Noncarcinogenic Effects
Organics:
Aldrin
garrma-BHC
Benzoic add
alpha-Chlordane
ganma-Chlordane
4 4'·DDT
oietdrin
RME
Exposure Point
Concentration
(ug/kg) (c)
4.SOE+OO
1.3OE+O2
2.7OE+O2
1.2OE+O2
4.2OE+O1
4.9OE+O1
3.7OE+O3
2.OOE+O3
9.OOE+O3 2.5OE+O2
3.7OE+O4
4.SOE+OO
1.2OE+O2
3.6OE+O3
4.2OE+O1
4.9OE+O1
9.OOE+O3
2.5OE+O2
RME
Chronic Daily
Intake
(mg/kg-day) (d)
3. 77E·1O
1.O9E·OB
2.26E·OB
1.O1E·OB
3.52E·O9
4.11E·O9 3.1OE·O7
1.68E·O7
7.55E·O7 2.1OE·OB
3.1OE·O6
1.O6E·O9
2.82E·OB
8.45E·O7
9.86E·O9
1.15E-OB
2.11E·O6 5.B7E-OB
(a) COis have been calculated for those chemicals of potential concern with toxicity criteria.
The following chemical of potential concern is not presented due to lack of toxicity
criteria: delta-BHC.
(b) Average concentration (including one-half the detection limit for non-detected values).
(c) RME concentration is the 95X upper confidence limit on the arithmetic mean.
(d) See text for exposure assL1T1ptions.
4-63
4.5.2.2 Dermal Absorption of Chemicals from On-Site Surface Soil/Sediment
This scenario evaluates potential exposures through dermal contact with
chemicals of potential concern in soil by a hypothetical future merchant and
future adult and child (1-6 years) residents on the site. The exposure point
concentrations for the dermal absorption pathway are the same as those
presented in Table 4-5 for the on-site soil ingestion pathway. The exposure
parameters used for the dermal absorption pathway are presented in Table 4-34.
CDI estimates for dermal contact with chemicals in soil/sediment were
calculated using the equation below:
where
CDI
cs
SA
AF
Ab
EF
ED
CF
BW
Days
· AT
chronic daily chemical intake (mg/kg-day),
chemical concentration in soil (ug/kg),
skin surface area available for contact (cm2),
soil-to-skin adherence factor (mg/cm2),
dermal absorption fraction (unitless),
frequency of exposure events (days/year),
duration of exposure (years),
conversion factor (1 kg/109 mg),
average body weight (kg),
conversion factor (365 days/year), and
averaging time (70 years for carcinogens, duration of
exposure for noncarcinogens).
The parameters describing duration of exposure (ED), body weight (BW) lifetime
(AT) were identical to those used for estimating ingestion of soil by a future
on-site child resident, adult resident and merchant. Again, it was assumed
that future residents and future merchants would pntentially contact outdoor
soil 170 and 120 days/year, respectively. A soil-to-,i1<in adherence factor
(AF) of 1.0 mg/cm2 was used (based on Driver et al. 1989). For child (1-6
4-64
J!l
I I TABLE 4-34
EXPOSURE PARAMETERS FOR DERMAL CONTACT
WITH ON-SITE SURFACE SOIL/SEDIMENT
FUTURE LAND-USE CONDITIONS
Parameters
Exposure Frequency (days/year) (a)
Exposure Duration (years) (b)
Skin Surface Area Available for
Contact (cm2) (c)
Soil to Skin Adherence Factor (mg/cm2)
(d)
Dermal Absorption Factor
(dimensionless) (e)
Chlorinated Pesticides
Benzoic Acid
Body Weight (kg) (f)
Period Over Which Risk is Being
Estimated (years)
Carcinogenic (g)
Noncarcinogenic
Residents
Child
(1-6
170
6
3,140
1.0
0.01
0.01
15
70
6
yrs)
Adult
170
30
820
1.0
0.01
0.01
70
70
30
Adult
Merchant
120
25
820
1.0
0.01
0.01
70
70
25
(a) A merchant is assumed to work 5 days/week, 50 weeks/year (2 weeks
subtracted for vacation), minus 9 days for federal holidays and is to
spend half of that time outside. Values for adult and child residents
are based on the recommendation of USEPA Region IV.
(b) Values based upon USEPA (1991a). Adult resident duration is the
national upper-bound tim~ at one residence (USEPA 1991a).
(c) Value for the adult resident and merchant is the mean surface area for
hands (USEPA 1989a). Surface area for child residents is based the
recommendation of USEPA Region IV, assuming hands, arms and legs are
uncovered and exposed.
(d) Average and RME case based on Driver et al. (1989) and Clement (1988).
(e) Based USEPA Region IV guidance.
(f) Standard default value provided by USEPA (1991a, 1989a).
(g) Based on USEPA (1991a, 1989a) standard assumption for lifetime. This
value is used in calculating exposures for potential carcinogens.
4-65
years) and adult residents, potentially exposed skin surface areas (SA) of
3,140 cm2 and 820 were assumed, using the.50th percentile values from USEPA
(1989a). For a child (1-6 years) it was assumed that ·the hands, arms and legs
are uncovered and exposed. For the adult resident and merchant, a potentially
exposed skin surface area of 820 cm2 was assumed based on the mean surface
area of adult hands (USEPA 1989a). The expected lifetime used in calculating
CDis for carcinogens was assumed to be 70 years (USEPA 1991a, 1989a). As
shown in Table 4-34, and discussed previously, a dermal absorption fraction of
1% was used for all organic chemicals.
Using these exposure parameter values, CDis of the chemicals of potential
concern dermally absorbed from on-site surface soil/sediment are summarized in
Tables 4-35, 36, and 37 for a child resident, adult resident and merchant,
respectively. The CDis are calculated differently for chemicals exhibiting
carcinogenic and noncarcinogenic effects (with respect to averaging time).
4.5.2.3 Ingestion of Groundwater
Ingestion of groundwater from the surficial aquifer and second uppermost
aquifer on the Geigy site and MW-11D in the second uppermost aquifer south of
the site will be evaluated in this scenario. Chronic daily intakes are
calculated for both future worker and residential drinking water exposures
using the exposure parameters presented in Table 4-38 and discussed below and
the exposure point concentrations presented earlier in Table 4-7 for the
surficial aquifer. For the second uppermost aquifer within the property
boundaries, the time-averaged maximum TCE concentration of 180 ug/L presented
earlier in Table 2-6 was used to calculate the CDis.
CDis were estimated using the equation presented below for groundwater
ingestion:
4-66
I I
TABLE 4-35
EXPOSURE POINT CONCENTRATIONS AND CHRONIC DAILY INTAKES FOR DERMAL CONTACT
OF ON-SITE SOIL/SEDIMENT BY A CHILD RESIDENT (1-6 YRS)
Chemical
Chemicals Exhibiting
Carcinogenic Effects
Organics:
Aldrin alpha-BHC
beta·BHC
ganma-BHC
alpha-Chlordane
ganma-Chlordane
4 4 1 -DDD
4:4 1 -DDE
4 4 1 -DDT
oieldrin
Toxaphene
Chemicals Exhibiting
Noncarcinogenic Effects
Organics:
Aldrin
ganma-BHC
Benzoic acid
alpha-Chlordane
ganma-Chlordane
4 4' -DOT
oieldrin
UNDER FUTURE LAND-USE CONDITIONS (al
RME
Exposure Point
Concentration
(ug/kg) (cl
4.SDE+DD
1.3DE+D2
2.7OE+O2
1.2OE+D2
4.2DE+O1
4.9OE+O1
3.7OE+O3
2.OOE+O3
9.OOE+O3
2.5OE+O2
3.7OE+O4
4.SOE+OO
1.2OE+O2
3.6OE+O3
4.2OE+O1
4.9OE+O1
9.OOE+O3 2.5OE+O2
RME
Chronic Daily
Intake
(mg/kg-day) Cd)
3.76E-1O
1.O9E-O8
2.26E-OB
1.OOE-O8
3.SlE-O9
4.O9E-O9
3.O9E-O7
1 .67E-O7
7.52E-O7
2.O9E-O8
3.O9E-O6
4.39E-O9 1.17E-O7 3.SlE-O6
4.O9E-O8
4.7BE-O8
B.77E-O6 2.44E-O7
Ca) COis have been calculated for those chemicals of potential concern with toxicity criteria.
The following chemicals of potential concern are not presented due to lack of toxicity
criteria: delta-BHC.
(b) Average concentration (including one-half the detection limit for non-detected values).
(c) RME concentration is the 95X upper confidence limit on the arithmetic mean.
(d) See text for exposure assi..mptions.
4-67
Chemical
Chemicals Exhibiting
Carcinogenic Effects
Organics:
Aldrin
alpha-BHC
beta-BHC
ganma-BHC
alpha-Chlordane
ganma-Chlordane
4 4'-DDD
4141 -ooe
4141 -DDT
oieldrin
Toxaphene
Chemicals Exhibiting
Noncarcinogenic Effects
Organics:
Aldrin
ganma-BHC
Benzoic acid
alpha-Chlordane
ganma-Chlordane
4 4'-DDT
oleldrin
\
TABLE 4-36
EXPOSURE POINT CONCENTRATIONS AND CHRONIC DAILY INTAKES FOR DERMAL CONTACT OF ON-SITE SOIL/SEDIMENT BY ADULT RESIDENTS UNDER FUTURE LAND-USE CONDITIONS (a)
RME
Exposure Point
Concentration
(ug/kg) (c)
4.SOE+OO
1.30E+02
2.70E+02
1.20E+02
4.20E+01
4.90E+01 3.70E+03
2.00E+03
9.00E+03
2.50E+02
3.70E+04
4.SOE+OO
1 .20E+02
3.60E+03
4.20E+01
4 .90E+01
9.00E+03
2.50E+02
·USEPA RME
Chronic Daily
Intake
(mg/kg-day) Cd)
1. OSE-10
3.04E-09 6.31E-09
2.81E-09
9.82E-10
1.15E-09
8.65E-08
4.68E-08
2. lOE-07
5.BSE-09
8.65E-07
2.46E-10
6.SSE-09
1.96E-07
2.29E-09
2.67E-09
4.91E-07 1 .36E-08
(a} COis have been calculated for those chemicals of potential Concern with toxicity criteria. The following chemicals of potential concern are not presented due to lack of toxicity criteria: delta-BHC.
(b} Average concentration (including one-half the detection limit for non-detected values). (c) RME concentration is the 95¾ upper confidence llmlt on the arlthmetlc mean. (d) See text for exposure assllllptions.
4-68
TABLE 4-37
EXPOSURE POINT CONCENTRATIONS AND CHRONIC DAILY INTAKES FOR DERMAL
CONTACT OF ON-SITE SOIL/SEDIMENT BY ADULT MERCHANTS
Chemical
Chemicals Exhibiting
Carcinogenic Effects
Organics:
Aldrin
alpha-BHC
beta-BHC
ganrna-BHC
alpha-Chlordane
ganrna-Chlordane
4 41 -DDO
4:4 1 -DDE
4,4'-DDT
Dieldrin
Toxaphene
Chemicals Exhibiting
Noncarcinogenic Effects
Organics:
Aldrin
ganrna-BHC
Benzoic acid
alpha-Chlordane
ganma-Chlordane
4 41 -DOT
oieldrin
UNDER FUTURE LAND·USE CONDITIONS (a)
RME
Exposure Point ·
Concentration
(ug/kg) (c)
4.SOE+OO
1.3OE+O2
2.7OE+O2
1 .2OE+O2
4.2OE+O1
4.9OE+O1 3.7OE+O3
2.OOE+O3
9.OOE+O3
2.SOE+O2
3.7OE+O4
4.SOE+OO
1.2OE+O2
3.6OE+O3
4.2OE+O1
4.9OE+O1
9.OOE+O3
2.SOE+O2
RME
Chronic Daily
Intake
(mg/kg-day) (d)
6.19E·11
1. 79E·O9
3.71E·O9
1.65E-O9
5. 78E·1O
6. 74E·1O S.O9E·O8
2. 75E·O8
1 .24E-O7
3.44E-O9
S.O9E·O7
1. 73E-1O
4.62E·O9
1.39E·O7
1 .62E·O9
1.89E·O9
3.47E-O7
9.63E·O9
(a) COis have been calculated for those chemicals of potential concern with toxicity criteria.
The following chemicals of potential concern are not presented due to lack of toxicity
criteria: delta·BHC.
(b) RME concentration is the 95X upper confidence limit on the arithmetic mean.
(with one-half the detection limit for non-detected values).
(d) See text for exposure ass~tions.
4-69
where
CDI
IR
.EF
ED
BW
AT
Days
CDI= CW•IR•EF•ED
BW•AT•Days
chronic daily intake (mg/kg-day),
chemical concentration in groundwater (mg/L),
water ingestion rate (L/day),
frequency of exposure (days/year),
duration of exposure (years),
average body weight (kg),
averaging time (70 years for carcinogens, duration of
exposure for noncarcinogens), and
conversion factor (365 days/year).
Drinking water exposures are evaluated for child and adult residents both on-
site and just south of the site at MW-llD. Groundwater ingestion exposures
were evaluated for adult merchants only on-site. For child residents 1-6
years, a time-weighted average body weight of 15 kg, and a time-weighted
drinking water rate of one liter/day (based on USEPA Region IV) are used as
parameters for the RME case. A drinking water consumption rate of two
liters/day (USEPA 1991a, 1989a), and an exposure duration of 30 years, the
upper-bound time at one residence is assumed for adult residents (EPA 1991a,
1989a). Again, standard default assumptions were made regarding body weight
(70 kg), and lifetime (70 years) (USEPA 1989a) for the adult resident.
Adult merchants are assumed to weigh 70 kg and ingest one liter of water per
day USEPA (1991a), 241 days/year for 25 years throughout their 70-year
lifetime. The exposure frequency (EF) assumes that a merchant works 5
days/week, 50 weeks/year (minus 2 weeks vacation), minus 9 days for federal
holidays. The exposure duration is the USEPA (1991a) default value.
CDis for chemicals exhibiting carcinogenic effects.and chemicals exhibiting
noncarcinogenic effects due to ingestion of groundwatsr from the surficial
aquifer at the Geigy site are summarized in Tables 4-39 through 4-41. Tables
4-70
.!i
TABLE 4-38
EXPOSURE PARAMETERS FOR INGESTION
OF GROUNDWATER
FUTURE LAND-USE CONDITIONS
Residents
Parameters
Exposure Frequency (days/year) (a)
Exposure Duration (years) (b)
Ingestion Rate (liter/day) (c)
Body Weight (kg) (d)
Period Over Which Risk is Being
Estimated (years)
Carcinogenic (e)
Noncarcinogenic
Child Adult
(1-6 yrs)
350
6
1
15
70
6
350
30
2
70
70
30
Adult
Merchant
241
25
1
70
70
25
(a) A merchant is assumed to be at work 5 days/week, 50 weeks/year (2
weeks subtracted for vacation), minus 9 days for federal holidays.
Values for adult and child residents are based on USEPA (1991a).
(b) All three values based upon USEPA (1991a). Value for the adult
resident is based on the upper bound time at one residence (USEPA
1991a).
(c) Value for a
Region IV.
(1991a).
1-6 years old is based on the recommendation of USEPA
Value for adult resident and merchant is based on USEPA
(d) Standard default value provided by USEPA (1991a, 1989a).
(e) Based on USEPA (1991a, 1989a) standard assumption for lifetime.
This value is used in calculating exposures for potential
carcinogens.
4-71
4-42 and 4-43 summarize the CDis for chemicals in the on-site second uppermost
aquifer for a child (1-6 years) and adult resident, respectively. Tables 4-44
and 4-45 summarize the CDis for chemicals in the off-site second uppermost
aquifer (MW-llD) for a child (1-6 years) and adult resident, respectively.
4.5.2.4 Chronic Inhalation Exposure to Chemicals Volatilized During
Showering
For inhalation exposure while showering, the surficial aquifer concentrations
for volatile organic chemicals presented in Tables 4-7 and exposure parameters
presented in Table 4-46 and discussed below are input into a shower model
(Foster and Chrostowski 1987). Additionally, the time-averaged maximum TCE
concentration detected in the second uppermost aquifer is input into the same
shower model. As previously discussed in Section 4.4.4, the outputs from the
shower model are mg/m3 of the organic chemicals released from groundwater.
The shower model uses a one-compartment indoor air model to estimate indoor
air VOC levels which assumed instantaneous and complete mixing in the room air
and no chemical decay of the VOCs once they are released into the room air.
The model does not estimate potential dermal absorption of contaminants while
showering. However, dermal absorption from short-term exposures to dilute
water concentrations is expected to be minimal. in comparison to potential
inhalation exposures. Details of the shower model are given in Appendix C.
Residential exposures associated with inhalation of volatile organic chemicals
released during showering are calculated using the following equation and
assumptions:
4-72
TABLE 4-39
EXPOSURE POINT CONCENTRATIONS AND CHRONIC DAILY INTAKES FOR INGESTION
OF GROUND~ATER FROM THE SURFICIAL AQUIFER BY A CHILD ·c1-6 YRS)
RESIDENT UNDER FUTURE LAND USE CONDITIONS (a)
Chemical
Chemicals Exhibiting
Carcinogenic Effects
Organics:
Aldrin
alpha-BHC
beta·BHC
garrrna-BHC
Bis(2-ethylhexyl)phthalete
Dieldrin
4,4'-DDE
Toxaphene
Chemicals Exhibiting
Noncarcinogenic Effects
Organics:
Aldrin
garrrna-BHC
Bis(2·ethylhexyl)phthalate
Dieldrin
1,2,4-Trichlorobenzene
lnorganics:
Barillll
Manganese
Mercury
VanadillTI
Zinc
RME
Exposure Point
Concentration
(ug/1)
2.00E-01
3.60E+D1
2.SOE+D1 3.00E+01
6.40E+OO
1.20E+OO
1.00E-01
5.90E+OO
2.DOE-01
3.00E+01
6.40E+OO
1.20E+OO
5.00E+OO
2.80E+02
1.00E+02
1.00E+OO
3.80E+01
5 .80E+02
RME
Chronic Daily
Intake
(mg/kg-day) (b)
1.10E-06
1.97E-04
1.37E-04
1.64E-04
3.51E-D5 6.SBE-06
5.48E-07
3.23E-05
1.28E-05
1 .92E-03 4.09E-04
7.67E-05
3.20E-04
1.79E-02
6.39E-03
6.39E-05
2.43E-03
3.71E-02
(a) COis have been calculated for those chemicals of potential concern with toxicity
criteria. The following chemicals of potential concern are not presented due to
lack of toxicity criteria: aluninun, delta·BHC, calciun, endrin ketone, heptachlor epoxide, iron, magnesiun, and potassiun.
(b) See text for exposure assumptions.
4-73
TABLE 4-40
EXPOSURE POINT CONCENTRATIONS ANO CHRONIC DAILY INTAKES FOR INGESTION
OF GROUNDWATER FROM THE SURFICIAL AOUIFER BY AN ADULT RESIDENT
UNDER FUTURE LAND USE CONDITIONS (a)
Chemical
Chemicals Exhibiting
Carcinogenic Effects
Organics:
Aldrin
alpha-BHC
beta-BHC
garrma-BHC
Bis(2-ethylhexyl)phthalate
Dieldrin
,4,4'-DDE·
Toxaphene
Chemicals Exhibiting
Noncarcinogenic Effects
Organics:
Aldrin
garrma-BHC
Bis(2-ethylhexyl)phthalate Dieldrin
1,2,4-Trichlorobenzene
Inorganics:
Barit.JTI
Manganese
Mercury
VanadillJl
Zinc
RME
Exposure Point
Concentration
Cug/l)
2.00E-01 3.60E+01
2.50E+01
3.00E+01
6.40E+OO
1.20E+OO
1.00E-01
5.90E+OO
2.00E-01
3.00E+01
6.40E+OO
1.20E+OO 5.00E+OO
2.80E+02
1.00E+02
1.00E+OO
3.80E+01
5.80E+02
RME
Chronic Dai Ly
Intake
(mg/kg-day) Cb)
2.35E-06
4.23E·04
2.94E·04
3.52E·04
7.51E-05
1.41E-05
1.17E-06
6.93E-05
5.48E·06
8.22E·04
1. 75E-04 3.29E-05
1.37E-04
7.67E-03
2.74E-03
2. 74E-05
1.04E-03
1.59E·02
(a) COis have been calculated for those chemicals of potential concern with toxicity
criteria. The following chemicals of potential concern are not presented due to
lack of toxicity criteria: alllflinllfl, delta-BHC, calcillfl, endrin ketone, heptachlor epoxide, iron, magnesillfl, and potassillJI.
Cb) See text for exposure assllllptions.
4-74
'· I
TABLE 4·41
EXPOSURE POJ NT CONCENTRATIONS AND CHRONIC DA 1 L.Y I NT AKES FOR l NGEST I ON
OF GROUNDWATER FROM THE SURFICIAL AQUIFER BY AN ADULT MERCHANT
UNDER FUTURE LAND USE CONDITIONS (a)
Chemical
Chemicals Exhibiting
Carcinogenic Effects
Organics:
Aldrin
alpha·BHC
beta-BHC
garrma-BHC
Bis(2-ethylhexyl)phthalate
Dieldrin
4 41 -DDE
T~xaphen~
Chemicals Exhibiting
Noncarcinogenic Effects
Organics:
Aldrin
ga!Tll1a-BHC
Bis(2-ethylhexyl)phthalate
Oieldrin
1,2,4-Trichlorobenzene
lnorganics:
Barium
Manganese
Mercury
Vanadiun
Zinc
RME
Exposure Point
Concentration
(ug/ll
2.OOE-O1
3.6OE+O1
Z.SOE+Ol
3.OOE+Ol
6.4OE+OO
1.ZOE+OO
1.OOE-O1
5.9OE+OO
2.OOE-O1
3.OOE+Ol
6.4OE+OO
1.ZOE+OO
5.OOE+OO
2.BOE+OZ
1.OOE+OZ
1.OOE+OO
3.80E+01
5.BOE+OZ
RME
Chronic Daily
Intake
(mg/kg-day) Cb)
6. 74E·O7
1 .ZlE-O4
8.42E·O5
1.OlE-O4
2.16E·O5
4.O4E·O6
3.37E·O7
1.99E·O5
1.89E·O6
2.83E·O4
6.O4E·O5
1. 13E·O5
4.72E·O5
2.64E·03
9.43E-04 9.43E·06
3.58E·04
5.47E·03
(a) COis have been calculated for those chemicals of potential concern with toxicity
criteria. The following chemicals of potential concern are not presented due to
lack of toxicity criteria: aluminun, delta-BHC, calciun, endrin ketone, heptachlor
epoxide, iron, magnesiun, and potassillll.
Cb) See text for exposure ass~tions.
4-75
TABLE 4·42
EXPOSURE POINT CONCENTRATIONS AND CHRONIC DAILY INTAKES FOR INGESTION OF GROUND~ATER
FROM THE SECOND UPPERMOST AQUIFER BENEATH THE SITE PROPERTY BY A CHILD RESIDENT
UNDER CURRENT LAND USE CONDITIONS (a)
Chemical
Carcinogenic Effects
Organics:
Trichloroethene
Noncarcinogenic Effects
Organics:
Trichloroethene
RME
Exposure Point
Concentration
( ug/ I)
1 .8DE+02
1.80E+02
RME
Chronic Daily
Intake
(mg/kg-day) (bl
9.86E·O4
1.1SE·D2
(a) COi's have been calculated for the carcinogenic and noncarcinogenic effects of
trichloroethene
(b) See text for exposure assLJnptions.
4-76
2 1
TABLE 4-43
EXPOSURE POINT CONCENTRATIONS AND CHRONIC DAILY INTAKES FOR INGESTION OF GROUND~ATER
FROM THE SECOND UPPERMOST AQUIFER BENEATH THE SITE PROPERTY BY AN ADULT RESIDENT UNDER CURRENT LAND USE CONDITIONS (a)
Chemical
Carcinogenic Effects
Organics:
Trichloroethene
Noncarcinogenic Effects
Organics:
Trichloroethene
RME
Exposure Point
Concentration
(ug/l)
1.8DE+02
1 .80E+02
RME
Chronic Daily
Intake
(mg/kg-day) (b)
2.11E·03
4.93E·03
(a) COi's have been calculated for the carcinogenic and noncarcinogenic effects of
trichloroethene
Cb) See text for exposure assllnptions.
4-77
TABLE 4-44
EXPOSURE POINT CONCENTRATIONS AND CHRONIC DAILY INTAKES FOR INGESTION OF OFF-SITE GROUNDWATER FROM THE SECOND UPPERMOST AQUIFER BY A CHILD . (1-6 YRS) RESIDENT UNDER FUTURE LAND USE CONDITIONS (a)
Chemical
Chemicals Exhibiting
Carcinogenic Effects
Organics:
alpha-BHC
beta-BHC
ganma-BHC
Dieldrin
Chemicals Exhibiting
Noncarcinogenic Effects
Organics:
ganma-BHC
Dieldrin
4-methyl-2-pentanone
RME
Exposure Point
Concentration
(ug/l)
1.60E+01
6.60E+OO
1.10E+01
2.BOE-01
1. 1 OE+01 2.BOE-01 2.00E+OO
RME
Chronic Daily
Intake
(mg/kg-day) (b)
8. TTE-05 3.62E-05
6.03E-05
1 .53E-06
7.03E-04
1.79E-05
1.28E-04
Ca) COis have been calculated for those chemicals of potential concern with toxicity criteria. The following chemicals of potential concern are not presented due to lack of toxicity criteria: delta-BHC Cb) See text for exposure assumptions.
4-78
TABLE 4·45
EXPOSURE POI NT CONCENTRAT I CNS AND CHRONIC DA IL Y I NT AKES FOR ·INGEST ION
OF OFF·SITE GROUNDWATER FROM THE SECOND UPPERMOST AQUIFER BY AN ADULT RESIDENT UNDER FUTURE LAND USE CONDITIONS (a)
Chemical
Chemicals EXhibiting
Carcinogenic Effects
Organics:
alpha·BHC
beta-SHC ganma-BHC
Dieldrin
Chemicals Exhibiting
Noncarcinogenic Effects
Organics:
ganma·BHC
Dieldrin
4-methyl-2-pentanone
RME
Exposure Point
Concentration
(ug/l)
1 ,60E+01
6,60E+OO
1.10E+01
2.80E·01
1.10E+01
2.80E·01
2.00E+OO
RME
Chronic Deily
Intake
(mg/kg·day) Cb)
1 .88E·04
7.75E·05
1.29E·04 3.29E·06
3.01E-04
7.67E·06
5.48E·05
(a) COis have been calculated for those chemicals of potential concern with toxicity
criteria. The following chemicals of potential concern are not presented due to
lack of toxicity criteria: delta-BHC and Endrin ketone
Cb) See text for exposure ass~tions.
4-79
TABLE 4·46
EXPOSURE PARAMETERS FOR INHALATION OF
VOLATILES RELEASED DURING SHOWERING
.FUTURE LAND-USE CONDITIONS
Residents
Parameters
Exposure Frequency (days/year) (a)
Exposure Duration (years) (b)
Inhalation Rate (m3/hour) (c)
Shower Duration (hour) (d)
Skin surface area available for contact
(cm2)(e)
Dermal Permeability constant (cm/hr)(f)
Body Weight (kg) (g)
Metabolized Dose Fractions (h)
Trichloroethene
Period Over Which Risk is Being
Estimated (years)
Carcinogenic (i)
Noncarcinogenic
Child Adult
(1-6 yrs)
350
6
0.6
0.2
6,990
8x10-4
15
0.35
70
6
350
30
0.6
0.2
18,150
8xl0"4
70
0.35
70
30
(a) Values for adult and child residents are based on USEPA (1991a). (b) Based upon USEPA (1991a). Value for the adult resident is based on the upper bound time at one residence (USEPA 1991a). (c) Based on USEPA (1991a, 1989a).
(d) Based upon USEPA (1989a). The shower duration is assumed to be 12 minutes per day.
(e) Based on 50th percentile values in USEPA (1989b, 1989a). (f) Based on USEPA (1989a). Assumes all chemicals penetrate the skin at the same rate as water.
(g) Standard default value provided by USEPA (1991a, 1989a). (h) Derived from EPA toxicity criteria to convert administered CDis into metabolized CDis for those chemicals with slope factors based on a metabolized dose.
(i) Based on USEPA (1991a, 1989a) standard assumption for lifetime .. This value is used in calculating exposures for potential
carcinogens.
4-80
where
CDI
IR
ET
EF
ED
BW
AT
Days
· C • IR • ET • EF • ED CDI = -•----~~~---BW •AT• Days
chronic daily intake (mg/kg-day),
exposure point concentration in air
(mg/m3); estimated using the shower model
described in Appendix C,
inhalation rate (m3/hr),
shower duration (hours),
shower fre.quency (days/year),
exposure duration (years),
body weight over the period of exposure (kg),
averaging time (70 years for carcinogens, duration of
exposure for noncarcinogens), and
conversion factor (365 days/year).
In estimating inhalation CDis and associated health risks from showering, it
is conservatively assumed that once inhaled, the volatilized organic compounds
are all absorbed across the lung lining at 100% efficiency. Adult and child
(1-6 years) residents are assumed to inhale 0.6 m3 air/hour while showering
(USEPA 1989a). The standard default body weights of 15 kg and 70 kg are used
for a child (1-6 years), and adult, respectively (USEPA 1991a). The duration
·of exposure while showering is assumed to be 12 minutes per day (USEPA 1989a).
Child and adult residents are each assumed to shower 350 days/year for a
duration of 6 and 30 years, respectively (USEPA 1989a).
CDis calculated using these exposure assumptions are presented in Tables 4-47
and 4-48 for inhal'ation of volatilized organic chemicals from the surfic'ial
aquifer by a child (1-6 years) and adult resident, respectively. Tables 4-49
and 4-50 summarize the CDis for chemicals in the second uppermost aquifer for
a child (1-6 years) and adult resident, respectively.
4-81
TABLE 4-47
EXPOSURE POINT CONCENTRATIONS AND CHRONIC DAILY INTAKES FOR INHALATION OF VOLATILES
WHILE SHOWERING WITH GROUNDWATER FROM THE SURFICIAL AOUIFER BY A CHILD (1-6 YRS) RESIDENT UNDER FUTURE LAND USE CONDITIONS (a)
Chemical
Chemicals Exhibiting
Carcinogenic Effects
Organics:
Aldrin
alpha-BHC
beta-SHC
Dieldrin
Toxaphene
Chemicals Exhibiting
Noncarcinogenic Effects
Organics:
1,2,4-Trichlorobenzene
RME
Exposure Point
Concentration
(mg/m3)
6.21E-07
4. 76E-06
2.58E-07
2.54E-07
4.57E-06
2.60E-05
RME
Chronic Daily
Intake
(mg/kg-day) (bl
4.0BE-10
3.13E-09
1. 70E-10
1.67E-10
3.00E-09
1.99E-07
(a) COis have been calculated for those chemicals of potential concern with toxicity
criteria. The following chemicals of potential concern are not presented due to
lack of toxicity criteria: delta-BHC, garrma·BHC, 4,4'-DDE, bis(2-ethylhexyl)
phthalate, endrin ketone, and heptachlor epoxide.
(b) See text for exposure aSS1.J11Jtions •
•
4-82
TABLE 4-4B
EXPOSURE POINT CONCENTRATIONS AND CHRONIC DAILY INTAKES FOR INHALATION OF VOLATILES
WHILE SHOWERING WITH GROUNDWATER FROM THE SURFICIAL AQUIFER BY ADULT RESIDENTS UNDER FUTURE LAND USE CONDITIONS (a)
Chemical
Chemicals Exhibiting
Carcinogenic Effects
Organics:
Aldrin
alpha-BHC
beta-BHC
Oieldrin
Toxaphene
Chemicals Exhibiting
Noncarcinogenic Effects
Organics:
1,2,4-Trichlorobenzene
RME
Exposure Point
Concentration
(mg/m3)
6.21E-O7
4.76E-O6
2.SBE-O7
2.54E-O7
4.57E-O6
2.6OE-O5
RME
Chronic Daily
Intake
(mg/kg-day) (b)
4.37E-1O
3.35E-O9
1.82E-1O 1.79E-1O
3.22E-O9
4.27E-O8
Ca) COis have been calculated for those chemicals of potential concern with toxicity
criteria. The following chemicals of potential concern are not presented due to
lack of toxicity criteria: delta-BHC, garrrna-BHC, 4,4'-DDE, endrin ketone,
bis(2·ethylhexyl)phthalate, and heptachlor epoxide.
(b) See text for exposure ass~tions.
4-83
TABLE 4-49
EXPOSURE POINT CONCENTRATIONS AND CHRONIC DAILY INTAKES FOR INHALATION OF
VOLATILES WHILE SHOWERING WITH GROUNDWATER FROM THE SECOND UPPERMOST AQUIFER BENEATH THE SITE PROPERTY BY CHILD RESIDENTS
Chemical
Chemicals Exhibiting
Carcinogenic Effects
Organics:
Trichloroethene
UNDER CURRENT LAND USE CONDITIONS (a)
RME-Mater
Exposure Point
Concentration (b)
( ug/L)
1.BOE+02
Calculated
Shower Air
Concentration
(mg/m3) (C)
8.SOE-01
RME
Chronic Dai Ly
Intake
(mg/kg-day) Cd)
1 .96E-04
(a) COis have been calculated for the carcinogenic effects of trichloroethene.
Trichloroethene lacks noncarcinogenic inhalation toxicity criteria.
(b) Concentration used represents the maxiffll.lTI concentration in the second uppermost aquifer.
(c) Based on Foster 8nd Chrostowski (1987).
Cd) See text for exposure assU11ptions. CDI presented represents a metabolized dose calculated based on USEPA (1991).
4-84
TABLE 4-50
EXPOSURE POINT CONCENTRATIONS AND CHRONIC DAILY INTAKES FOR INHALATION OF
VOLATILES WHILE SHOWERING WITH GROUNDWATER FROM THE SECOND UPPERMOST
AQUIFER BENEATH THE SITE PROPERTY BY ADULT RESIDENTS
Chemical
Chemicals Exhibiting
Carcinogenic Effects
Organics:
-Trichloroethene
UNDER CURRENT LAND USE CONDITIONS (a)
RME·Water
Exposure Point
Concentration (b)
(ug/L)
1.BDE+D2
Calculated
Shower Air
Concentration
(mg/m3) (C)
B.SOE·D1
RME
Chronic Daily
Intake
(mg/kg-day) Cd)
2.10E·04
(a) COis have been calculated for the carcinogenic effects of trichloroethene.
Trichloroethene lacks noncarcinogenic inhalation toxicity criteria.
Cb) Concentration used represents the maxinun concentration in the second uppermost
aquifer. ·
Cc) Based on Foster and Chrostowski (1987).
Cd) See text for exposure assurptions. COi presented represents a metabolized dose
calculated based on USEPA (1991).
4-85
4.5.2.5 Dermal Exposure to Chemicals During Showering
CDis are calculated for dermal exposures during showering for child (1-6
years) and adult residents using estimated exposure point concentrations
presented in Table 4-7 and exposure parameters presented previously in Table
4-46 and discussed below. Residential exposures associated with dermal
absorption of chemicals in water during showering are calculated using the
following equation and assumptions:
where
CDI
Cw
SA
PC
ET
EF
ED
CF
BW
AT
Days
C • SA • PC • ET • EF • ED • CF CDI = ....:•:.._ ____________ _
BW •AT• Days
chronic daily intake (mg/kg-day, absorbed dose),
exposure point concentration in groundwater (mg/1),
skin surface area available for contact (13,600 cm2),
chemical-specific dermal permeability constant (cm/hr),
exposure time (hr/day),
frequency of exposure (days/year),
exposure duration (years),
volumetric conversion factor for water (1 liter/1000 cm3),
average body weight (kg),
averaging time (70 years for carcinogens, duration of
exposure for noncarcinogens), and
conversion factor (365 days/year).
The parameters describing e_xposure time (ET), exposure frequency (EF),
exposure duration (ED), body weight (BW), and lifetime (AT) were identical to
those used for estimating inhalation of volatiles by a child (1-6 years) and
adult resident. Again, it was assumed that future residents would shower 12
minutes/day for 350 days/year. The standard body weight of 15 kg and 70 kg
were used for a child (1-6 years) and adult, respectively (USEPA 1991a).
Further, a child and adult are to have a total body surface area of 6,990 cm2
(weighted-average surface area for 1 to 6 year-olds) and 18,150 cm2,
4-86
respectively (USEPA 1989b ,. 1989a). Because chemical-specific permeability
constants are not available, the permeability of water, 8xl0"4 cm/hr based on
data reported by Blank et al. (1984), is used as a default permeability
constant for both organic and inorganic chemicals, as recommended by USEPA
(1989a).
CDis calculated using these exposure assumptions are presented in Tables 4-51
and 4-52 for the dermal absorption of organic chemicals by a child and adult
resident, respectively.
4.5.2.6 Inhalation of Volatilized Chemicals from Surface Soil/Sediment
Under future site use conditions, inhalation exposures to volatile chemical
emissions from the site are estimated for hypothetical future on-site
merchants, and residents (young child and adult). As discussed previously in
Section 4.5, exposure point concentrations on site were calculated using
volatilization and air dispersion models. Details of these models are
described in Appendix D. Estimated exposure point concentrations were
presented earlier in Table 4-9. Note that CDis are calculated differently for
chemicals exhibiting carcinogenic versus noncarcinogenic effects. In the
former case, exposure is extrapolated over a·lifetime while in the latter
case, CDis are estimated over the actual duration of exposure.
CDis are calculated using the following equation:
where
CDI
IR
ET
EF
CDI = C• • IR • ET • EF • ED
BW. AT. Days
chronic daily intake (mg/kg-day),
exposure point concentration in air
(mg/m3);
inhalation rate (m3/hr),
exposure time (hours/day),
frequency of exposure (days/year),
4-87
TABLE 4-51
EXPOSURE POINT CONCENTRATIONS AND CHRONIC DAILY INTAKES FDR DERMAL CONTACT WHILE
SHOWERING WITH GROUNDWATER FROM THE SURFICIAL AQUIFER BY A CHILD (1-6 YRS)
RESIDENT UNDER FUTURE LAND USE CONDITIONS (a)
Chemical
Chemicals Exhibiting
Carcinogenic Effects
Organics:
Aldrin
atpha-BHC
beta-BHC
ganrna-BHC
Bis(2-ethylhexyl)phthalate
Dieldrin
4 4'-DDE
T~xaphene
Chemicals Exhibiting
Noncarcinogenic Effects
Organics:
Aldrin
garrma-BHC
Bis(2-ethylhexyl)phthalate
Dieldrin
1,2,4-Trichlorobenzene
lnorganics:
Bariun
Manganese
Mercury
Vanadium
Zinc
RME
Exposure Point
Concentration
(ug/1)
2.00E-01
3.60E+01
2.50E+01
3.00E+01
6.40E+OO
1.20E+OO
1.00E-01
5.90E+OO
2.00E-01
3.00E+01
6.40E+OO
1.20E+OO
5.90E+OO
2.8E+02 1.0E+02
1.0E+OO
3.8E+01
5.2E+02
RME
Chronic Daily
Intake
(mg/kg-day) (b)
1.23E-09
2.21E-07
1.53E-07
1.84E-07
3.92E-08
7.35E-09
6.13E-10
3.62E-08
1.43E-08
2. 14E-06
4.SBE-07
8.SBE-08
4.22E-07
2.00E-05
7. 15E-06 7.15E-08
2.72E-06
3.72E-05
Ca) COis have been calculated for those chemicals of potential concern with tox1c1ty
criteria. The following chemicals of potential concern are not presented due to lack
of toxicity criteria: aluninun, calciLm, iron, magnesillll, potassillTI, delta-BHC and
endrin ketone.
(b) See text for exposure assllfPtions.
4-88
r-
TABLE 4-52
EXPOSURE POINT CONCENTRATIONS AND CHRONIC DAILY INTAKES FOR DERMAL CONTACT WHILE
SHOWERING WITH GROUNDWATER FROM THE SURFICIAL AQUIFER BY AN ADULT .
RESIDENT UNDER FUTURE LAND USE CONDITIONS Ca)
Chemical
Chemicals Exhibiting
Carcinogenic Effects
Organics:
Aldrin
alpha·BHC
beta-BHC
garrma-BHC
Bis(2-ethylhexyl)phthalate
Dieldrin
4,4'-DDE
Toxaphene
Chemicals Exhibiting
Noncarcinogenic Effects
Organics:
Aldrin
ganma-BHC
Bis(2-ethylhexyl)phthalate
Dieldrin
1,2,4-Trichlorobenzene
Inorganics:
Bariiin
Manganese
Mercury
Vanadiun
Zinc
RME
Exposure Point
Concentration
(ug/l)
2.OOE-O1
3.6OE+O1
2.5OE+O1
3.OOE+O1
6.4OE+OO
1.2OE+OO
1.OOE-O1 5.9OE+OO
2.OOE-O1
3.OOE+O1
6.4OE+OO
1.2OE+OO
5.9OE+OO
2.8E+O2
1.OE+O2
1.OE+OO 3.BE+O1
5 .2E+O2
RME
Chronic Dai Ly
Intake
(mg/kg-day) Cb)
3.41E-O9
6.14E-O7
4.26E-O7
5.11E-O7
1.O9E-O7
2.OSE-O8 1.?OE-O9
1.O1E-O7
7.96E·O9
1.19E·O6
2.SSE-O7 4.m-os
2.35E·O7
1.11E-O5
3.98E-06
3.9BE·OB
1.51E-06
2.O?E-O5
(a) COis have been calculated for those chemicals of potential concern with toxicity
criteria. The following chemicals of potential concern are not presented due to lack
of toxicity criteria: elllllin1n, calciun, iron, magnesi1i11, potassillTI, delta-BHC and
endrin ketone.
Cb) See text for exposure assllllptions.
4-89
ED
BW
AT
Days
duration of exposure (years),
body weight over the period of exposure (kg),
averaging time (70 years for carcinogens, duration of
exposure for noncarcinogens),
conversion factor (365 days/year).
The parameter values used to estimate CDis for a hypothetical future on-site
merchant, and future adult and child (1-6 years) residents are presented in
Table 4-53. Parameters describing duration of exposure, body weight and
lifetime were identical to those used for estimating inhalation of volatiles
to nearby merchants, and residents under current land-use conditions (Section
4.5.1.3). Children were assumed to weigh (BW) 15 kg (USEPA 1989b) and to be
exposed 350 days/year (EF) for 6 years (ED). Adult residents were assumed to
be at home 350 days/year (EF) for a duration of 30 years (ED). Both values
are based upon,USEPA (1991a, 1989a), and represent the upper-bound durations
at one residence. Again, standard default assumptions were made regarding
body weight (BW) (70 kg), and lifetime (AT) (70 years) (USEPA 1989a).
It was assumed that a future merchant would be at work 241 days/year (5
days/week, 50 weeks/year). This includes 2 weeks subtracted for vacation and
9 days for federal holidays. Standard default assumptions were made regarding
body weight (70 kg), and lifetime (70 years) (USEPA 1989a).
The resulting CDis for chemicals exhibiting carcinogenic effects and chemicals
exhibiting noncarcinogenic effects are summarized in Table 4-54 through 4-56.
4-90
TABLE 4-53
EXPOSURE PARAMETERS FOR INHALATION OF VOLATILIZED CHEMICALS
FUTURE LAND-USE CONDITIONS
Parameter
Exposure Frequency (days/year) (a)
Exposure Duration (years) (b)
Inhalation Rate (m3/day) (c)
Body Weight (kg) (d)
Period Over Which Risk is Being
Estimated (years)
Carcinogenic (e)
Noncarcinogenic
Residents
Child
(1-6 yrs)
350
6
15
15
70
6
Adult
350
30
20
70
70
30
Adult
Merchant
241
25
20
70
70
25
(a) A merchant is assumed to work 5 days/week, 50 weeks/year (2 weeks
subtracted for vacation), minus 9 days for federal holidays. Values for
adult and child residents are based on USEPA (1991a).
(b) Based upon USEPA (1991a). Value for adult residents is the upper bound
time at one residence (USEPA 1991a).
(c) Values for adult and merchant are the standard default value provided by
USEPA (1991a). Value for child 1-6 years is the age-weighted
ventilation rate, assuming 10 hours at rest and 14 hours of active play
(NCRP 1985).
(d) Standard default values provided by USEPA (1991a, 1989a).
(e) Based on USEPA (1991a, 1989a) standard assumption for lifetime. This
value is used in calculating exposures for potential carcinogens.
4-91
TABLE 4·54 ·
EXPOSURE POINT CONCENTRATIONS AND CHRONIC DAILY INTAKES FOR
INHALATION OF VOLATILIZED CHEMICALS BY AN ON·SITE CHILD ·c1·6 YRS)
RESIDENT UNDER FUTURE LAND·USE CONDITIONS (a)
Chemical
Chemicals Exhibiting
Carcinogenic Effects
Organics:
Aldrin
alpha·BHC
beta-BHC
alpha-Chlordane
ga1T1T1a-Chlordane
4,4' -DDT
Dieldrin
Toxaphene
RME
Exposure Point
Concentration
(ug/m3) Cb)
5.23E·O6
5.O6E·O5
2.81E·O5
4. 74E·O5
4.85E·OS
4.31E·O4
1.5OE·O4
1 .29E-O2
RME
Chronic Daily
Intake (COi)
(mg/kg·day) (C)
4.3OE·1O
4.16E·O9
2.31E·O9
3.9OE·O9
3.99E·O9
3.54E-O8
1.23E-O8
1.O6E·O6
Ca) COis have been calculated for those chemicals of potential concern with toxicity
criteria. The following chemicals of potential concern are not presented due to
lack of inhalation toxicity criteria: delta-BHC, ga1T1T1a·BHC, 4,4'-DDD and 4,4'-DDE.
Cb) RME concentration is the 95¾ upper confidence limit on the arithmetic mean
(which includes one-half the detection limit for non-detected values).
(c) See text for exposure assL1Tptions.
;t
4-92
.D
TABLE 4-55
EXPOSURE POINT CONCENTRATIONS AND CHRONIC DAILY INTAKES FOR INHALATION OF
VOLATILIZED CHEMICALS BY ON-SITE ADULT RESIDENTS UNDER
Chemical
Chemicals Exhibiting
Carcinogenic Effects
Organics:
Aldrin
alpha·BHC
beta·BHC
alpha-Chlordane
ganma-Chlordane
4 4'-DDT
oieldrin
Toxaphene
FUTURE LANO-USE CONDITIONS (a)
RME
Exposure Point
Concentration
(Ug/rn3) (C)
2.34E·06
2.26E-05
1.25E-05
2.12E·05
2.17E·05
1 .93E·04
6.71E-05 5.TTE-03
RME
Chronic Daily
Intake (CDI)
(mg/kg-day) (d)
2.75E-10
2.65E-09
1.47E-09
2.49E·09
2.55E·09
2.27E·08
7.BBE-09 6. 77E-07
Ca) COis have been calculated for those chemicals of potential concern with inhalation tox1c1ty
criteria. The following chemicals of potential concern are not presented due to lack of
inhalation toxicity criteria: delta-BHC, garnna•BHC, 4,4'·000 and 4,4'-DDE. Cb) Average concentration (including one-half the detection limit for non-detected values).
Cc) RME concentration is the 95X upper confidence limit on the arithmetic mean.
Cd) See text for exposure ass~tions.
4-93
TABLE 4-56
EXPOSURE POINT CONCENTRATIONS AND CHRONIC DAILY INTAKES FOR INHALATION
OF VOLATILIZED CHEMICALS BY ON-SITE ADULT MERCHANTS
Chemical
Chemicals Exhibiting
Carcinogenic Effects
Organics:
Aldrin
alpha-BHC
beta-BHC
alpha-Chlordane
galtllla-Chlordane
4,4'-DDT
Dieldrin
Toxaphene
UNDER FUTURE LAND-USE CONDITIONS (a)
RME
Exposure Point
Concentration (Ug/m3) (C)
2.56E-O6
2.48E-O5
1.3BE·O5
2.32E·O5
2.38E-O5
2.11E-O4
7.33E-O5
6.3OE·O3
RME
Chronic Daily
Intake (CDI)
(mg/kg-day)(d)
1. 72E-1O
1.67E-O9 9.3OE·1O
1.56E·O9
1.6OE-O9
1 .42E-O8 4.94E-O9
4.24E·O7
(a) COis have been calculated for those chemicals of potential concern with inhalation toxicity
criteria. The following chemicals of potential concern are not presented due to lack of
inhalation toxicity criteria: Benzoic acid, copper, delta-BHC, ganma·BHC, 4,4'-DDD, and 4,4'·00E.
(b) Average concentration (including one-half the detection limit for non-detected values).
Cc) RME concentration is the 95¾ upper confidence limit on the arithmetic mean.
Cd) See text for exposure asslllptions.
4-94
. I
5.0 RISK CHARACTERIZATION
In this section, the human health risks potentially associated with exposures
to media (soil/sediment, air and groundwater) from the Geigy Chemical
Corporation site are evaluated.
To quantitatively assess risks from the Geigy Chemical Corporation Site, the
chronic daily intakes (CDis) calculated in Section 4.4 were combined with the
health effects criteria presented in Section 3.0. For potential carcinogens,
excess lifetime upperbound cancer risks were obtained by multiplying the
estimated CDI for each chemical by its cancer slope factor. The total upper-
bound excess lifetime cancer risk for each pathway was obtained by summing the
chemical-specific risk estimates. This approach is consistent with the
USEPA's guidelines for evaluating the toxic effects of chemical mixtures
(USEPA 1989). A cancer risk level of lx10·6 , for example, represents an upper
bound probability of one in one million that an individual could develop
cancer due to exposure to the potential carcinogen under the specified
exposure conditions. The upper bound lifetime excess cancer risks derived in
this report were compared to USEPA's risk range for health protectiveness at
Superfund sites of 10·6 to 10·4 (USEPA 1990). USEPA's Office of Solid Waste
and Emergency Response (USEPA 1991) has recently issued a directive clarifying
the role of the risk assessment in the Superfund process. This directive
states that where the cumulative carcinogenic site risk to an individual based
on reasonable maximum exposure for both current and future land-use is less
than 10·4 and the non-carcinogenic hazard quotient is less than one, action
generally is not warranted unless there are adverse environmental impacts.
In general, USEPA cancer slope factors based on animal data are 95 percent
upper confident limit values based on the linearized multistage model. Thus,
actual risks associated with exposure to potential carcinogens such as alpha-,
beta and gamma-BHC, chlordane, DDT, dieldrin and toxaphene which are
quantitatively based on animal data are not likely to exceed the risks
estimated using these cancer slope factors, but may be considerably lower. It
5-1
is important to keep in m~nd that these risk levels are based on conservative
upperbound estimates, and are not actuarial risks, i;e., these estimates
cannot be translated directly into actual cancer cases.
Potential risks for noncarcinogens are presented as the ratio·of the CDI to
the reference dose (CDI/RfD) for each chemical. The sum of the ratios of all
chemicals under consideration is called the hazard index. The hazard index is
useful as a reference point for gauging the potential effects of environmental
exposures to complex mixtures. In general, hazard indices which are less than
one are not likely to be associated with any health risks, and are therefore
less likely to be of regulatory 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 greater than one
are "unacceptable". This is a consequence of the perhaps one order of
magnitude or greater uncertainty inherent in estimates of the RfD and CDI
ratio, in addition to the fact that there are uncertainties associated with
assuming the individual terms in the hazard index calculation are additive.
If the hazard index was greater than one, the chemicals of concern were
subdivided into categories based on target organ affected by exposure (e.g.,
liver, kidney, etc.) in accordance with USEPA (1989) guidance. Hazard indices
were then recalculated for these categories to better identify the potential
for noncarcinogenic effects to occur.
When risk from the dermal absorption of chemicals is quantified, the oral
cancer slope factor or reference dose may require modification if it was based
upon an administered dose rather than an absorbed dose. The modification
required in this case is the absorption efficiency of the chemical under the
conditions of the study from which the cancer slope factor was derived. For
example, if the slope factor was derived from an animal study where the
chemical was administered by gavage, then a factor which represents the extent
of absorption of the chemical from the gut under such conditions should be
applied. In other cases, the chemical may have been administered during a
dietary study. The absorption efficiency used in this situation should
5-2
r
reflect the conditions of .a dietary study. (It should be noted that this type
of absorption is difference from the relative oral absorption which takes into
account differences in absorption of a chemical adsorbed on sediment/soil
versus the vehicle used in the animal study.) However, since most human
health effects criteria are based upon administered doses to the study animal,
the extent of absorption under the study conditions in not generally known.
Because sufficient information regarding this absorption factor is not readily
available for the chemicals of concern, an absorption efficiency of 100% (a
factor of 1.0) was applied to the oral human health effects criteria when
estimating risk through the route of dermal absorption.
USEPA guidance considers exposure periods of less than 7 years to be
subchronic (USEPA 1989). In this risk assessment, chronic, rather than
subchronic toxicity criteria (RfDs) were used to evaluate exposure periods of
less than 7 years involving young and older children. This was because Region
IV is concerned that the use of subchronic RfDs in evaluating non-carcinogenic
risk may not afford sufficient protection to children.
5.1 RISKS ASSOCIATED WITH CURRENT SITE AND SURROUNDING LAND-USE CONDITIONS
The risk estimates for each pathway evaluated under current site use
conditions are presented in Tables 5-1 through 5-11. Highlighted below are
those pathways for which the lifetime excess cancer risk fall within or exceed
USEPA's target risk range of 10·6 to 10·4 risk range and hazard indices exceed
one.
5.1.1 Risks Due to Surface Soil/Sediment Exposures
Several of the surface soil exposure pathways evaluated in this risk
assessment had upper bound lifetime excess cancer risk levels lower than
USEPA's 10·6 to 10·4 range of risk for human health protectiveness, in addition
5-3
TABLE 5-1
POTENTIAL RISKS ASSOCIATED WITH INCIDENTAL INGESTION OF ON-SITE SOIL/SEDIMENT BY AN OLDER CHILD TRESPASSER UNDER CURRENT LAND-USE CONDITIONS (a)
RME
Chemicals Exhibiting
Carcinogenic Effects
RME
Chronic Dai Ly
Intake (CDI)
(mg/kg-day)
Slope
Factor
(mg/kg·day)-1
Weight of
Evidence
Class (b)
Upper Bound
Excess Lifetime
Cancer Risk
Organics:
Aldrin
alpha-BHC
beta·BHC
ganma-BHC
alpha-Chlordane
ganrna-Chlordane
4,4'-D00 4 4'-DOE·
4 '4, -DDT
oieldrin
Toxaphene
TOTAL
Chemicals Exhibiting
Noncarcinogenic Effects
Organics:
Aldrin ganma-BHC
Benzoic acid
alpha-Chlordane
ganma-Chlordane
4 4'·DDT
oieldrin
HAZARD INDEX
6.00E-11
1.73E-09
3.60E·09
1.60E·09
5.60E·10
6.53E-10
4.93E·08
2.67E-08
1.20E-07
3.33E·09
4.93E-07
RME
Chronic Daily
Intake (CDI)
(mg/kg-day)
7.00E-10
1.87E-08
5.60E-07
6.53E-09
7.62E-09
1.40E-06
3.89E-08
1. 7E+01
6.3E+OO
1.BE+OO
1.3E+OO (c) 1.3E+OO
1.3E+OO
2.4E-01
3.4E·01
3.4E·01
1.6E+01
1.1E+OO
Reference Dose
(mg/kg-day)
[Uncertainty
Factor] Cd)
3.0E·DS [1,000]
3.0E:04 [1,000] 4.0E+OO [1 J
6.0E-05 [1,000]
6.0E-05 [1,000]
5.0E-04 [100]
5.0E-05 [100]
82
82
C
82/C
82
82
82
82
82
82
82
Target Organ/
critical Effect Ce)
Liver
Liver/Kidney
Malaise Liver
Liver
Liver
Liver
< 1 (
1E·09
1E-08
6E-09
2E·09
7E· 10
BE· 10
1E·08
9E-09 4E-08
SE-08
SE-07 --------
?E-07
RME
CDl:RfD
Rafio
2E·05
6E·05
1E-07
1E·04
1E-04
3E-03
BE-04 --------4E-03
(a) Risks are calculated for those chemicals of potential concern with toxicity criteria. The following chemical of potential concern is not presented due to lack of toxicity criteria: delta-BHC. (b) USEPA ~eight of Evidence for Carcinogenic Effects: [82) Probable hllll8n carcinogen based on inadequate evidence from hunan studies and adequate evidence from animal studies.
[CJ Possible hunan carcinogen based on limited evidence from animal studies in the absence of hunan studies. (c) Under review by CRAVE Workgroup. (d) Uncertainty factors represent the amount of uncertainty in extrapolation from the available data. (e) A target organ/critical effect is the most sensitive organ/effect to a chemical's tOxic effect. RfDs are based on toxic effects in the target organ or on an effect elicited by the chemical. lf an RfD was based on a study in which a target organ was not identified, the organ listed is one known to be affected by the particular chemical of concern.
5-4
TABLE 5-2
POTENTIAL RISKS ASSOCIATED ~ITH INCIDENTAL INGESTION OF OFF-SITE SOIL/SEDIMENT BY
AN OLDER CHILD TRESPASSER UNDER CURRENT LAND-USE CONDITIONS (a)
Chemicals Exhibiting
Carcinogenic Effects
Organics:
beta-BHC
4 41 -DDD
4:41 -DDE
4 4'-DDT
Dieldrin
Toxaphene
TOTAL
Chemicals Exhibiting
Noncarcinog~nic Effects
Organics:
4,4'-DOT
Dieldrin
HAZARD INDEX
RME
Chronic Daily
Intake (CDI)
(mg/kg-day)
1. 71E·OB
7.93E·07
2.09E·07
1.65E·06 3.81E·10
6.03E·06
RME
Chronic Daily
Intake (CDI)
(mg/kg-day)
1.93E·05
4.44E·09
Slope
Factor
(mg/kg·day)-1
1.BE+OO
2.4E·01
3.4E·01
3.4E·01 1.6E+01
1. 1E+OO
Reference Dose (mg/kg-day)
[Uncertainty
Factor] (c)
S.OE-04 [100]
5.0E-05 [100]
Weight of
Evidence
Class Cb)
C
B2
B2
B2
82
B2
Target Organ/
Critical Effect
Liver
Liver
(a) Risks are calculated for those chemicals of potential concern with toxicity criteria.
(b) USEPA Weight of Evidence for Carcinogenic Effects:
(d)
RME Upper Bound
Excess Lifetime
Cancer Risk
< 1
3E·OB
2E·07
7E·OB
6E·07
6E·09
7E-06 --------
7E·06
RME
CDI :RfD
Ratio
4E·02
9E·05
4E·02)
[B21 Probable hunan carcinogen based on inadequate evidence from hunan studies and adequate evidence from animal studies.
[C] Possible human carcinogen based on limited evidence from animal studies in the absence of human studies.
Cc) Uncertainty factors represent the amount of uncertainty in extrapolation from the available data.
Cd) A target organ/critical effect is the most sensitive organ/effect to a chemical's toxic effect. RfDs are based
on toxic effects in the target organ or on an effect elicited by the chemical. If an RfD was based on a study in
which a target organ was not identified, the organ listed is one known to be affected by the particular chemical
of concern.
5-5
TABLE 5-3
POTENTIAL RISKS ASSOCIATED WITH DERMAL CONTACT OF ON-SITE SOIL/SEDIMENT BY
AN OLDER CHILD TRESPASSER UNDER CURRENT LAND-USE CONDITIONS ·ca)
Chemicals Exhibiting
Carcinogenic Effects
Organics:
Aldrin
alpha·BHC
beta-BHC
garrrna-BHC
alpha-Chlordane
garrma-Chlordane
4 4' -ODO
(4'-DDE
4,4'-DDT
Dieldrin
Toxaphene
TOTAL
Chemicals Exhibiting
Noncarcinogenic Effects
Organics:
Aldrin
gama-BHC
Benzoic acid
alpha-Chlordane
ganma-Ch lordane
4 4' -DDT
oieldrin
RME
Chronic Daily
Intake (CDI)
(mg/kg-day)
4.41E-11
1.27E-09
2.64E-09
1.18E·09
4. llE-10
4.SOE-10
4.llE-10
4.80E-10
3.62E-08
1.96E-08
8.81E-08
RME
Chronic Daily
Intake (CDI)
(mg/kg-day)
5.14E-10
1 .37E-08
4.llE-07
4.llE-07
4.BOE-09
5.60E·09
1 .03E-06
Slope
Factor
(mg/kg-day)-1
1. 7E+01
6.3E+OO
1.8E+OO
1.3E+OO Cc)
1.3E+OO
1.3E+OO
2.4E·01
3.4E-01
3.4E-01
1.6E+01
1.1E+OO
Reference Dose
(mg/kg-day)
[Uncertainty
Factor] Cd)
3.0E-05 [1, DOOJ
3.0E-D4 [1,000]
4.0E+OO [1]
6.0E-05 [1,000]
6.0E-05 [1,000]
5.0E-04 [100]
5.0E-05 [100]
Weight of
Evidence
Class Cb)
B2
82
C
B2/C
82
B2
B2
82
B2
B2
B2
Target Organ
or Critical
Effect (e)
Liver
Liver/Kidney
Malaise
Liver Liver
Liver
Liver
RME
Upper Bound
Excess Lifetime
Cancer Risk
7E-10
BE-09
SE-09
2E·09
SE-10
6E· 10
lE-10
2E-10
lE-08
3E-07
lE-07
4E·07
RME
CDI :RfD
Ratio
2E·05
SE-05
lE-07
7E-03
BE-05
lE-05
2E-02
HAZARD INDEX < 1 ( 3E·02)
(a) Risks are calculated for those chemicals of potential concern with toxicity criteria. The following
chemicals of potential concern are not presented due to lack of toxicity criteria: delta-BHC.
(b) USEPA Weight of Evidence for Carcinogenic Effects:
(B2] Probable hunan carcinogen based on inadequate evidence from hU'llan studies and adequate evidence from animal studies.
[C] Possible hlB'Tlan carcinogen based on limited evidence from animal studies in the absence of hllTIBn studies;
Cc) Under review by CRAVE Workgroup.
Cd) Uncertainty factors represent the amount of uncertainty in extrapolation from the available data.
(e) A target organ is the organ most sensitive to a chemical's toxic effect. RfDs are based on toxic effects
in the target organ. If an RfD was based on a study in which a target organ was not "identified, the organ
listed is one known to be affected by the particular chemical Of concern.
5-6
TABLE 5-4
POTENTIAL RISKS ASSOCIATED WITH DERMAL CONTACT· OF OFF-SITE SOIL/SEDIMENT BY
AN OLDER CHILO TRESPASSER UNDER CURRENT LAND-USE CONDITIONS (a)
Chemicals Exhibiting
Carcinogenic Effects
Organics:
beta·BHC
4 4'-000
4'4•-ooE
4
1
4'·DDT
oieldrin
Toxaphene
TOTAL
Chemicals Exhibiting
Noncarcinogenic Effects
Organics:
4 4'-00T
oieldrin
HAZARD INDEX
RME
Chronic Daily
Intake (CDI)
(mg/kg-day)
S.29E-09
2.4SE-07
6.46E-08
S.09E-07
1.18E-10
1.86E-06
RME
Chronic Daily
Intake (COi)
(mg/kg-day)
S.94E-06
1.37E-09
Slope
Factor
(mg/kg-day)-1
1.8E+00
2.4E-01
3.4E-01
3.4E-01
1.6E+01
1.1E+OO
Reference Dose
(mg/kg-day)
(Uncertainty
Factor] (c)
S.OE-04 [1001
S.OE-05 [100]
Weight of
Evidence
Class Cb)
C
B2
B2
B2
B2
B2
Target Organ
or Critical Effect (d)
Liver
Liver
(a)
Cb)
are calculated for those chemicals of potential concern with toxicity criteria.
Weight of Evidence for Carcinogenic Effects:
RME
Upper Bound
Excess Lifetim
Cancer Risk
1E-0B
6E-08
2E-08
2E-07
2E-09
2E-06
2E-06
RME
COi :RID
Ratio
1E-02
3E-OS
< 1 ( 1E-02 )
Risks
USEPA
[B2] Probable human carcinogen based on inadequate evidence from human studies and adequate evidence from
animal studies.
(c)
(d)
[CJ Possible human carcinogen based on limited evidence from animal studies in the absence of
human studies;
Uncertainty factors represent the amoUnt of uncertainty in extrapolation from the available data.
A target organ is the organ most sensitive to a chemical's toxic effect. RfOs are based on toxic effects
in the target organ. If an RfD was based on a study in which a target organ was not identified, the organ
listed is one known to be affected by the particular chemical of concern.
5-7
Chemicals Exhibiting
Carcinogenic Effects
Organics~
Aldrin alpha-BHC
beta-BHC
alpha-Chlordane
garrma·Chlordane
4 4' -DDT
oieldrin
Toxaphene
TOTAL
TABLE 5-5
POTENTIAL RISKS ASSOCIATED WITH INHALATION OF VOLATILIZED CHEMICALS BY AN ON-SITE OLDER CHILD TRESPASSER UNDER CURRENT LANO-USE CONDITIONS (a)
RME
Chronic•Daily
Intake (COi)
(mg/kg-day)
7.3DE-12
7.D7E-11
3.92E-11
6.62E-11
6.77E-11
6.02E-10
2.09E-10
1.B0E-08
Slope
Factor
(mg/kg-day)-1
1. 7E+D1
6.3E+00
1.BE+00
1.3E+00
1.3E+00
3.4E-01
1.6E+01
1.1E+00
Weight of
Evidence
Class (b)
B2
B2
C
B2
B2
B2
B2
B2
RME ·
Upper Bound
Excess Lifetime
cancer Risk
1E-10
4E-10
7E-11
9E-11
9E-11
2E-10
3E-09
2E-08
2E-08
Ca) Risks are calculated for those chemicals of potential concern with inhalation toxicity criteria. The following chemicals of potential concern are not presented due to lack of inhalation toxicity criteria: delta·BHC, ganma·BHC, 4,4'·00D, and 4,4'-DDE. Cb) USEPA Weight of Evidence for Carcinogenic Effects: [821 Probable hl.DTlan carcinogen based on inadequate evidence from hl.lll8n studies and adequate evidence from animal studies. [Cl Possible hl.11\an carcinogen based on limited evidence from animal studies in the absence of hunan studies.
s-s
/
TABLE 5-6
POTENTIAL RISKS ASSOCIATED WITH INHALATION OF VOLATILIZED CHEMICA.LS BY A NEARBY
ADULT MERCHANT TO THE NORTH UNDER CURRENT LAND-USE CONDITIONS (a)
Chemicals Exhibiting
Carcinogenic Effects
Organics:
Aldrin
alpha-BHC
beta-BHC
alpha-Chlordane
gamna·Chlordane
4,4'-DDT
Dieldrin
Toxaphene
TOTAL
RME
Chronic Daily
Intake (COi)
(mg/kg-day)
1.68E-10
1.63E-09
9.10E-10
1.53E-09
1.56E-09
1.39E-08
4.82E-09
4.14E-07
Slope
Factor
(mg/kg-day)-1
1. 7E+01
6.3E+OO
1.BE+OO
1.3E+OO
1.3E+OO
3.4E-01
1.6E+01
1.1E+OO
Weight of
Evidence
Class Cb)
B2
B2
C B2
B2
B2 B2
B2
RME
Upper Bound
Excess Lifetime
Cancer Risk
3E-09
1E-08
2E-09
2E-09
2E-09
SE-09
BE-08
SE-07
6E-07
(a) Risks are calculated for those chemicals of potential concern with toxicity criteria. The following
chemicals of potential concern are not presented due to lack of inhalation toxicity criteria: delta·BHC,
ganma-BHC, 4,4'·000 and 4,4'-00E.
(b) USEPA Weight of Evidence for Carcinogenic Effects:
(B2] Probable hunan carcinogen based on inadequate evidence from hunan studies and adequate evidence from
animal studies.
[Cl Possible hllllan carcinogen based on limited evidence·from animal studies in the absence of
hunan studies.
5-9
TABLE 5-7
POTENTIAL RISKS ASSOCIATED ~ITH INHALATION OF VOLATILIZED CHEMICALS
BY A CHILO (1-6 YRS) RESIDENT TO THE NORTHEAST
Chemicals Exhibiting
Carcinogenic Effects
Organics:
Aldrin
alpha-BHC
beta-BHC
alpha-Chlordane
ga1Tma·Chlordane 4,41-DDT
Dieldrin
Toxaphene
TOTAL
UNDER CURRENT LANO-USE CONDITIONS (a)
RME
Chronic Daily
Intake (CDI)
(mg/kg-day)
4.23E-11 4.09E-10
2.28E-10
3.84E-10
3.93E-10
3.49E-09
1.21E-09
1.04E-07
Slope
Factor (mg/kg-day)-1
1. 7E+D1
6.3E+OO
1.BE+OO
1.3E+OO
1.3E+OO
3.4E-01
1.6E+01 1.1E+OO
Weight of
Evidence
Class Cb)
B2
B2
C
B2
B2
B2
B2
B2
RME Upper Bound
Excess Lifetime
Cancer Risk
7E-10 3E-09
4E-10
SE-10
SE-10 1E-09
2E-08
1E-07
1E-07
Ca) Risks are calculated for those chemicals of potential concern with toxicity criteria. The following
chemical~ of potential concern are not presented due to lack of inhalation toxicity criteria: delta·BHC, gamna•BHC, 4,4'·0D0 and 4,4'-DDE. Cb) USEPA Weight of Evidence for Carcinogenic Effects:
[82] Probable hunan carcinogen based on inadequate evidence from hLll'IBn studies and adequate evidence from animal studies.
[Cl Possible hl.lTI8n carcinogen based on limited evidence from animal studies in the absence of hunan studies.
5-10
' !
Chemicals Exhibiting
Carcinogenic Effects
Organics:
Aldrin
alpha-BHC
beta-BHC
alpha-Chlordane
galll!la-Chlordane
4,4'-DDT
Dieldrin
Toxaphene
TOTAL
TABLE 5-8
POTENTIAL RISKS ASSOCIATED WITH INHALATION OF VOLATILIZED CHEMICALS SY AN ADULT RESIDENT TO THE NORTHEAST
UNDER CURRENT LAND-USE CONDITIONS (a)
RME
Chronic Daily
Intake (CDI)
(mg/kg-day)
2.7OE·11
2.62E·1O
1.46E-1O
2.45E-1O
2.51E-1O 2.23E-O9
7.74E-1O
6.65E-O8
Slope
Factor
Cmg/kg-day)-1
1. 7E+O1
6.3E+OO
1.8E+OO
1.3E+OO
1.3E+OO
3.4E·O1 1.6E+O1
1.1E+OO
Weight of
Evidence
Class Cb)
82
82
C
B2
B2
82
82
82
RME
Upper Bound
Excess Lifetime
Cancer Risk
SE-1O
2E-O9
3E·1O
3E·1O 3E-1O 8E·1O 1E-O8
7E-O8
9E·O8
(a) Risks are calculated for those chemicals of potential concern with tox1c1ty criteria. The following
chemicals of potential concern are not presented due to lack of inhalation toxicity criteria: delta·BHC
ganma-BHC, 4,4'-DDD and 4,4'-DOE. Cb) USEPA Weight of Evidence for Carcinogenic Effects:
[B2] Probable hiinan carcinogen based on inadequate evidence from hiinan studies and adequate evidence from
animal studies.
[C] Possible human carcinogen based on limited evidence from animal studies in the absence of hunan studies.
5-11
Chemicals EXhibiting
Carcinogenic Effects
Organics:
Aldrin
alpha-BHC
beta-BHC
alpha-Chlordane
galTl!la-Chlordane
4,4' -DOT .
Dieldrin
Toxaphene
TOTAL
TABLE 5-9
POTENTIAL RISKS ASSOCIATED ~ITH INHALATION OF OUST PARTICULATES BY A NEARBY ADULT MERCHANT TO THE NORTH UNDER UNDER CURRENT LAND-USE CONDITIONS (a)
RME
Chronic Dai Ly
Intake (CDI)
(mg/kg-day)
1.24E-13
2.33E-12
3.38E-12
1.15E-12
1.18E-12
1.04E-10
4.22E-12
4.SOE-10
Slope
Factor
(mg/kg-day)-1
1. 7E+01
6.3E+OO
1.BE+OO 1.3E+OO
1.3E+OO
3.4E-01 1.6E+01
1.1E+OO
Weight of
Evidence
Class Cb)
B2
B2
C
B2
B2
B2
B2
B2
RME
Upper Bound
Excess Lifetime
Cancer Risk
2E-12
1E-11
6E-12 1 E-12
2E-12
4E-11
7E-11
SE-10
6E-10
(a) Risks are calculated for those chemicals of potential concern with toxicity criteria. The following chemicals of potential concern are not presented due to lack of inhalation toxicity criteria: delta-BHC, garrrna-BHC, 4,4'·0D0 and 4,4'-0DE. (b) USEPA Weight of Evidence for Carcinogenic Effects: [B21 Probable human carcinogen based on inadequate evidence from human studies and adequate evidence from animal studies. [Cl Possible hlll'lan carcinogen based on limited evidence from animal studies in the absence of human studies.
5-12
TABLE 5-10
POTENTIAL RISKS ASSOCIATED YITH INHALATION OF OUST PARTICULTATEs·
BY A CHILO (1·6 YRS) RESIDENT TO THE NORTHEAST
Chemicals Exhibiting
Carcinogenic Effects
Organics:
Aldrin
alpha·BHC
beta-BHC
alpha-Chlordane
garrma-Chlordane
4,4'-0DT
Dieldrin
Toxaphene
TOTAL
UNDER CURRENT LANO-USE CONDITIONS (a)
RME
'Chroni C Daily
Intake (CDI)
(mg/kg-day)
1.52E·14
2.87E-13
4.15E·13
1.42E·13
1.45E·13
1.28E·11
5.19E-13
5.53E·11
Slope
Factor
(mg/kg·day)-1
1. 7E+01
6.3E+OO
1.8E+OO
1.3E+OO
1.3E+OO
3.4E·01
1.6E+01
1. 1E+OO
Weight of
Evidence
Class Cb)
82
B2
C
B2
B2 B2
B2
B2
RME
Upper Bound
Excess Lifetime
Cancer Risk
3E-13
2E· 12
7E-13
2E·13
2E·13 4E·12
BE· 12
6E· 11
BE· 11
(a) Risks are calculated for those chemicals of potential concern with toxicity criteria. The following
chemicals of potential concern are not presented due to lack of inhalation toxicity criteria:
delta-BHC, garrma-BHC, 4,4'-000 and 4,4'-DDE.
(b) USEPA Weight of Evidence for Carcinogenic Effects:
[B2] Probable human carcinogen based on inadequate evidence from human studies and adequate evidence
from animal studies.
[C] Possible human carcinogen based on limited evidence from animal studies in the absence of
hlmlan studies.
5-13
Chemicals Exhibiting Carcinogenic Effects
Organics:
Aldrin
alpha·BHC beta-BHC
alpha-Chlordane
garrma-Chlordane 4 4'-DDT
oleldrin
Toxaphene
TOTAL
TABLE 5-11
POTENTIAL RISKS ASSOCIATED YITH INHALATION Of DUST PARTltULATES BY AN ADULT RESIDENT TO THE NORTHEAST UNDER CURRENT LAND-USE CONDITIONS (a)
RME
Chronic Daily Intake (CDI) (mg/kg-day)
2.17E-14
4.10E·13
5.93E·13
2.03E-13
2.0BE-13 1.83E·11
7.41E·13
7.90E·11
Slope
Factor (mg/kg-day)-1
1. 7E+01
6.3E+OO 1.8E+OD
1.3E+OO
1.3E+OO
3.4E-01
1 .6E+01
1.1E+OD
Weight of
Evidence
Class (b)
B2
B2
C
B2
B2
B2
B2
B2
RME
Upper Bound
Excess Lifetime
Cancer Risk
4E-13
3E·12
1 E-12
3E·13
3E·13
6E· 12
1E·11
9E· 11
1E·10
Ca) Risks are calculated for those chemicals of potential concern with toxicity criteria. The following chemicals of potential concern are not presented due to lack of inhalation toxicity criteria: delta-BHC garrma-BHC, 4,4'-DDD and 4,41 -DDE. Cb) USEPA Weight of Evidence for Carcinogenic Effects: [B21 Probable hunan carcinogen based on inadequate evidence from hl.11\an studies end adequate evidence from • animal studies. [CJ Possible human carcinogen based on limited evidence from animal studies in the absence of human studies.
5-14
\'----_ \ to hazard indices which we.re less than one. This encompasses the following
pathways:
• Incidental ingestion of on-site surface soil/sediment by
trespassing children (8-13 years) (Table 5-1) and;
• Dermal absorption of chemicals in on-site surface·soil/sediment by
trespassing children (8-13 years) (Table 5-3).
Scenarios with cancer risks within USEPA's risk range of 10-6 to 10·4 for human
health protectiveness or hazard indices greater than one are discussed in more
detail below. No exposure pathways were associated with risks greater than
7x10·6.
5.1.1.1 Risks Associated with Incidental Ingestion of Off-Site Surface
Soil/Sediment by Older Children (8-13 years)
Table 5-2 shows that the potential upper bound lifetime excess cancer risk to
off-site older child (8-13 years) through incidental ingestion of off-site
surface soil/sediment is 7xlo-6. This value is attributable to toxaphene and
is within USEPA's target risk range of 10·6 to 10·4. For noncarcinogenic
chemicals, the hazard index is less than one indicating that adverse
noncarcinogenic effects are not likely to occur.
5.1.1.2 Risks Associated with Dermal Contact with Off-Site Surface
Soil/Sediment by Older Children (8-13 years)
Table 5-4 shows that the potential upper bound lifetime excess cancer risk to
an older child (8-13 years) who may absorb chemicals in off-site surface
soil/sediment through dermal contact is 2xlo-6. Again, this value is
attributable to toxaphene and is at the lower bound of USEPA's risk range of
10-6 to 10-4. For noncarcinogenic chemicals, the hazard index is less than one
indicating that older children are not likely to experience adverse
noncarcinogenic effects.
5-15
5.1.2 Risks Due to the Inhalation of Airborne Volatiles and Dust Particulates
All of the exposure pathways which evaluated the inhalation of chemicals
volatilized from on-site soil/sediment and the inhalation of wind blown
particulates migrating off-site had upper bound lifetime excess cancer risks
levels lower than USEPA's 10-6 to 10-4 risk range for human health
protectiveness, in addition to hazard indices which were less than one. This
includes the following pathways:
• Inhalation of volatilized surface soil/sediment
chemicals by on-site child trespassers (Table 5-5);
• Inhalation of volatilized surface soil/sediment chemicals by merchants north of the site (Table 5-6);
• Inhalation of volatilized surface soil/sediment chemicals by nearby child residents, northeast of the site (Table 5-7);
• Inhalation of volatilized surface soil/sediment chemicals by nearby adult residents, northea_st of the site (Table 5-8);
• Inhalation of dust particulates by merchants north of the site
(Table 5-9);
• Inhalation of dust particulates by nearby child residents,
northeast of the site (Table 5-10); and
• Inhalation of dust particulates by nearby adult residents, northeast of the site (Table 5-11).
5.2 SUMMARY OF CUMULATIVE RISKS UNDER CURRENT LAND-USE CONDITIONS
For the purposes of this assessment, the effects of exposure to the pesticides
present in soil have been considered separately for each pathway. However,
receptors may be exposed at one time by a combination of pathways, and
therefore, the combined pathway risks were estimated for each of the receptors
of concern. In this assessment, an older trespassing child, nearby merchant
and nearby residents may be exposed to the chemicals of potential concern
through multiple pathways. The total cancer risks associated with multiple
pathway exposure for these receptors are summarized on Table 5-12.
r.
I
5.2.1 Cumulative Risks to an On-Site Trespasser
The total risks for a on-site older child trespasser (8-13 years) who may
contact surface soil dermally and through incidental ingestion, and may inhale
chemicals released from.surface soil/sediment through volatilization is lxio-6
for the RME case. This means that an individual over a lifetime of 70 years
would have a chance of one in one million of developing cancer from the
combined ingestion, dermal and inhalation exposure pathways for these exposure
scenarios. This is at the lower bound of the risk range of concern to
regulatory agencies.
Individual exposure pathways were combined in order to estimate the total
potential for adverse noncarcinogenic effects to occur. Risks of
noncarcinogenic effects are not expressed as a probability as are cancer
risks. Instead, noncarcinogenic effects are assumed to occur through a
threshold mechanism, and adverse noncarcinogenic effects could potentially
occur if the total hazard index for a single target organ is greater than one.
Total hazard indices much less than one are indicative of exposures of non-
concern. The total noncancer risks for each receptor, associated with
incidental ingestion, dermal absorption and inhalation, are summarized on
Table 5-12.
The total noncancer risk across pathways for an on-site older child trespasser
are at least two orders of magnitude below one and range from 4xlo-3 to 3xlo-2
for the RME case. This clearly indicates that potential adverse
noncarcinogenic effects associated with all of the evaluated exposures are not
of concern.
5.2.2 Cumulative Risks to a Off-Site Receptors
Nearby merchants north of the site, in addition to nearby child and adult
residents to the northeast of the site may be exposed by a combination of
5-17
TABLE 5-12
TOTAL RISKS ASSOCIATED WITH CURRENT LAND-USE CONDITIONS
Area/Pathway
Ingestion of Surface Soil/Sediment
Dermal Absorption from Surface
Soil/Sediment
Inhalation of Volatile Chemicals Released from surface Soil/Sediment
Inhalation of Dust Particulates
Total Cancer Risk
Area/Pathway
Ingestion of Surface Soil/Sediment
Dermal Absorption from Surface
Soil/Sediment
Inhalation of Volatile Chemicals
Released from Surface Soil/Sediment
Inhalation of Oust Particulates
On-Site
Older Child
Trespasser
(8-13 yrs)
7.0E·O?
4.0E-07
2.0E-08
1E·D6
On-Site
Older Child
Trespasser (8·13 yrs)
4.0E·D3
3.0E·D2
Cal
• • • Ca)
Cancer Risk Due to All Chemicals
Off-Site
Older Child
(8-13 yrs)
7.0E-06
2.0E-06
9E·06
Off-Site
Adu It Merchant
6.0E·D7
6.0E-10
6E·07
Off-Site
Adu It
Resident
9.0E·D8
1.0E·10
9E·08
Noncancer Risk Due to All Chemicals
Off-Site Off-Site Off·Site
Older Child Adu It Adu It (8·13 yrs) Merchant Resident
4.0E·D2
1.0E·D2
Ca) Cal Ca)
Ca) . . . Ca) • . • Ca)
Ca) No inhalation toxicity criteria were available to assess noncercinogenic risks.
= Not evaluated.
5-18
Off-Site
Young Child
Resident
(1-6 yrs)
1.0E·D7
8.00E-11
1E·D7
Off-Site
Young Child
Resident
(1·6 yrs)
Ca)
... Ca)
_fl
i '· '
' •.
pathways, and therefore, t~e combined pathway risks were estimated in order to
be protective. The total cancer _risks for a nearby merchant, and nearby child
and adult residents associated with inhalation of volatile chemicals and dust
particulates are summarized on Table 5-12.
The total risks for a nearby merchant, young child (1-6 years) resident and
adult resident who may inhale both volatilized chemicals and dust particulates
migrating from the site are 6x10·7, lx10·7, and 9x10·8 respectively. These
risks are below USEPA's target risk range of 10·6 to 10·4 for human health
protectiveness at Superfund sites. Noncarcinogenic effects could not be
evaluated due to an absence of USEPA inhalation toxicity criteria.
5.3 RISKS ASSOCIATED WITH FUTURE LAND-USE CONDITIONS
The potential risks associated with the future land-use pathways are
summarized in Tables 5-13 through 5-30. Highlighted below are those pathways
for which the lifetime excess cancer risk fall within or exceed USEPA's target
risk range of 10·6 to 10"4 risk range and hazard indices exceed one under
future land-use conditions.
5.3.1 Risks Due to Surface Soil/Sediment Exposures
5.3.1.1 Risks Associated with Incidental Ingestion of Surface
Soil/Sediment by a Future Merchant and a Child (1-6 years) and
Adult Resident
Tables 5-13, 5-14 and 5-15 show that the potential upper bound lifetime excess
cancer risks to a future on-site child (1-6 years) resident, adult resident
and merchant through incidental ingestion of surface soil/sediment are 3x10·5,
lxlo-5, and 4xio-6, respectively. These values are attributable to toxaphene
and are within USEPA's target risk range of 10·6 to 10-4 • For noncarcinogenic
chemicals, the hazard index is less than one for all three scenarios,
indicating that young children, adult residents and merchants are not likely ~
to_exp~rience adverse noncarcinogenic effects.
5-19
Chemicals Exhibiting
Carcinogenic Effects
Organics:
Aldrin
alpha-BHC
beta-BHC
ganrna-SHC
alpha-Chlordane
ganma-Chlordane
4,4'·000
4 4'·DDE
4:4'-0DT
Dieldrin
Toxaphene
TOTAL
Chemicals Exhibiting
Noncarcinogenic Effects
Organics:
Aldrin
ganrna•BHC
Benzoic acid
alpha-Chlordane
garrma·Chlordane
4 4'-DDT
oieldrin
HAZARD INDEX
TABLE 5-13
POTENTIAL RISKS ASSOCIATED WITH INCIDENTAL INGESTION OF
ON-SITE SOIL/SEDIMENT BY A CHILD RESIDENT (1-6 YRS) UNDER FUTURE LAND-USE CONDITIONS (a)
USEPA RME
Chronic Daily
Intake (CDI)
(mg/kg-day)
2.40E-09
6.92E-08
1.44E-07
6.39E-08
2.24E-08
2.61E-08
1.97E·06
1.06E-06
4. 79E-06
1.33E·07
1.97E-OS
USEPA RME
Chronic Daily
Intake (CDI)
(mg/kg-day)
2.79E-08
7.4SE·07
2.24E-OS
2.61E·07
3.04E·07
S.59E-05
1.SSE-06
Slope
Factor
(mg/kg-day)-1
1. 7E+01
6.3E+OO
1.BE+OO
1.3E+OO (c)
1.3E+OO
1.3E+OO
2.4E-01
3.4E-01
3.4E·01
1 . 6E+01
1.1E+OO
Reference Dose
(mg/kg-day)
[Uncertainty
Factor] (d)
3.0E-05 [1,000]
3.0E-04 [1,000]
4.0E+OO [1 J
6.0E·OS [1,000]
6.0E-05 [1,000]
S.OE-04 [100] S.OE-05 [100]
Ueight of
Evidence
Class (b)
B2
B2
C
B2/C
B2
B2
B2
B2
B2
B2
B2
Target Organ/
Critical
Effect (e)
Liver
liver/Kidney
Malaise
Liver
Liver
Liver
Liver
USEPA RME
Upper Bound
Excess Lifetime
Cancer Risk.
4E-08
4E-07
3E-07
BE-08
3E-OB
3E-0B
SE-07
4E·07
2E-06
2E-06
2E-05
3E-05
USEPA RME
CDI :RfD
Ratio
9E-04
2E-03
6E-06
4E-03
SE-03
1E-01
3E-02
< 1 ( 2E-01 )
(a) Risks are calculated for those chemicals of potential concern with toxicity criteria. The following
chemical of potential concern is not presented due to lack of toxicity criteria: delta·BHC. (b) USEPA Weight of Evidence for Carcinogenic Effects:
[82] Probable hlll'l8n carcinogen based on inadequate evidence from hlll'l8n studies and adequate evidence from animal studies.
[C] Possible human carcinogen based on limited evidence from animal studies in the absence of hl.lTlan studies.
(c) Under review by CRAVE Workgroup.
(d) Uncertainty factors represent the amount of uncertainty in extrapolation from the available data.
(e) A target organ/critical effect is the most sensitive organ/effect to a chemical's toxic effect. RfOs are based
on toxic effects in the target organ or on an effect elicited by the chemical. If an RfO was based on a study in
which a target organ was not identified, the organ listed is one known to be affected by the particular chemical of concern.
(f) The drinking water standard of 1.3 mg/L has been converted to a dose asslllling a 70 kg individual ingests 2 liters of water per day.
5-20
Chemicals Exhibiting
Carcinogenic Effects
Organics:
Aldrin
alpha·BHC
beta-BHC
garrma-BHC
alpha-Chlordane
garrma-Chlordane
4 4'-DD0
414'-DOE
41 4'-0DT
oietdrin
Toxaphene
TOTAL
Chemicals Exhibiting
Noncarcinogenic Effects
Organics:
Aldrin
garrma-BHC
Benzoic acid
alpha-Chlordane
ganma-Chlordane
4 41 -DDT oietdrin
HAZARD INDEX
TABLE 5·14
POTENTIAL RISKS ASSOCIATED WITH INCIDENTAL INGESTION OF
ON·SITE SOIL/SEDIMENT BY ADULT RESIDENTS UNDER FUTURE LANO·USE CONDITIONS (a)
USEPA RME
Chronic Dai Ly
Intake (CDI)
(mg/kg-day)
1.28E·09
3.71E·08
7.70E·08
3.42E·08
1.20E·08
1.40E·08 1.06E·06
5.70E·07
2.57E·06
7.13E·08
1.06E·05
USEPA RME
Chronic Daily
Intake (COi)
(mg/kg·day)
2.99E·09
7.98E·08
2.40E·06
2.79E·08
3.26E·08
5.99E·06
1 .66E·07
Slope
Factor
(mg/kg·day)·l
1. 7E+01
6.3E+OO
1.8E+OO
1.3E+OO (cl 1.3E+OO
1.3E+OO
2.4E·01
3.4E·01
3.4E·01
1.6E+01
1.1E+OO
Reference Dose
(mg/kg-day)
[Uncertainty·
Factor] (dl
3.0E-05 [1,000]
3.0E-04 [100]
4.0E+OO [1]
6.0E·OS [1,000]
6.0E·0S [1,000]
5.0E-04 [100]
5.0E·0S [100]
~eight of
Evidence
Class Cb)
82
82
C
82/C
B2
B2
82
82
B2
82
82
Target Organ/
Critical
Effect Ce)
Liver
Liver/Kidney
Malaise
Liver
Liver
Liver
Liver
USEPA RME
Upper Bound
Excess Lifetime
Cancer Risk
2E·08
2E·07
1E·07 4E·08
2E·08
2E·08 3E·07
2E·07
9E·07
1E·06
1E·05 --------
1E·05
USEPA RME
COi :RIO
Ratio
1E·04
3E·04
6E·07
5E·04 SE-04
1E·02
3E-03 --------
< 1 2E·02 l
(a) Risks are calculated for those chemicals of potential concern with toxicity criteria. The following
chemicals of potential concern are not presented due to lack of toxicity criteria: delta-BHC.
Cb) USEPA Weight of Evidence for Carcinogenic Effects:
[B2] Probable hunan carcinogen based on inadequate evidence from hunan studies and adequate evidence from
animal studies.
[C] Possible hunan carcinogen based on limited evidence from animal studies in the absence of hunan studies;
(c) Under review by CRAVE Workgroup.
(d) Uncertainty factors represent the amount of uncertainty in extrapolation from the available data.
Ce) A target organ/critical effect is the most sensitive organ/effect to a chemical's toxic effect. RfDs are based
on toxic effects in the target organ or on an effect elicited by'the chemical. If an RfD was based on a study in
which a target organ was not identified, the organ listed is one known to be affected by the particular chemical of concern.
5-21
TABLE 5-15
POTENTIAL RISKS ASSOCIATED ~ITH INCIDENTAL INGESTION Of ON-SITE SOIL/SEDIMENT BY
ADULT MERCHANT UNDER FUTURE LANO-USE CONDITIONS (a)
Chemicals Exhibiting
Carcinogenic Effects
Organics:
Aldrin
alpha-BHC
beta-BHC
galTITla·BHC
alpha-Chlordane
ganma-Chlordane
4,4'-DDD
4,4'-DDE
4 4'-DOT
oieldrin Toxaphene
TOTAL
Chemicals Exhibiting
Noncarcinogenic Effects
Organics:
Aldrin
ganma•BHC
Benzoic acid
alpha-Chlordane garrma-Chlordane
4 4'·DDT
oieldrin
HAZARD INDEX
RME
Chronic Daily
Intake (CDI)
(mg/kg-day)
3.??E-10
1.09E·08
2.26E·08
1.01E·08
3.52E·09 4.11E·09
3.10E·07
1.68E-07
7.55E-07
2.10E-08
3.10E-06
RME
Chronic Daily
Intake (CD!)
(mg/kg-day)
1.06E·09
2.82E·08
8.45E-07
9.86E·09
1.15E-08
2.11E·06
5.87E-08
Slope
Factor
(mg/kg·day)-1
1. 7E+D1
6.3E+OO
1 .BE+OO
1.3E+OO (C)
1.3E+OO
1.3E+OO
2.4E·01
3.4E·01
3.4E:01
1 . 6E+01
1.1E+OO
Reference Dose · (mg/kg-day)
[Uncertainty
Factor] (d)
3.0E-05 [1,000]
3.0E-04 [1,000]
4.0E+OO [1 J
6.0E-05 [1,000]
6.0E-05 [1,000]
5.0E-04 [100]
5.0E-05 [100]
Weight of·
Evidence
Class (b)
B2
B2
C
B2/C
B2
B2
82
B2
B2
B2
B2
Target Organ/
Critical
Effect Ce)
Liver
Liver/Kidney
Malaise
Liver
Liver
Liver
Liver
RME
Upper Bound
Excess Lifetime
Cancer Risk
6E·D9
?E-08
4E·08
1E·08
5E·09
5E·09
?E-08
6E·08
3E-07
3E-07
3E·06 --------4E·06
RME.
CDl:RfD
Ratio
4E·05
9E·05
2E·07
2E·04
2E·04
4E·03
1E·03 --------
< 1 6E·03 l
(a) Risks are calculated for those chemicals of potential concern with toxicity criteria. The following
chemicals of potential concern are not presented due to lack of toxicity criteria: delta-BHC.
(b) USEPA ~eight of Evidence for Carcinogenic Effects:
[82) Probable hllTl8n carcinogen based on inadequate evidence from hunan studies and adequate evidence from animal studies. ·
[CJ Possible hunan carcinogen based on limited evidence from animal studies in the absence of h1.11'18n studies;
Cc) Under review by CRAVE Workgroup.
(d) Uncertainty factors represent the amount of uncertainty in extrapolation from the available data.
(e) A target organ/critical effect is the most sensitive organ/effect to a chemical's toxic effect. RfDs are based
on toxic effects in the target organ or on an effect elicited by the chemical. If an RfD was based on a study in
which a target organ was not identified, the organ listed is one known to be affected by the particular chemical of concern.
5.22
5.3.1.2 Risks Associat_ed with Dermal Contact with Surface Soil/Sediment by
a Future Merchant and a Child (1-6 years) and Adult Resident
Tables 5-16, 5-17 and 5-18 show that the potential upper bound lifetime excess
cancer risks to a child (1-6 years) resident, adult resident and merchant who
may absorb chemicals in surface soil/sediment through dermal contact are
4xl0"6 , lxlo-6 , and 6x10·7, respec_tively. Again, the risks for a child and
adult resident are due primarily to toxaphene. The risks to a child and adult
resident are at the lower bound of USEPA's target risk range of 10·6 to 10·4 .
The risk to a future merchant is less than USEPA's risk range. For
noncarcinogenic chemicals, the hazard indices are less than one for all three
receptors indicating that adverse noncarcinogenic effects are not likely to
occur through dermal contact with surface soil.
5.3.1.3 Risks Associated with Incidental Ingestion and Dermal Absorption
of Off-Site Surface Soil/Sediment by a Future Resident
(Qualitative)
Direct contact with off-site surface soil/sediment by a hypothetical future
resident could occur if the property south of the Geigy site were developed
for residential use. Hence, inadvertent ingestion of soils and absorption of
chemicals through the skin could occur. The RME concentration for toxaphene,
the risk-driving chemical, in off-site soil/sediment was higher than the RME
concentration on-site (190 mg/kg versus 37 mg/kg). However, it should be kept
in mind that the RME exposure point concentration of 190 mg/kg for toxaphene
is equal to the maximum measured value because of the small sample size used
to evaluate off-site surface soil/sediment. This maximum concentration
represents a single sampling point, and it is not likely that a future
resident will consistently contact this single concentratio'n over several
years. The average off-site surface soil/ sediment concentration of 51 mg/kg
is very close to the on-site 95th UCL surface soil concentration of 37 mg/kg.
Future residents in the area may thus experience an excess upperbound li'fetime
cancer risk which is comparable to that predicted for future on-site
residents, if exposure over this limited off-site area occurs over a prolonged
period of time.
5-23
Chemicals Exhibiting
Carcinogenic Effects
Organics:
Aldrin
alpha·BHC
beta-BHC
ganrna-BHC
alpha-Chlordane
ganrna-Chlordane
4,41 -DOD
4,4'-0DE
4,4'-DDT
Dieldrin
Toxaphene
TOTAL
Chemicals Exhibiting
Noncarcinogenic Effects
Organics:
Aldrin
garrma-BHC
Senzoic acid alpha-Chlordane
ganrna-Chlordane
4 4' -DDT oieldrin
HAZARD INDEX
TABLE 5-16
POTENTIAL RISKS ASSOCIATED WITH DERMAL CONTACT·OF ON-SITE SOIL/SEDIMENT BY A CHILD RESIDENT (1-6 YRS) UNDER FUTURE LANO-USE CONDITIONS (a)
USEPA RME
Chronic Daily
Intake (COi)
(mg/kg-day)
3.76E·10
1 .09E-08
2.26E-08
1.00E-08
3.51E-09.
4.09E-09
3.09E-07
1 .67E-07
7.52E-07
2.09E·08
3.09E-06
USEPA RME
Chronic Daily
Intake (CDI)
(mg/kg-day)
4.39E-09
1.17E-07
3.51E-06
4.09E-08
4. 78E-08
s.m-06
2.44E-07
Slope
Factor
(mg/kg·day)-1
1.7E+01
6.3E+OO
1.BE+OO 1.3E+OO (c)
1 .3E+OO
1 .3E+OO
2.4E·01
3.4E·01
3.4E·01
1.6E+01 1.1E+OO
Reference Dose
(mg/kg-day)
[Uncertainty
Factor] Cd)
3.0E-05 [1,000]
3.0E-04 [1,000] 4.0E+OO [1J
6.0E-05 [1,000] 6.0E-05 [1,000]
5.0E-04 [100]
5.0E-05 [100]
Weight of
Evidence
Class Cb)
B2
B2
C
B2/C
B2
B2
B2
B2
B2
B2
B2
Target Organ
or Critical
Effect (e)
Liver
Liver/Kidney
Malaise Liver
Liver
Liver
Liver
USEPA RME
Upper Bound
Excess Lifetime
Cancer Risk
6E·09
?E-08
4E·08
1E·08
5E·09
5E·09
7E·08
6E·08
3E·07
3E·07
3E·06
4E·06
USEPA RME
COi :RfO
Ratio
1E-04
4E-04
9E·07
7E·04
BE-04
2E·02
5E·03
< 1 ( 2E·02
Ca) Risks are calculated for those chemicals of potential concern with tox1c1ty criter1a. The following chemicals of potential concern are not presented due to lack of toxicity criteria: delta·BHC. Cb) USEPA Weight of Evidence for Carcinogenic Effects: (82] Probable hllJ'lan carcinogen based on inadequate evidence from hllnan studies and adequate evidence from animal studies.
[Cl Possible hiinan carcinogen based on limited evidence from animal studies in the absence of hunan studies; (c) Under review by CRAVE Workgroup.
(d) Uncertainty factors represent the amount of uncertainty in extrapolation from the available data. (e) A target organ is the organ most sensitive to a chemical's toxic effect. RfDs are based on toxic effects in the target organ. If an RfD was based on a study in which a target organ was not identified, the organ listed is one known to be affected by the particular chemical of concern.
5-24
J
Chemicals Exhibiting
Carcinogenic Effects
Organics:
Aldrin
alpha-BHC
beta-BHC
garrma-BHC
alpha-Chlordane
garrrna-Chlordane
4 4'-DDD
4:4, -DOE
4,4' -DDT
Dieldrin
Toxaphene
TOTAL
Chemicals Exhibiting
Noncarcinogenic Effects
Organics:
Aldrin
ganma-BHC
Benzoic acid
alpha-Chlordane
gamna-Chlordane
4 4' -DDT
oieldrin
HAZARD INDEX
TABLE 5·17
POTENTIAL RISKS ASSOCIATED WITH DERMAL CONTACT WITH
ON-SITE SOIL/SEDIMENT BY ADULT RESIDENTS
UNDER FUTURE LANO-USE CONDITIONS (a)
RME
Chronic Daily
Intake (CDI)
(mg/kg-day)
1.0SE-10
3.04E·09
6.31E·09
2.81E·09
9.82E·10
1 .15E·09
8.65E-08
4.68E·08
2.10E·07
5.BSE-09
8.65E-07
RME
Chronic Daily
Intake (CDI)
(mg/kg-day)
2.46E·10
6.SSE-09
1 .96E·07
2.29E·09
2.67E-09
4.91E·07
1.36E-08
Slope
Factor
(mg/kg-day)-1
1. 7E+01
6.3E+OO
1.BE+OO
1.3E+OO (C)
1.3E+OO
1.3E+OO
2.4E·01
3.4E·01
3.4E-01
1 .6E+01 1.1E+OO
Reference Dose
(mg/kg-day)
[Uncertainty
Factor] Cd)
3.0E-05 [1, ODO]
3.0E-04 [1,000]
4.0E+OO [1 J
6.0E-05 [1,000]
6.0E-05 [1,000]
5.0E-04 [100]
5.0E-05 [100]
Weight of
Evidence
Class (b)
B2
B2
C
B2/C
B2
B2 B2
B2
B2
B2
B2
Target Organ
or Critical
Effect Ce)
Liver
Liver/Kidney
Malaise
Liver Liver
Liver
Liver
RME
Upper Bound
Excess Lifetime
Cancer Risk
2E·09
2E·08 1E·08 4E·09
1E·09
1E·09
2E·08
2E-08
7E-08
9E·08 1E·06
1E·06
RME
COi :RID
Ratio
BE-06
2E·05
SE-08
4E-05
4E·05
1E-03
3E·04
< 1 C 1E-03
(a) Risks are calculated for those chemicals of potential concern with toxicity criteria. The following
chemicals of potential concern are not presented due to lack of toxicity criteria: calcilJTI,
magnesiun, and strontilJTI.
(b) USEPA Weight of Evidence for Carcinogenic Effects:
[B2J Probable human carcinogen based on inadequate evidence from human studies and adequate evidence from animal studies.
[C] Possible human carcinogen based on limited evidence from animal studies in the absence of
human studies;
(c) Under review by CRAVE Workgroup.
(d) Uncertainty factors represent the amount of uncertainty in extrapolation from the available data.
(e) A target organ is the organ most sensitive to a chemical's toxic effect. RfOs are based on toxic effects
in the target organ. If an RfD was based on a study in which a target organ was not identified, the organ
listed is one known to be affected by the particular chemical of concern.
5-25
TABLE 5·18
POTENTIAL RISKS ASSOCIATED ~ITH DERMAL CONTACT OF ON-SITE SOIL/SEDIMENT BY ADULT MERCHANTS UNDER FUTURE LAND·USE CONDITIONS (aj
Chemicals Exhibiting Carcinogenic Effects
Organics:
Aldrin
alpha·BHC
beta-BHC
galTITla-BHC
alpha-Chlordane
ganma-Chlordane
4 4'-0D0
<4'-0DE
4,4'-DDT
Dieldrin
Toxaphene
TOTAL
Chemicals Exhibiting
Noncarcinogenic Effects
Organics:
Aldrin
ganma-BHC
Benzoic acid
alpha-Chlordane
ganma-Chlordane
4 4'-DDT
oieldrin
HAZARD INDEX
RME
Chronic Daily
Intake (CDI)
(mg/kg·day)
6.19E·11
1. 79E·09
3.71E·09
1.6SE·09
S.78E·10
6. 74E· 10
S.78E·10
6.74E·10
S.09E·08
2. 7SE·08
1.24E·07
RME
Chronic Dai Ly
Intake (COi)
Cmg/kg·day)
1.73E·10
4.62E·09
1.39E·07
1.39E·07
1.62E·09
1.89E-09
3.47E-07
Slope
Factor
(mg/kg·day)-1
1. 7E+01
6.3E+OO
1.BE+OO
1.3E+OO ( C)
1 .3E+OO
1.3E+OO
2.4E·01
3.4E·01
3.4E·01
1.6E+01
1.1E+OO
Reference Dose
(mg/kg•day)
(Uncertainty
Factor] (d)
3.0E·OS [1,000]
3.0E·04 [1,000]
4.0E+OO [1]
6.0E·OS [1,000]
6.0E·OS [1,000]
5.0E-04 [100]
5 .OE·OS [100]
Weight of
Evidence
Class Cb)
B2
B2
C
B2/C
B2
B2
B2
B2
B2
B2
B2
Target Organ
or Critical
Effect Ce)
Liver
Liver/Kidney
Malaise
Liver
Liver
Liver
Liver
RME
Upper Bound
Excess Lifetime Cancer Risk
.1E-09
1E-08
7E-09
2E·09
BE-10
9E·10
1E·10
2E· 10
2E·08
4E·07
1E-07
6E-07
RME
CDI :RfD
Ratio
6E·06
2E-05
3E·08
2E·03
3E·05
4E·06
7E·03
< 1 ( 9E·03)
Ca) Risks are calculated for those chemicals of potential concern with toxicity criteria. The following chemicals of potential concern are not presented due to lack of toxicity criteria: calciun, magnesium, and strontium. (b) USEPA Weight of Evidence for Carcinogenic Effects: [B2] Probable h1.man carcinogen based on inedeq_Jate evidence from hllllBn studies end adequate evidence from animal studies.
[CJ Possible hLATian carcinogen based on limited evidence from animal studies in the absence of hLman studies; Cc) Under review by CRAVE Workgroup. Cd) Uncertainty factors represent the amount of uncertainty in extrapolation from the available data. Ce) A target organ is the organ most sensitive to a chemical's toxic effect. RfDs are based on toxic effects in the target organ. If an RfD was based on a study in which a target organ was not identified, the organ listed is one known to be affected by the particular chemical of concern.
5-26
Ji
5. 3. 2 Risks Due to the Gr_oundwater Exposures
The risks associated with the Surficial Aquifer and MW-11D in the Second
Uppermost Aquifer at the Geigy Chemical Corporation site were evaluated
quantitatively.
5.3.2.1 Risks Associated with Ingestion of Untreated Groundwater from the
Surficial Aquifer by a Future Merchant and a Child (1-6 years) and
Adult Resident
Carcinogenic and noncarcinogenic risks associated with the ingestion of
untreated groundwater from the surficial aquifer by a hypothetical future
child resident, adult resident and merchant are presented in Tables 5-19, 5-20
and 5-21, respectively. The estimated upper bound excess lifetime cancer
risks for ingestion of untreated water from this aquifer are 2xlo-3 and 4xlo-3
for future child (1-6 years) and adult residents, respectively. The risk to a
future merchant is lxlo-3 . The risks to both child and adult residents and
the merchant exceeds USEPA's target risk range of 10-6 to 10-4 range for human
health protectiveness. These risks are primarily due to alpha-BHC, beta-BHC,
gamma-BHC, and dieldrin.
The hazard indices for ingestion of untreated water from the surficial aquifer
are greater than one for a future child (1-6 years) resident, adult resident
and merchant. When the hazard index is greater than one, the chemicals of
concern were subdivided by target organ in accordance with USEPA (1989)
guidance. The resulting hazard index for the liver was greater than one for
all three receptors due primarily to gamma-BHC. The hazard index for the
kidney also exceeded one for the child and adult resident, again due
predominantly to gamma-BHC. Thus, adverse effects on the liver may result
from prolonged consumption of the surficial aquifer by all three receptors.
Additionally, child and adult residents are likely to experience adverse,
kidney effects.
5-27
TABLE 5-19
POTENT I AL RISKS ASSOCIATED UI TH INGESTION OF GROUNDUATER
FROM THE SURFICIAL AQUIFER BY A CHILD (1-6 YRS) RESIDENT
UNDER FUTURE LAND-USE CONDITIONS (a)
Chemicals Exhibiting Carcinogenic Effects
Organics:
Aldrin
alpha·BHC
beta-BHC
9a1TTI1a-BHC
Bis(2·ethylhexyl)phthalate
Dieldrin
4 4'-DDE
T~xaphene
TOTAL
Chemicals Exhibiting
Noncarcinogenic Effects
Organics:
Aldrin
garmia·BHC
Bis(2-ethylhexyl)phthalate
Dieldrin
1,2,4-Trichlorobenzene
Inorganics:
BarilDTI
Manganese
Mercury
Vanadillll
Zinc
HAZARD INDEX
RME
Chronic Dai ty
Intake (COi)
(mg/kg-day)
1.10E·D6
1.97E·04
1.37E·04 1.64E·04
3.51E-05
6.SBE-06
5.48E-07
3.23E·05
RME
Chronic Daily
Intake (COi)
(mg/kg-day)
1.28E-05
1.92E·03
4.09E-04
7.67E-05
3.20E-04
1.79E-02
6.39E·03
6.39E-05
2.43E003
3.71E·02
Slope
Factor
(mg/kg·day)-1
1. 7E+01
6.3E+OO
1.BE+OO 1.3E+OO (c)
1.4E-02
1.6E+01
3.4E·D1
1.1E+OO
Reference Dose
(mg/kg-day)
[Uncertainty
Factor] Cd)
3.0E-05 [1,000]
3.0E-04 [1,000] 2.0E-02 [1,000]
5.0E-05 [100]
1.3E·03 [1,000]
5.0E-02 [100]
1.0E-01 [1]
3.0E-04 [1000]
7.0E-03 [100]
2.0E-01 [1 OJ
Weight of
Evidence
Class (b)
B2
B2
C
B2/C
B2
B2
B2
B2
Target Organ
or Critical
Effect (e)
Liver
Liver/Kidney
Liver
Liver
Liver
Cardiovascular
CNS
Kidney
Liver/Kidney
Anemia
RME
Upper Bound
Excess Lifetime
Cancer Risk
2E·05
1E-03
2E·04 2E-04
SE-07
1E-04
2E-07 4E-05
2E·03
RME
CDI:RfO
Ratio
4E·D1
6E+OO
2E·D2
2E+OO
2E-01
4E-01
6E·02
2E-01
3E-01
2E-01 --------
> 1 (f)
Ca) Risks are calculated for those chemicals of potential concern with toxicity criteria.
The following chemicals of potential concern are not presented due to lack of toxicity
criteria: alllTlinllTI, delta·BHC, calcillTI, endrin ketone, heptachlor epoxide, iron, magnesillTI, and potassil.lTI.
(b) USEPA Weight of Evidence for Carcinogenic Effects:
[B21 Probable hllT\an carcinogen based on inadequate evidence from hllT\an studies and adequate evidence from animal studies.
[CJ Possible hllnan carcinogen based on limited evidence from animal studies in the absence of hr.,nan studies.
Cc) Under review by CRAVE Workgroup.
(d) Uncertainty factors represent the amount of uncertainty in extrapolation from the
available data.
(e) A target organ is the organ most sensitive to a chemical's toxic effect. RfDs are based
on toxic effects in the target organ. If an RfD was based on a study in which a
target organ was not identified, the organ listed is one known to be affected by the particular chemical of concern.
Cf) Hazard Index greater than 1.0 for liver effects (8.9) and kidney effects (6.5).
5-28
TABLE 5-20
POTENTIAL RISKS ASSOCIATED ~ITH INGESTION OF GROUND~ATER FROl4 THE SURFICIAL AQUIFER BY AN ADULT RESIDENT
UNDER FUTURE LAND-USE CONDITIONS (a)
RME RME
Chemicals Exhibiting
Carcinogenic Effects
Chroni C Daily
Intake (CDI)
(mg/kg-day)
Slope
factor
(mg/kg-dayJ-1
IJeight of
Evidence
Class (b)
Upper Bound
Excess Lifetime
Cancer Risk
Organics:
Aldrin
alpha·8HC
beta-BHC
garrma-BHC
Bis(2-ethylhexyl)phthalate
Dieldrin
4,41 -DOE
Toxaphene
TOTAL
2.35E·D6
4.23E·04
2.94E·04
3.52E-04
7.SlE-05
1.41E·05
1.17E·06
6.93E·05
RME
Chronic Dai Ly
1. 7E+01
6.3E+OO
1.8E+00
1.3E+OO (cl
1.4E·02
1.6E+01
3.4E·01
1.1E+OO
Reference Dose
(mg/kg-day)
82 4E·05
82 3E·03
C SE-04
B2/C SE-04
82 lE-06
82 2E·04
82 4E-07
82 8E-05
4E·03
Target Organ RME
Chemicals Exhibiting
Noncarcinogenic Effects
Intake (CDI) [Uncertainty or Critical CDI :RfD
Organics:
Aldrin
ganrna-BHC
8is(2-ethylhexyl)phthalate
Dieldrin
1,2,4-Trichlorobenzene
lnorganics:
Barium Manganese
Mercury
VanadillJI
Zinc
HAZARD INDEX
(mg/kg-day)
5 .48E-06
8.22E-04
1.75E·04
3.29E-05
1.37E-04
7.67E-03
2.74E-03
2.74E-05
1.04E·03
1.59E·02
Factor] (dl Effect (e)
3.0E-05 [1,000] Liver
3.0E-04 [1,000] liver/Kidney
2.0E-02 [1,000] Liver
5.0E-05 C100] Liver
1.3E·03 Cl ,0001 Liver
7.0E-02 [3] Cardiovascular
1.0E-01 m CNS
3.0E-04 C,000] Kidney
7.0E-03 C100] Liver/Kidney
2.0E-01 [10] Anemia
(a) Risks are calculated for those chemicals of potential concern with toxicity criteria.
The following chemicals of potential concern are not presented due to lack of toxicity
criteria: aluminun, delta·BHC, calciun, endrin ketone, heptachlor epoxide, iron,
magnesiun, and potassillTI.
(b) USEPA Weight of Evidence for Carcinogenic Effects:
[82] Probable hunan carcinogen based on inadequate evidence from hunan studies and·
adequate evidence from animal studies. [Cl Possible hunan carcinogen based on limited evidence from animal studies in the
absence of hunan studies.
(c) Under review by CRAVE Workgroup.
(d) Uncertainty factors represent the amount of uncertainty in.extrapolation from the
available data.
Ratio
2E·01 3E+OO
9E-03
7E-01
1E·01
1E ·01
3E·02
9E·02
lE-01
8E·02
> 1
(e) A target organ is the organ most sensitive to a chemical's toxic effect. RfDs are based
on toxic effects in the target organ. If an RfD was based on a study in which a
target organ was not identified, the organ listed is one known to be affected by the
particular chemical of concern.
Cf) Hazard Index greater than 1.0 for liver effects (4.1) and kidney effects (3.2).
5-29
(f)
TABLE 5-21
POTENTIAL RISKS ASSOCIATED WITH INGESTION OF GROUNDWATER
FROM THE SURFICIAL AOUIFER BY AN ADULT MERCHANT UNDER FUTURE LAND-USE CONDITIONS Ca)
RME
Chemicals Exhibiting
Carcinogenic Effects
RME
Chronic Daily
Intake (COi)
(mg/kg-day)
Slope
Factor
(mg/kg·day)-1
Weight of
Evidence
Class Cb)
Upper Bound
Excess Lifetime
Cancer Risk
Organics:
Aldrin
alpha·BHC
beta-BHC
garrma-BHC
Bis(2-ethylhexyl)phthalate
Dieldrin ·
4 41 -DOE
T~xaphene
TOTAL
Chemicals Exhibiting
Noncarcinogenic Effects
Organics:
Aldrin
ganma-BHC
Bis(2·ethylhexyl)phthalate
Dieldrin
1,2,4-Trichlorobenzene
I norgan i cs:
BarillTl Manganese
Mercury
Vanadii..m
Zinc
HAZARD INDEX
6. 74E·07
1.21E-04
8.42E·05
1.01E-04
2.16E·05 4.04E·06 ·3.37E-07
1.99E·05
RME
Chronic Daily
Intake (CDI)
(mg/kg-day)
1.89E-06
2.83E·04
6.04E·05
1.13E·05
4.72E-05
2.64E-03
9.43E-04
9.43E·06
3.58E·04
5.47E-03
1. 7E+01 B2 1E·05
6.3E+OO B2 BE-04 1.BE+OO C 2E·04 1.3E+OO (C) B2/C 1E-04
1.4E-02 B2 3E-07 1.6E+01 B2 6E-05
3.4E-01 B2 1E-07 1.1E+OO B2 2E·05
1E·03
Reference Dose (mg/kg-day) Target Organ RME
[Uncertainty or Critical CDl:RfD Factor] (d) Effect Ce) Ratio
3.0E·OS [1,000] Liver 6E·02 3.0E-04 [1,000] Liver/Kidney 9E·01 2.0E-02 [1,000] Liver 3E·03 5.0E-05 [100] Liver 2E·01 1.3E-03 [1,000] Liver 4E·02
7.0E-02 [3] Cardiovascular 4E-02 1.0E-01 [1 l CNS 9E·03
3.0E-04 [1000] Kidney 3E-02 7.0E-03 [100] Liver/Kidney SE-02 2.0E-01 [1 OJ Anemia 3E·D2
> 1
(a) Risks are calculated for those chemicals of potential concern with toxicity criteria.
The following chemicals of potential concern are not presented due to leek of toxicity
criteria: aluninllll, delta-BHC, calciun, endrin ketone, heptachlor epoxide, iron,
magnesiun, and potassiun.
(b) USEPA Weight of Evidence for Carcinogenic Effects:
[B21 Probable hll'l'lan carcinogen based on inadequate evidence from hUT1an studies and
adequate evidence from animal studies.
[Cl Possible hunan carcinogen based on limited evidence from animal studies in the absence of hunan studies.
(c) Under review by CRAVE Workgroup.
(d) Uncertainty factors represent the amount of uncertainty in extrapolation from the
available data.
(e) A target organ is the organ most sensitive to a chemical's toxic effect. RfDs are based
on toxic effects in the target organ. If an RfD was based on a study in which a
target organ was not identified, the organ listed is one known to be affected by the
particular chemical of concern.
(f) Hazard Index greater than 1.0 for liver effects (1.2).
5-30
(f)
5.3.2.2 Risks Associated with Ingestion of Untreated Groundwater from the
Second Uppermost Aquifer by a Future Child (1-6 years) and Adult
Resident
Carcinogenic and noncarcinogenic risks associated with the ingestion of
untreated groundwater from the second uppermost aquifer by a hypothetical
future child and adult resident are presented in Tables 5-22 and
5-23, respectively. The estimated upper bound excess lifetime cancer risks
for ingestion of untreated water from this aquifer are lx10·5 and 2xl0"5 for
future child (1-6 years) and adult residents, respectively. The risks to both
child and adult residents are within USEPA's target risk range of 10·6 to 10·4
range for human health protectiveness. These risks are due solely to the
presence of TCE.
The hazard indices for ingestion of untreated water from the second uppermost
aquifer are greater than one for a future child (1-6 years) and less than one
for a future adult resident. When the hazard index is greater than one, the
chemicals of concern were subdivided by target organ in accordance with USEPA
(1989) guidance. The resulting hazard index for the liver was greater than
one for child residents due to TCE. Thus, adverse effects on the liver may
result from prolonged consumption of groundwater from the second uppermost
aquifer by child residents.
5.3.2.3 Risks Associated with Ingestion of Untreated
Groundwater from MW-11D by a Future Child (1-6 years)
and Adult Resident
The excess lifetime cancer risks for a future child (1-6 years) and adult
resident are 7xio·4 and 2xio·3, respectively as presented in Tables 5-24 and
5-25. The values for the child and adult resident are within and exceed
USEPA's risk range for human health protectiveness, respectively. The primary
chemicals contributing to these risks are alpha-BHC, beta-BHC, and gammaaBHC.
For noncarcinogenic chemicals, the hazard index exceeds one for both the child
and adult resident. The hazard index for the liver exceeds one for both the
5-31
TABLE 5-22
POTENTIAL RISKS ASSOCIATED WITH INGESTION OF GROUNDWATER FROM THE SECOND U_PPERMOST
AQUIFER BENEATH THE SITE PROPERTY BY A CHILD RESIDENT
UNDER FUTURE LAND-USE CONDITIONS (a)
RME
Carcinogenic Effects
RME
Chronic Dai Ly
Intake (CDI)
(mg/kg-day)
Slope
Factor
(mg/kg-day)-1
Weight of
Evidence
Class Cb)
Upper Bound
Excess lifetime
Cancer Risk
Organics:
Tri ch loroethene
TOTAL
Noncarcinogenic Effects
Organics:
Trichloroethene
HAZARD INDEX
9.86E-04
RME
Chronic Daily
Intake (COi)
(mg/kg-day)
1.15E-02
1.1E-02 B2
Reference Dose
(mg/kg-day) Target Organ
[Uncertainty or Critical
Factor} (C) Effect (d)
7.3E-03 [1,000] Liver
(a)
(b)
Risks
USEPA
[B2J
are calculated for carcinogenic and noncarcinogenic effects of trichloroethene. Weight of Evidence for Carcinogenic Effects:
Probable hunan carcinogen based on inadequate evidence from hi.man studies and
adequate evidence from animal studies.
Uncertainty factors represent the amount of uncertainty in extrapolation from the
available data.
1E-05 --------
1E-05
RME
COi :RIO
Ratio
1.6E+OO
> 1
(c)
(d) A target organ is the organ most sensitive to a chemical's toxic effect. RfDs are based
on toxic effects in the target organ. If an RfD was based on a study in which a
target organ was not identified, the organ listed is one known to be affected by the particular chemical of concern.
(e) Hazard index is greater than 1.0 for liver effects (1.6).
5-32
(e)
TABLE 5-23
POTENTIAL RISKS ASSOCIATED WITH INGESTION OF GROUNDWATER FROM THE SECOND UPPERMOST
AQUIFER BENEATH THE SITE PROPERTY BY AN ADULT RESIDENT .
UNDER FUTURE LANO-USE CONDITIONS (a)
RME
Carcinogenic Effects
RME
Chronic Daily
Intake (COi)
(mg/kg-day)
Slope Factor
(mg/kg•day)-1
\Jeight of
Evidence
Class Cb)
Upper Bound
Excess Lifetime
Cancer Risk
Organics:
Trichloroethene
TOTAL
Noncarcinogenic Effects
Organics:
Trichloroethene
HAZARD INDEX
2.11E·03
RME
Chronic Daily
Intake (CD!)
(mg/kg-day)
4.93E·03
1.1E·02 B2
Reference Dose (mg/kg-day) Target Organ
[Uncertainty or Critical
Factor] (C) Effect (d)
7.3E·03 [1,000] Liver
(a)
(b)
Risks
USEPA
[B2J
are calculated for carcinogenic and noncarcinogenic effects of trichloroethene.
Weight of Evidence for Carcinogenic Effects:
Probable hiinan carcinogen based on inadequate evidence from hunan studies and
adequate evidence from animal studies.
(c) Uncertainty factors represent the amount of uncertainty in extrapolation from the
available data.
2E·OS --------
2E·05
RME
COl:RfD
Ratio
6. 7E-01
< 1
(d) A target organ is the organ most sensitive to a chemical's toxic ·effect. RfDs are based
on toxic effects in the target organ. If an RfD was based on a study in which a
target organ was not identified, the organ listed is one known to be affected by the
particular chemical of concern.
5-33
adult (1.2) and child (2.4) residents, respectively. The hazard index for the
kidney also exceeds one for the child resident (2.4), but is equal to one
(1.003) for the adult resident. This indicates that a future child and adult
resident may experience noncarcinogenic effects •in the liver if groundwater
from this aquifer is ingested on a daily basis over 6 and 30 years,
respectively. Additionally, adverse kidney effects may occur in children.
5.3.2.4 Risks Associated with Inhalation of Volatiles While
Showering with Surficial Groundwater by a Future Child
(1-6 years) and Adult Resident
Carcinogenic and noncarcinogenic risks associated with the inhalation of
volatiles while showering with groundwater from the surficial aquifer by
hypothetical future child (1-6 years) and adult residents are presented in
Tables 5-26, and 5-27, respectively. The estimated upper bound excess
lifetime cancer risks for inhalation of volatiles from this aquifer are 3x10·8
and 4x10-B for future child (1-6 years) and adult residents, respectively.
These risks to both residents are less than USEPA's target risk range of 10-6
to 10-4 for human·health protectiveness. For noncarcinogenic chemicals, the
hazard indices are less than one, for both child (1-6 years) and adult
residents, indicating that adverse noncarcinogenic effects are not likely to
occur through inhalation of volatiles while showering.
5.3.2.5 Risks Associated with Inhalation of Volatiles While
Showering with Second Uppermost Aquifer Groundwater by
a Future Child (1-6 years) and Adult Resident
Carcinogenic and nonc~~~inogenic risks associated with the inhalation of
• ¥ ••
volatiles while showering with groundwater from the second uppermost aquifer
by hypothetical future child (1-6 years) and adult residents are presented in
Tables 5-28, and 5-29, respectively. The estimated upper bound excess
lifetime cancer risks for inhalation.of volatiles from this aquifer are
3xlo-6 and 4xl0"6 for future child (1-6 years) and adult residents,
respectively. These risks to both residents are within USEPA's target risk
range of 10-6 to 10-4 for human health protectiveness.
5-34
Chemicals Exhibiting
Carcinogenic Effects
Organics:
alpha-BHC
beta-BHC
ganma-BHC
Dieldrin
TOTAL
TABLE 5-24
POTENTIAL RISKS ASSOCIATED WITH INGESTION OF OFF-SITE GROUNDWATER FROM THE SECOND UPPERMOST AQUIFER (MW·11D) BY A CHILD (1·6 YRS)
RESIDENT UNDER FUTURE LAND-USE CONDITIONS (a)
RME
Chronic Daily
Intake (COi)
(mg/kg-day)
B.TTE-05
3.62E·05
6.03E·05
1.53E·06
RME
Chronic Daily
Slope
Factor
(mg/kg-day)-1
6.3E+OO
1.BE+OO 1.3E+OO (C)
1 .6E+01
Reference Dose
Weight of
Evidence
Class (b)
B2
C B2/C
B2
Target Organ
Chemicals Exhibiting Noncarcinogenic Effects
Intake (COi)
(mg/kg-day)
(mg/kg-day) or Critical
[Uncertainty Factor] Cd) Effect Ce)
Organics:
ganma-BHC
Dieldrin 4·methyl-2-pentanone
HAZARD INDEX
7.03E·04
1.79E·05
1.28E·04
3.0E-04 [1,000]
5.0E-05 [100]
5.0E-02 [1,000]
Liver/Kidney
Liver.
Liver/Kidney
RME
Upper Bound
Excess Lifetime
Cancer Risk
6E·04
7E-05 BE-05
2E·05
7E-04
RME
CDI :RfD
Ratio
2E+OO
4E·01
3E-03
> 1 Cf)
(a) Risks are calculated for those chemicals of potential concern with toxicity criteria. The following
chemicals of potential concern ere not presented due to lack of toxicity criteria: delta·BHC
and Endrin ketone
(b) USEPA Weight of Evidence for Carcinogenic Effects:
(821 Probable hllllan carcinogen based on inade(luate evidence from hllllan studies and adequate evidence from
animal studies.
[Cl Possible hllllan carcinogen ba'sed on limited evidence from animal studies in the absence of
hllnan studies; (c) Under review by CRAVE Workgroup. .
Cd) Uncertainty factors represent the amount of uncertainty in extrapolation from the available data.
(e) A target organ is the organ most sensitive to a chemical's toxic effect. RfDs are based on toxic effects
in the target organ. If an RfD was based on a study in which a target organ was not identified, the organ
listed is one known to be affected by the particular chemical of concern:
(f) Hazard Index greater than 1.0 for liver effects (2.4) and kidney effects (2.0).
5-35
TABLE 5·25
POTENTIAL RISKS ASSOCIATED WITH INGESTION OF OFF·SITE GROUNDWATER FROM THE SECOND UPPERMOST AQUIFER (MW·11D) BY AN ADULT RESIDENT
UNDER FUTURE LAND·USE CONDITIONS (a)
RME
Chemicals Exhibiting Carcinogenic Effects
RME
Chronic Daily
Intake (CDI) (mg/kg•day)
Slope
Factor
(mg/kg·day)-1
Weight of
Evidence
Class Cb)
Upper Bound
Excess Lifetime
Cancer Risk
Organics:
alpha·BHC
beta-BHC
garrma·BHC
Dieldrin
TOTAL
Chemicals Exhibiting
Noncarcinogenic Effects
Organics:
garrma•BHC
Dieldrin
4-methyl-2-pentanone
HAZARD INDEX
1.BBE-04
7.75E·05
1.29E·04
3.29E·06
RME
Chronic Dai ty
Intake (CDI)
(mg/kg•day)
3.01E·04
7.67E·06
5.48E·05
6.3E+OO
1.BE+OO 1.3E+OO (C)
1.6E+01
Reference Dose
(mg/kg·day)
[Uncertainty
Factor] Cd)
3.0E·D4 [1,000]
5.0E·D5 [100]
5.0E·D2 [1,000]
B2
C
B2/C B2
Target Organ
or Critical
Effect (e)
Liver/Kidney
liver
Liver/Kidney
1E·03
1E·04
2E·04
5E·D5
2E·03
RME COi :RfD
Ratio
1E+OO
2E·D1 1E·03
> 1
(a) Risks are calculated for those chemicals of potential concern with toxicity criteria. The following
chemicals of potential concern are not presented due to lack of toxicity criteria: delta-BHC and Endrin ketone.
(b) USEPA Weight of Evidence for Carcinogenic Effects:
(f)
[B21 Probable hllllan carcinogen based on inadequate evidence from hllllan studies and adequate evidence from animal studies.
[Cl Possible hllllan carcinogen based on limited evidence from animal studies in the absence of hLman studies;
Cc) Under review by CRAVE Workgroup.
Cd) Uncertainty factors represent the amount of uncertainty in extrapolation from the available data.
Ce) A target organ is the organ most sensitive to a chemical's toxic effect. RfDs are based on toxic effects
in the target organ. If an RfD was based on a study in which a target organ was not identified, the organ listed is one known to be affected by the particular chemical of concern.
Cf) Hazard Index greater than 1.0 for liver effects (1.2) and equal to 1.0 for kidney effects.
5-36
TABLE 5-26
POTENTIAL RISKS ASSOCIATED WITH INHALATION OF VOLATILES WHILE SHOWERING WITH GROUNDWATER
FROM THE SURFICIAL AQUIFER BY A CHILD (1·6 YRS) RES.IOENT
Chemicals Exhibiting
Carcinogenic Effects
Organics:
Aldrin
alpha·BHC
beta-BHC
Dieldrin
Toxaphene
TOTAL
Chemicals Exhibiting
Noncarcinogenic Effects
Organics:
1,2,4-Trichlorobenzene
HAZARD INDEX
UNDER FUTURE LANO·USE CONDITIONS (a)
RME
Chronic Daily
Intake (COi)
(mg/kg-day)
4.0BE-10
3.13E-09
1. 70E·10
1.67E-10
3.00E-09
RME
Chronic Daily
Intake (COi)
(mg/kg-day)
1.99E-07
, Slope
Factor
(mg/kg·day)-1
1 • 7E+01
6.3E+OO
1 .BE+OO
1 .6E+01
1.1E+OO
Reference Dose
(mg/kg-day)
[Uncertainty
Factor] (c)
Weight of
Evidence
Class Cb)
B2
B2
C
B2
B2
Target Organ
or Critical
Effect (d)
3.0E-03 [1,000] Liver
RME
Upper Bound
Excess Lifetime
Cancer Risk
7E·09
2E·OB
3E· 10
3E·09
3E-09
3E·OB
RME
COi :RfO
Ratio
7E·05
<1(7E-05
(a) Risks are calculated for those chemicals of potential concern with toxicity criteria.
The following chemicals of potential concern ere not presented due to lack of toxicity
criteria: delta-BHC, endrin ketone, and heptachlor epoxide.
(b) USEPA Weight of Evidence for Carcinogenic Effects:
[B2] Probable hlil18n carcinogen based on inadequate evidence from hiinan studies and
adequate evidence from animal studies.
[C] Possible hllllan carcinogen based on limited evidence from animal studies in the
absence of human studies.
(c) Uncertainty factors represent the amount of uncertainty in extrapolation from the
available data.
(d) A target organ is the organ most sensitive to a chemical's tox"ic effect. RfDs are based
on toxic effects in the target organ. If an RfD was based on a study in which a
target organ was not identified, the organ listed is one known to be affected by the ·
particular chemical of concern. ·
5-37
TABLE 5-27
POTENTIAL RISKS ASSOCIATED WITH INHALATION OF VOLATILES WHILE SHOWERING
WITH GROUNDWATER FROM THE SURFICIAL AQUIFER BY ADULT RESIDENTS
UNDER FUTURE LANO-USE CONDITIONS (a)
Chemicals Exhibiting
Carcinogenic Effects
Organics:
Aldrin
alpha-BHC
beta-BHC
Dieldrin
Toxaphene
TOTAL
Chemicals Exhibiting
Noncarcinogenic Effects
Organics:
1,2,4-Trichlorobenzene
HAZARD INDEX
RME
Chronic Daily
lntake (CDI)
(mg/kg-day)
4.37E-10
3.35E-09
1.82E-10
1. 79E-10
3.22E-09
RME
Chronic Dai Ly
Intake (COi)
(mg/kg-day)
4.27E-08
Slope
Factor
(mg/kg-day)-1
1. 7E+D1
6.3E+OO
1.8E+OO
1 .6E+01
1.1E+OO
Reference Dose
(mg/kg-day)
[Uncertainty
Factor] (c)
\Jeight of
Evidence
Class Cb}
82
82
C
82
82
Target Organ
or Critical
Effect (d)
3.0E-03 [1,000] Liver
RME
Upper Bound
Excess L Hetime
Cancer'Risk
?E-09
2E-OB
3E-10
3E-09
4E-09
4E-08
RME
CDl:RfO
Ratio
lE-05
< 1 ( lE-05
(a) Risks are calculated for those chemicals of potential concern with toxicity criteria.
The following chemicals of potential concern are not presented due to lack of toxicity
criteria: delta-BHC, endrin ketone, and heptachlor epoxide. (b) USEPA Weight of Evidence for Carcinogenic Effects:
(82] Probable hLrnan carcinogen based on inadequate evidence from hLrnan studies and adequate evidence from animal studies.
[Cl Possible human carcinogen based on limited evidence from animal studies in the absence of hLrnan studies.
(c) Uncertainty factors represent the amount of uncertainty in extrapolation from the available data.
Cd) A target organ is the organ most sensitive to a chemical's toxic effect. RfOS are based
on toxic effects in the target organ. If an RfO was based. on a study in which a
target organ was not identified, the organ listed is one known to be affected by the particular chemical of concern.
5-38
_c
TABLE 5-28
POTENTIAL RISKS ASSOCIATED WITH INHALATION OF VOLATILES WHILE SHOWERING
WITH GROUNDWATER FROM THE SECOND UPPERMOST BENEATH
THE SITE PROPERTY BY CHILO RESIDENTS
UNDER FUTURE LANO-USE CONDITIONS (a)
RME
Chemicals Exhibiting
Carcinogenic Effects
RME
Chronic Daily
Intake (COi) (mg/kg-day)
Slope
Factor (mg/kg-day)-1
Weight of
Evidence
Class Cb)
Upper Bound
Excess Lifetime
Cancer Risk
Organics:
Trichloroethene
TOTAL
1.96E·D4 1. 7E-02 Cc) B2 3E-06
3E-06
(a)
(bl
(c)
Risks are calculated for the carcinogenic effects of trichloroethene. Trichloroethene
lacks noncarcinogenic inhalation toxicity criteria.
USEPA Weight of Evidence for Carcinogenic Effects:
[B2] Probable hunan carcinogen based on inadequate evidence from hunan studies and
adequate evidence from animal studies.
The slope factor for this chemical is based on a metabolized dose (USEPA 1991).
5-39
TABLE 5-29
POTENTIAL RISKS ASSOCIATED WITH INHALATION OF VOLATILES WHILE SHOWERING
WITH GROUNDWATER FROM THE SECOND UPPERMOST BENEATH
Chemicals Exhibiting
Carcinogenic Effects
Organics:
Trichloroethene
TOTAL
THE SITE PROPERTY BY ADULT RESIDENTS
UNDER FUTURE LAND-USE CONDITIONS (a)
RME
Chronic Daily
Intake (CDI) (mg/kg-day)
2.10E-04
Slope
Factor
(mg/kg-day)-1
1. 7E-02 (c)
Weight of
Evidence
Class Cb)
82
RME Upper Bound
Excess Lifetime
Cancer Risk
4E-06
4E-06
(a) Risks are calculated for the carcinogenic effects of trichloroethene. Trichloroethene
lacks noncarCinogenic inhalation toxicity criteria.
(b) USEPA Weight of Evidence for Carcinogenic Effects:
[B2) Probable hllnan carcinogen based on inadequate evidence from hunan studies and
adequate evidence from animal studies.
(c) The slope factor for this chemical is based on a metabolized dose (USEPA 1991).
5-40
5.3.2.6 Risks Associated with Dermal Exposures While Showering
with Surficial Groundwater by a Future Child (1-6
years) and Adult Resident
Tables 5-30 and 5-31 show that the potential upper bound lifetime excess
cancer risks to a child (1-6 years) and adult resident who may absorb
chemicals in the surficial groundwater while showering are 2x10·6 and 6x10·6 ,
respectively. The risks for a child and adult resident are due primarily to
alpha-BHC and are at the lower bound of USEPA's target risk range of 10-6 to
10-4 . For noncarcinogenic chemicals, the hazard indices are less than one,
for both child and adult residents indicating that adverse noncarcinogenic
.effects are not likely to occur through dermal absorption of chemicals in
groundwater.
5.3,3 Risks Due to the Inhalation of Airborne Volatiles
All of the exposure pathways which evaluated the inhalation of chemicals
volatilized from on-site soil/sediment by future child (1-6 years) and adult
residents and merchants had upper bound lifetime excess cancer risks levels
equal to or lower than USEPA's 10·6 to 10·4 risk range for human health
protectiveness. No hazard indices were calculated due to an absence of USEPA
inhalation RfCs. This includes the following pathways:
• Inhalation of volatilized surface soil/sediment chemicals by a
hypothetical future child (1-6 years) resident (Table 5-32);
• Inhalation of volatilized surface soil/sediment chemicals by a
hypothetical future adult resident (Table 5-33); and
• Inhalation of volatilized surface soil/sediment chemicals by a
hypothetical future merchant (Table 5-34).
5-41
TABLE 5-30
POTENTIAL RISKS ASSOCIATED WITH DERMAL CONTACT WHILE SHOWERING WITH
GROUNDWATER FROM THE SURFICIAL AQUIFER BY A CHILO (1-6 YRS)
RESIDENT UNDER FUTURE LANO-USE CONDITIONS (a)
Chemicals Exhibiting
Carcinogenic Effects
Organics:
Aldrin
alpha-BHC
beta-BHC
ganma-BHC
Bis(2-ethylhexyl)phthalate
Dieldrin
4,4-00E
Toxaphene
TOTAL
Chemicals Exhibiting Noncarcinogenic Effects
Organics:
Aldrin
gamma-BHC
Bis(2-ethylhexyl)phthalate
Oieldrin
1,2,4-Trichlorobenzene
lnorganics:
Bariun Manganese
Mercury
Vanadi1ir1
Zinc
HAZARD INDEX
RME
Chronic Daily
Intake (CDI)
(mg/kg-day)
1.23E-09
2.21E-07
1.53E-07
1.84E-07
3.92E-08
7.35E-09
6. 13E-10
3.62E-08
RHE
Chronic Daily
Intake (CDI)
(mg/kg-day)
1.43E·08
2.14E·06 4.SBE-07
8.58E·08
4.22E-07
2.00E-05
7.15E·06
7.15E-08
2.ne-06
3.nE-05
Slope
Factor (mg/kg-dayJ-1
1. 7E+01
6.3E+OO
1.BE+OO
1.3E+OO
1.4E-02
1.6E+01
3.4E+01
1.1E+OO
Reference Dose
(mg/kg-day)
[Uncertainty
Factor] (d)
(cl
3.0E-05 [1,000]
3.0E-04 [1,000]
2.0E-02 [1,000]
5.0E-05 [100]
1.3E-03 [1,000]
7.0E-02 [3]
1.0E-01 [1 J
3.0E-04 [1,000]
7.0E-03 [100]
2.0E-01 [10]
Weight of
Evidence
Class (bl
82
82 C
82/C
82 82
82
82
Target Organ (e)
Liver
Liver/Kidney
Liver
Liver
Liver
Cardiovascular
CNS
Kidney
Liver/kidney
Anemia
RME
Upper Bound
Excess Lifetime
Cancer Risk
2E-08
1E-06
3E-07
ZE-07
6E· 10
1E-07
ZE-08
4E-08
2E-06
RME
CDI :RfD
Ratio
5E-04
7E·03
ZE-05
ZE-03
3E-04
3E·04
?E-05
2E-04
4E-04
ZE-04
< 1 ( 1E-02
(a) Risks are calculated for those chemicals of potential concern with toxicity criteria. The following
chemicals of potential concern are not presented due to lack of toxicity criteria: alllTiinllll, calcillll, iron, magnesiiin, potassillll, delta·BHC and endrin ketone. (b) USEPA Weight of Evidence for Carcinogenic Effects:
[B2) Probable hllJ'lan carcinogen based on inadequate evidence from hl.11\an studies and adequate evidence from animal studies.
[C] Possible hunan carcinogen based on limited evidence from animal studies in the absence of
hl.lT'lan studies; ·
Cc) Under review by CRAVE Workgroup.
(d) Uncertainty factors represent the amount of uncertainty in extrapolation from the available data.
Ce) A target organ is the organ most sensitive to a chemical's toxic effect. RfDs are based on toxic effects
in the target organ. If an RfD was based on a study in which a target organ was not identified, the organ
listed is one known to be affected by the particular chemical of concern.
5-42
TABLE 5-31
POTENTIAL RISKS ASSOCIATED WITH DERMAL CONTACT WHILE SHOWERING WITH
GROUNDWATER FROM THE SURFICIAL ACUIFER BY AN ADULT
RESIDENT UNDER FUTURE LAND-USE CONDITIONS (a)
Chemicals Exhibiting
Carcinogenic Effects
Organics:
Aldrin
alpha·BHC
beta-BHC
ganrna-BHC
Bis(2-ethylhexyl)phthalete
Oieldrin
4,4-DDE
Toxaphene
TOTAL
Chemicals Exhibiting
Noncarcinogenic Effects
Organics:
Aldrin
ganrna-BHC
Bis(2-ethylhexyl)phthalate
Dieldrin
1,2,4-Trichlorobenzene
lnorganics:
Barillll Manganese
Mercury
VanadiLm
Zinc
HAZARD INDEX
RME
Chronic Dai Ly
Intake (COi) (mg/kg-day)
3.41E-09
6.14E-07
4.26E-07
5.11E·07
1.09E·07
2.05E-08
1. 70E-09
1.01E-07
RME
Chronic Daily
Intake (COi)
(mg/kg-day)
7.96E-09
1.19E·06
2.55E·07
4.ffi-08
2.35E-07
1 .11E-05
3.98E-06
3.98E·08
1.51E-06
2c07E-05
Slope
Factor
(mg/kg-day)-1
1 . 7E+01
6.3E+OO
1.8E+OO
1.3E+OO (C)
1.4E-02
1.6E+01
3.4E+01
1.1E+OO
Reference Dose
(mg/kg-day)
[Uncertainty
Factor] Cd)
3.0E-05 [1,000]
3.0E-04 [1,000]
2.0E-02 [1,000]
5.0E-05 [100]
1.3E-03 [1,000]
7.0E-02 [3]
1.0E-01 [1]
3.0E-04 [1,000]
7.0E-03 [100]
2.0E-01 [10]
•
Weight of
Evidence
Class (b)
B2
B2 C
B2/C
B2 B2
B2
B2
Target Organ Ce)
liver
Liver/Kidney
Liver
Liver
Liver
Cardiovascular
CNS
Kidney
Liver/kidney
Anemia
RME
Upper Bound
Excess Lifetime
Cancer Risk
< 1
6E·08
4E·06
BE-07
7E-07
2E·09 3E-07
6E·08
1E·07
6E-06
RME
COi :RfD
Ratio
3E·04
4E-03
1E·05
1E·03
2E·04
2E-04
4E·05
1E-04
2E·04
1E-04
C 5E·03)
Ca) Risks are calculated for those chemicals of potent;al concern with toxicity criteria. The following
chemicals of potential concern are not presented due to lack of toxicity criter;a: alllTlinllll, calcil.111,
iron, magnesiU'll, potassiU'll, delta-BHC and endrin ketone.
Cb) USEPA Weight of Evidence for Carcinogenic Effects:
[B21 Probable h1.1nan carcinogen based on inadequate evidence from h1.1nan studies and adequate evidence from animal studies.
[C] Poss;ble human carcinogen based on limited evidence from animal studies in the absence of
h1.1nan studies;
(c) Under review by CRAVE Workgroup.
Cd) Uncertainty factors represent the amount of uncertainty in extrapolation from the available data.
Ce) A target organ is the organ most sensitive to a chemical's toxic effect. RfDs are based on toxic effects
in the target organ. If an RfD was based on a study in which a target organ was not identified, the organ
listed is one known to be affected by the particular chemical of concern.
5-43
TABLE 5-32
POTENTIAL RISKS ASSOCIATED WITH INHALATION OF VOLATILIZED CHEMICALS BY AN ON-SITE CHILD (1-6 YRS) RESIDENT UNDER
FUTURE LAND-USE CONDITIONS (a)
RME RME Chronic Daily Slope Weight of Upper Bound Chemicals Exhibiting Intake (CD!) Factor Evidence Excess Lifetime Carcinogenic Effects (mg/kg-day) (mg/kg-day)-1 Class Cb) Cancer Risk
Organics: --------
Aldrin 4.30E-10 1. 7E+01 B2 ?E-09 alpha-8HC 4.16E-09 6.3E+OO B2 3E-08 beta-BHC 2.31E-09 1.8E+OO C 4E-09 alpha-Chlordane 3.90E-09 1.3E+OO B2 SE-09 ganma-Chlordane 3.99E-09 1.3E+OO 82 SE-09 4,4' -DDT 3.54E-08 3.4E-01 82 1E-08 Dieldrin 1.23E-08 1.6E+01 82 2E-07 Toxaphene 1.06E-06 1.1E+OO 82 1E-06
TOTAL 1E-06
(a) Risks are calculated for those chemicals of potential concern with toxicity criteria. The
following chemicals of potential concern are not presented due to lack of inhalation toxicity
criteria: delta-BHC, garrrna-BHC, 4,4'·00D and 4,4'-DDE.
(b) USEPA Weight of Evidence for Carcinogenic Effects:
[82) Probable hiinan carcinogen based on inadequate evidence from hi.nnan studies and adequate evidence from animal studies.
[CJ Possible hunan carcinogen based on limited evidence from animal studies in the absence of hunan studies,
5-44
Chemicals Exhibiting
Carcinogenic Effects
Organics:
Aldrin
alpha-BHC
beta-BHC
alpha-Chlordane
ganma-Chlordane
4,4' -DDT
Dieldrin
Toxaphene
TOTAL
TABLE 5-33
POTENTIAL RISKS ASSOCIATED WITH INHALATION OF. VOLATILIZED
CHEMICALS BY ON-SITE ADULT RESIDENTS UNDER
FUTURE LAND-USE CONDITIONS (a)
RME
Chronic Daily
Intake (CD! J
(mg/kg-day)
2.75E-1O
2.65E-O9
1.47E-O9
2.49E-O9
2.SSE-O9 2.27E-OB
7.BBE-O9
6. 77E-O7
Slope
Factor
(mg/kg-dayJ-1
1. 7E+O1
6.3E+OO
1 .8E+00
1.3E+OO
1.3E+OO
3.4E-O1
1.6E+O1
1.1E+OO
Weight of
Evidence Class (b)
B2
B2
C
82
B2
B2
82
82
RME
Upper Bound
Excess lifetime
Cancer Risk
SE-O9
2E-OB
3E-O9
3E-O9
3E-O9
BE-O9
1E-O7
7E-O7
9E-O7
(a) Risks are calculated for those chemicals of potential concern with toxicity criteria. The following
chemicals of potential concern are not presented due to lack of inhalation toxicity criteria: delta-BHC
gamna-BHC, 4,4'·00D and 4,4'-DDE.
Cb) USEPA Weight of Evidence for Carcinogenic Effects:
[B2] Probable h1.1nan carcinogen based on inadequate evidence from human..studies and adequate evidence from animal studies.
[CJ Possible hl.lTlan carcinogen based on limited evidence from animal studies in the absence of
hl.lTlan studies.
5-45
Chemicals Exhibiting
Carcinogenic Effects
Organics:
Aldrin
alpha-BHC
beta-BHC
alpha-Chlordane
garrma-Chlordane
4,4'-DDT
Dieldrin
Toxaphene
TOTAL
TABLE 5-34
POTENTIAL RISKS ASSOCIATED WITH INHALATION OF VOLATILIZED CHEMICALS
BY ON-SITE ADULT MERCHANTS UNDER FUTURE LAND-USE CONDITIONS (a)
RME
Chronic Daily
Intake (COi)
(mg/kg-day)
1.72E-1O
1.67E-O9
9.3OE-1O
1.56E-O9
1 .6OE-O9
1.42E-O8
4.94E·O9
4.24E-O7
Slope
Factor
(mg/kg-day)-1
1. 7E+O1
6.3E+OO
1.BE+OO
1 .3E+OO
1.3E+OO
3.4E-O1
1 .6E+O1
1.1E+OO
Weight of
Evidence
Class Cb)
B2
B2
C
B2
B2
B2
B2
82
RME
Upper Bound
Excess Lifetime
Cancer Risk
3E-O9
1E-O8
2E-O9
2E-O9
2E-O9
5E-O9
BE-O8 5E-O7
6E-O7
Ca) Risks are calculated for those chemicals of potential concern with toxicity criteria. The following
chemicals of potential concern are not presented due to lack of inhalation toxicity criteria:
Benzoic acid, copper, delta-BHC, garrma·BHC, 4,4'-DDD, and 4,4'-DDE.
(b) USEPA Weight of Evidence for Carcinogenic Effects:
[B2] Probable hllnan carcinogen based on inadequate evidence from human studies and adequate evidence from animal studies.
[C] Possible hlJllan carcinQgen based on limited evidence from animal studies in the absence of human studies;
5-46
5.4 SUMMARY OF CUMULATIVE RISKS UNDER FUTURE LAND-USE CONDITIONS
5.4.1 Cumulative Residential Risks
The cumulative risks to child (1-6 years) and adult residents are presented in
Table 5-35. This table shows that the total cancer risks to future child and
adult residents living on the Geigy Chemical Corporation site are 2xlo-3 and
4xlo-3 , respectively. These risks are attributed primarily to the ingestion
of groundwater from the surficial aquifer. If risks from the ingestion of
groundwater were reduced to acceptable levels through remediation, the
remaining risks across pathways for a young child and adult resident are
4xlo-5 and 2xlo-5, respectively. These risks are within USEPA's risk range of
10-4 to 10-6 used for the selection of remedial alternatives. With respect to
noncarcinogenic effects, the cumulative hazard index for the liver and kidney
exceeds one indicating that adverse effects may occur. Again these risks are
associated with ingestion of pesticides in the surficial aquifer. If
pesticides concentrations in groundwater were reduced to levels of non-
concern, the remaining inorganics would not pose an unacceptable risk.
5.4.2 Cumulative Risks to Merchants
A hypothetical future merchant may be exposed at one time by a combination of
pathways, and therefore, the combined pathway risks were estimated in order to
be health protective. The total cancer risks for the hypothetical future on-
site merchant associated with incidental ingestion and dermal absorption of
surface soil, in conjunction with inhalation of volatilized chemicals and
consumption of groundwater from the surficial aquifer are summarized on Table
5-35.
The total risk for an on-site future merchant is lxlo-3 • This risk exceeds
USEPA's target risk range of 10-6 to 10-4 range for.;human health protectiveness
at Superfund sites. If risks from the ingestion of groundwater were reduced ~
to acceptable levels through remediation, the remaining risks across pathways
5-47
TABLE 5-35
TOTAL RISKS ASSOCIATED WITH FUTURE LAND-USE CONDITIONS
Cancer Risk
Due to All Chemicals
Child Adult Area/Pathway Resident Resident
Surface Soil/Sediment:
Ingestion of Surface Soil/ 3E-05 1E·D5 Sediment
Dermal Absorption from
Surface Soil/Sediment 4E-06 1E·06
Inhalation of Chemicals Released 1E-06 9E-07 from Surface Soil/Sediment
Groundwater:
Ingestion of surficial 2E·03 4E-03 groundwater
Inhalation of Volatiles 3E-08 4E-08 while Showering
Dermal Absorption
while Showering
of Chemicals 2E-06 6E·06
-------. Total Cancer Risk 2E·03 4E-03
Noncancer Risk
Due to All Chemicals
Child Area/Pathway Resident
Surface Soil/Sediment:
Ingestion of Surface Soil/ 2E-01
Sediment
Dermal Absorption from 2E-02
Surface Soil/Sediment
Inhalation of Chemicals Released ---(a)
from Surface Soil/Sediment
Groundwater:
Adult
Resident
2E-02'
1E-03
---(a)
Merchant
4E-06
6E·07
6E·07
1E-03
1E-03
Merchant
6E·03
9E·03
···Ca)
Ingestion of Surficial
groundwater
>1
liver = 8.9
kidney = 6.5
>1
liver=4.1
kidney= 3.2
>1
liver 1.2
(kidney = 1.0)
Inhalation of Volatiles
while Showering
Dennal Absorption of Chemicals
while Showering
?E-05
1E-02
1E-05
5E-03
(a) No inhalation toxicity criteria were available to assess noncarcinogenic risks.
= This pathway was not evaluated.
5-48
for a merchant· is 5xl0-6 • This risk is within US EPA' s risk range of 10-4 to
10-6 used for the selection of remedial alternatives. Risks to a future
merchant were highest for the ingestion of groundwater pathway.
Individual exposure pathways were combined to estimate the total potential for
adverse noncarcinogenic effects to occur. As described previously,
noncarcinogenic effects are not expressed as a probability but rather are
assumed to occur through a threshold mechanism. Adverse noncarcinogenic
effects could potentially occur if the total hazard index estimated across
pathways for an individual target organ is greater than one. The total non-
cancer risks for a hypothetical future on-site worker, associated with
incid1~ntal ingestion of soil, dermal contact with soil, ingestion of
groundwater and inhalation of volatilized chemicals are summarized on Table
5-35. The only target organ which had a hazard index that exceeded one was
the liver. Again this risk was due primarily to the ingestion of groundwater
from the surficial aquifer.
5.5 SUMMARY OF POTENTIAL HEALTH RISKS
Table 5-36 summarizes the potential health risks under current and future land
use conditions associated with the RME exposure case for each of the receptors
evaluated.
5-49
TABLE 5-36
SUMMARY OF POTENTIAL HEALTH RISKS ASSOCIATED WITH THE
GEIGY CHEMICAL CORPORATION SITE
Exposure Pathway
CURRENT LAND USE:
Soil Ingestion:
On-Site Child/teenage trespasser (8-13 years)
Off-Site Child/teenager (8-13 years)
Dermal Absorption from Soil Matrix:
On-Site Child/teenage trespasser (8-13 years)
Off-Site Child/teenager (8-13 years)
Inhalation of Volatilized Chemicals
On-Site Child/teenager trespasser (8-13 years)
Merchant North of Site
Child (1-6 years) Resident North.east of Site
Adult Resident Northeast of Site
Inhalation of Dust Particulates
Merchant North of Site
Child (1-6 years) Resident Northeast of Site
Adult Resident Northeast of Site
Upper·Bound.
Excess Lifetime
Cancer Risk•
7E-07
7E-06
4E-07
2E-06
2E-08
6E-07
lE-07
9E-08
6E-10
8E-ll
lE-10
Hazard Index for
Noncarcinogenic
Effectsb
< 1
< 1
< 1
< 1
This exposure pathway could not be evaluated due to the absence of EPA toxicity
criteria.
• The upperbound individual excess lifetime cancer risk represents the additional
probability that an individual may develop cancer over a 70-year lifetime as a result
of exposure conditions evaluated.
b The hazard index indicates whether or not exposure to mixtures of noncarcinogenic
chemicals may result in adverse health effects. A hazard index less than one
indicates that adverse human health effects are unlikely to occur.
5-50
I
I
I
TABLE 5-36 (Continued)
SUMMARY OF POTENTIAL HEALTH RISKS.ASSOCIATED WITH THE
GEIGY CHEMICAL CORPORATION SITE
Exposure Pathway
FUTURE LAND USE:
Soil Ingestion:
Merchant
Child (-16 years) Resident
Adult Resident
Dermal Absorption from Soil Matrix:
Merchant
Child (1-6 years) Resident
Adult Resident
Ingestion of Surficial Aquifer Groundwater:
Merchant
Child (1-6 years) Resident
Adult Resident
Ingestion of Second Uppermost Aquifer
Groundwater:
Child (1-6 years) Resident
Adult Resident
Ingestion of Off-Site MW-llD Groundwater:
Child (1-6 years) Resident
Adult Resident
Inhalation of Volatiles While Showering with
Surficial Groundwater:
Child (1-6 years) Resident
Adult Resident
Upper Bound
Excess Lifetime
Cancer Risk•
4E-06
3E-05
lE-05
6E-07
4E-06
lE-06
lE-03
2E-03
4E-03
lE-05
2E-05
7E-04
2E-03
3E-08
4E-08
Hazard Index for
Noncarcinogenic
Effectsb
> 1
> 1
> 1
> 1
> 1
> 1
< 1
< 1
< 1
< 1
< 1
< 1
(liver:
(liver:
kidney:
(liver:
kidney:
(liver:
< 1
(liver:
kidney:
(liver:
kidney:
< 1
< 1
1. 2)
8.9,
6.5)
4.1,
3.2)
1. 6)
2.4,
2.0)
1.2'
1.0)
This exposure pathway could not be evaluated due to the absence of EPA _toxicity
criteria.
• The upperbound indivi_dual excess lifetime cancer risk represents the additional
probability that an individual may develop cancer over a 70-year lifetime as a result
of exposure conditions evaluated.
b The hazard index indicates whether or not exposure to mixtures of noncarci~ogenic
chemicals may result in adverse health effects.· A hazard index less than one
indicates that adverse human health effects are unlikely to occur.
5-51
TABLE 5-36 (Continued)
SUMMARY OF POTENTIAL HEALTH RISKS.ASSOCIATED WITH THE
GEIGY CHEMICAL CORPORATION SITE
Exposure Pathway
FUTURE LAND USE (cont.):
Inhalation of Volatiles While Showering with
Second Uppermost Aquifer Groundwater:
Child (1-6 years) Resident
Adult Resident
Dermal Absorption While Bathing with Surficial
Groundwater:
Child (1-6 years) Resident
Adult Resident
Inhalation of Volatilized Chemicals:
Merchant
Child (1-6 years) Resident
Adult Resident
Upper Bound
Excess Lifetime
Cancer Risk8
3E-O6
4E-O6
2E-O6
6E-O6
6E-O7
lE-O6
9E-O7
Hazard Index for
Noncarcinogenic
Effectsb
< 1
< 1
----This exposure pathway could not be evaluated due to the absence of EPA toxicity
criteria.
• The upperbound individual excess lifetime cancer risk represents the additional
probability that an individual may develop cancer over a 7O-year lifetime as a result
of exposure conditions evaluated.
b The hazard index indicates whether or not exposure to mixtures of noncarcinogenic
chemicals may result in adverse health effects. A hazard index less than one
indicates that adverse human health effects are unlikely to occur.
5-52
6.0 ENVIRONMENTAL ASSESSMENT
This section contains an assessment of potential impacts to nonhuman receptors
associated with the chemicals of potential concern at the Geigy Chemical
Corporation Site. The approaches used in this environmental assessment
parallel those used in the human health risk assessment, in that potentially
exposed populations (receptors) are identified and then information on
exposure and toxicity is combined to predict impacts.
6.1 SITE DESCRIPTION AND POTENTIAL RECEPTOR SPECIES
The Geigy Chemical Corporation Site is located west of the town of Aberdeen in
Moore County, North Carolina. It is bounded to the north by State Highway 211
and to the south by the Aberdeen and Rockfish Railroad. The highway and,
tracks converge at the western end of the site, The site totals one acre in
size.
The vegetative community at the site is dominated by native grasses, which
were planted following a previous removal action, Other herbaceous species
which occur infrequently and along the perimeter of the site include poison
ivy (Rhus radicans), cinquefoil (Potentilla simplex), honeysuckle (Lonicera
sp,), passionflower (Passiflora incarnata), great ragweed (Ambrosia trifida),
and goldenrod (Solidago spp,), A stand of bamboo occurs in the northeast
corner of the site and a small number of pine trees occur in the eastern and
western portions of the site. Vegetative communities in the surrounding areas
are more diverse and include cropland, pastures, meadows, old fields, and
large tracts of forests.
The site is not expected to support extensive wildlife populations, given its
small size (i.e,, 1 acre), the limited diversity of the vegetative community
(which limits food and cover resources), and the availability of higher
quality habitat in adjacent areas. Resident vertebrate species of the site
(if they occur) are likely limited to small mammals such as voles (Microtus
spp.) and other field mice (e.g., Perornyscus leucopus), and the abundance of
6-1
these species is unlikely .to be great, given the lack of extensive cover at
the site. Some snakes and lizards also could occur at the site. Other
wildlife species could occasionally use the site while foraging.
There are no permanent surface water bodies at.the site. The drainage ditch
at the site does not contain enough water to sustain aquatic life. Water
reaching the ditch during and immediately following rain events quickly
infiltrates the ground. The nearest surface water body to the site is
Aberdeen Creek, which is located roughly 4,000 feet from the site.
No rare, threatened, or endangered species are expected to occur at the site.
However, based on information supplied by the NC Natural Heritage Program (in
the N.C. Department of Environment, Health, and Natural Resources), two
endangered species and one priority natural area occur within an approximate
1-mile radius of the site. Two colonies of the red-cockaded woodpe.cker
(Picoides borealis), a State and federally endangered bird species, occur in
the area. Sandhills pixie moss (Pyxidanthera brevifolia) is a State
endangered plant that occurs in the area. Paint Hill Natural Area is ranked
by the Natural Heritage Program as having national level significance. The
U.S. Fish and Wildlife Service also provided information regarding federal
species of concern known to occur in Moore County. Table 6-1 contains a
listing of State listed species, federal listed species, and federal candidate
species1 . The two State listed species are those mentioned above. In
addition to the red-cockaded woodpecker, there are four other federal listed
species known to occur in Moore County: the Cape Fear shiner (Notropis
mekistocholas), rough-leaved loosestrife (Lysimachia asperulaefolia),
Michaux's sumac (Rhus michauxii), and American chaffseed (Schwalbea
americana).
1Candidate species are not legally protected but are under status review
by the USFWS.
6-2
6.2 POTENTIAL EXPOSURES AND IMPACTS
Chlorinated insecticides are the principal chemicals of concern in the soils
and sediments of the site. Potential exposures and impacts are discussed
below by receptor type.
6.2.1 Plants
Terrestrial plants may be exposed to chemicals of potential concern in soil as
a result of direct contact with subsequent plant uptake via the roots. No
oata are available on the toxicity of the chlorinated insecticides of concern
on natural vegetation. The few data that are available from laboratory
studies with agricultural species (Eno and Everett 1958) suggest that
phytotoxic effects are likely to occur only at very high soil concentrations.
The low phytotoxicity of the chlorinated insecticides makes intuitive sense
from a mechanistic standpoint, given that the pesticides present at the site
were formulated to be toxic to insects and not plants. Although the
sensitivity of natural vegetation compared to agricultural species is not
known currently, it is unlikely that the insecticides of concern would be
extremely toxic ·to native vegetation given the mechanism of toxic action.
Therefore, impacts on the plant community at the site are not expected. The
successful revegetation of the site following soil remediation suggest that
the current level of insecticides in soils are below phytotoxic levels, at
least for some species.
6.2.2 Terrestrial Wildlife
Terrestrial wildlife may be exposed to chemicals of potential concern in
surface soil/sediment by several pathways: (1) ingestion of soil/sediment
while foraging or grooming; (2) dermal absorption; and (3) ingestion of.food
that has accumulated chemicals from soil/sediment. Potential exposures and
impacts associated with each of these pathways is discussed below.
6-3
TABLE 6-1
RARE, THREATENED, AND ENDANGERED SPECIES·POTENTIALLY
COMMON NAME
State Listed Species (a)
Birds:
Red-cockaded woodpecker
Plants:
Sandhills pixie moss
Federal Listed Species Cb)
Birds:
Red-cockaded woodpecker
Fishes:
Cape Fear shiner
Plants:
Rough-leaved loosestrife
Michaux's sunac
American chaffseed
OCCURRING NEAR THE GEIGY SITE .
SCIENTIFIC NAME
Picoides borealis
Pyxidanthera brevifolia
Picoides borealis
Notropis mekistocholas
Lysimachia asperulaefolia Rhus michauxi i
Schwalbea americana
Federal Candidate Species Cc)
Birds:
Bachman's sparrow
Fishes:
Pinewoods darter
Sandhills chub
Plants:
White-wicky
Nestronia Sun-facing coneflower
Spring-flowering
goldenrod
Georgia leadplant
Pine barrens boneset
Bog spicebush
Savanna cowbane
Conferva pondweed Pickering's morning
glory
Reptiles:
Northern pine snake
Insects:
Sandhills clubtail
dragonfly
Aimophila aestivalis
Etheostoma mariae
Semotilus lunbee
Kalmia cuneata
Nestronia lili>ellula Rudbeckia heliopsidis
Sol i dago verna
Amorpha georgiana georgiana
Eupatoriun resinosun
Lindera subcoriacea
Oxypolis ternata
Potamogeton confervoides
Styliema pickeringii var. pickeringii
Pituophis melanoleucus melanoleucus
Gorrphus parvidens carolinus
(a) Information provided by the N.C. Natural Heritage Program,
Septent>er 4, 1991. Encompasses area surrounding site but
but does not include all of Moore County.
STATUS
Endangered
Endangered
Endangered
Endangered
Endangered
Endangered
Proposed Endangered
(b) Endangered or threatened species known to occur in Moore County, NC.
Information provided by U.S. Fish and Wildlife Service (USFWS),
Raleigh Field Office, November 1, 1991.
(c) Candidate species are not legally protected but are under status
review by the USFWS.
6-4
Ingestion and Dermal Absorption of Chemicals in Soil and Sediment. Of
the potential receptors at the site, soi~ invertebrates such as earthworms
have the greatest potential for exposure as a result cf ingestion of soil or
sediment or dermal absorption of chemicals from soil and sediment. These
species are continuously in direct contact with soil and also·ingest soil
directly or indirectly during foraging, and therefore could be exposed
continuously to chemicals in soil.
Few data are available on the toxicity of the chlorinated insecticides of
concern at the site to soil invertebrate species. The data that are available
for selected insecticides suggest that some toxic effects can occur at
concentrations in the range of 3,000 to 17,000 ug/kg. Table 6-2 summarizes
the available toxicity data for soil invertebrates. The degree to which these
data represent possible toxic levels to soil invertebrate species at the site
is unknown and cannot be predicted given the available toxicity and exposure
data base. However, based on the toxic effect levels presented in Table 6-2
and the concentration data presented in Table 2-1 for surface soils and 2-2
and 2-4 for shallow subsurface soils (where soil invertebrates could live), it
is possible that soil invertebrates could experience toxic effects from
exposure to toxaphene and DDT in soils/sediments. If impacts are occurring
they are likely limited to 11hot spot" areas, as average concentrations of
toxaphene and DDT are below the reported toxic levels.
There is a tremendous amount of uncertainty associated with any predictions of
impacts in soil invertebrates at the site based on the limited toxicity data
base since the actual toxicity in invertebrates living at the site is not
known. Further, it is not known if the insecticides present in the site
soils/sediments are bioavailable. Van Gestel and Ma (1988) showed that the
toxicity of certain organic chemicals in earthworms was highly dependent on
bioavailability of the chemical from the soil.
The abundance of earthworms is also greatly influenced by soil characteristics
such as moisture, texture, and organic content. Earthworms often aggregate in
soil areas having a high organic content (Edwards and Lofty 1972). Even if
6-5
TABLE 6-2
SOIL INVERTEBRATE TOXICITY VALUES FOR CHEMICALS
OF POTENTIAL CONCERN IN SURFACE SOIL/SEDIMENT
Soil
Concentration
Chemical (ug/kg) Effect
Aldrin 15,DOO 20% mortality in earthworms
after 6 weeks exposure
BHC NA
Chlordane NA
DDT 6,OOD No-observed-Effect-Concentration
(NOEC) mortality in earthworms
Dieldrin 10,000 Decreased cocoon production
in earthworms
Endrin NA
Heptachlor 3,350 Reduced nlili>ers of springtails
(suborder: Arthropleona)
Toxaphene 16,800 24X mortality in English redworm
adults; no young observed
NA= Not available.
6-6
Reference
Cathey 19B2
Cathey 19B2
Reinecke and Venter 1985
Fox 1967
Hopkins and Kirk 1957
toxic effects in soil inv~rtebrates are possible in localized areas, it is
considered unlikely that impacts will be .extensive at the site because the
site is unlikely to support an abundant and diverse soil invertebrate
community given that the natural soil is very sandy and has an organic content
of less than 0.5%.
Ingestion of Food That Has Accumulated Chemicals. Terrestrial wildlife
exposures via the ingestion of food that has accumulated pesticides from the
site are not likely to be significant. None of the chemicals of potential
concern accumulate extensively in vegetation and therefore, significant
exposure in the herbivorous species that may inhabit the site is unlikely.
Some accumulation in soil invertebrates is possible and therefore animals that
feed on these organisms could be exposed to chemicals in the food.
The degree to which chemicals in soils at the site could be bioaccumulated is
unknown. However, because the site most likely does not support an abundant
invertebrate community (given its natural soil characteristics), it is
unlikely to be used extensively as a foraging area by invertebrate-eating
species. It is probable that the invertebrate-eating species would optimize
their foraging efforts to concentrate in areas yielding the highest return per
unit effort and therefore, would be more likely to feed in the surrounding
areas rather than at the site. Further, even if the site were used for
occasionally for foraging, it is unlikely to provide a significant portion of
the total food intake of an individual given its small size (1 acre) compared
to the total foraging area of an individual.
6.2.3 Endangered Species
Red-cockaded woodpeckers (a State and federal listed species) which live in
colonies located within one mile of the site are unlikely to be affected. by
chemicals in soil at the site. These woodpeckers feed on insects in trees,
and generally do not feed below the understory layer (USDA 1974). Therefore,
no pathway exists by which they could be exposed to chemicals in the
soil/sediments of the site.
6-7
It is not known if the State listed sandhills pixie moss or the federal listed
rough-leaved loosestrife, Michaux's sumac, or American chaffseed occur at the
site. However, given the historical disturbed nature·of the site, it is
considered unlikely. The Cape Fear shiner is unlikely to be impacted by the
site given that there is no surface water at or near the site:
No potential impacts are likely on the Paint Hill Natural Area, which is
located over a mile north of the site. No pathways exist by which chemicals
at the site would reach this natural area.
6.3 SUMMARY AND CONCLUSIONS
Adverse ecological impacts associated with the site are not expected. No
aquatic life impacts are expected, as the two drainage ditches that occur at
the site do not contain enough water to sustain aquatic life. No impacts on
the vegetative community are expected given the probable low phytotoxicity of
the insecticides of concern in soil. Adverse terrestrial wildlife impacts
also are not expected. The site is not expected to support extensive wildlife
populations, given its small size, the limited diversity of the vegetative
community (which limits food and cover resources), and the availability of
higher quality habitat in adjacent areas. Some impacts are possible for soil
invertebrates living in limited areas at the site, although these impacts
could not be evaluated with any degree of certainty given the available
toxicological and exposure database. Even if toxic effects in soil
invertebrates are possible in localized areas, it is considered unlikely that
impacts would be extensive because the site is unlikely to .support an abundant
and diverse soil invertebrate community given the sandy and low-organic
content soil present naturally at the site.
6-8
. .
7.0 UNCERTAINTIES
As in any risk assessment, the estimates of risk for the Geigy Chemical
Corporation Site have many associated uncertainties. The evaluation of
uncertainties is required by USEPA's Risk Assessment Guidance for Superfund
(USEPA 1989). This guidance states, "it is important to fully specify the
assumptions and uncertainties inherent in the risk assessment to place the
risk estimates in proper perspective11 • In general, the primary sources of
uncertainty are the following:
• Environmental sampling and analysis, and selection of chemicals
• Exposure assessment
• Toxicological data
Some of the more important sources of uncertainty in this assessment are
discussed below. As a result of the uncertainties described below, this risk
assessment should not be construed as presenting an absolute estimate· of risk
to persons or ecological receptors potentially exposed to chemicals from the
site. Rather, it is a conservative analysis intended to indicate the
potential for adverse impacts to occur.
7.1 ENVIRONMENTAL SAMPLING AND ANALYSIS
Table 7-1 highlights some uncertainties associated with environmental sampling
and analysis. In general, environmental sampling and analysis at the Geigy
site was adequate to support data quality objectives for risk assessment and
should not add appreciably to the uncertainty in this assessment.
Environmental chemistry analysis error can stem from several sources including
errors inherent in the sampling or analytical methods. Analytical precision
or accuracy errors can be the source of a great deal of uncertainty. For
example, sample dilution, matrix interferences, a~d samples which were
extracted days beyond the holding time specified by the Contract Laboratory ~
7-1
TABLE 7-1
UNCERTAINTIES IN THE BASELINE.RISK ASSESSMENT
FOR THE GEIGY CHEMICAL CORPORATION SITE
ENVIRONMENTAL SAMPLING AND ANALYSIS
AND SELECTION OF CHEMICALS
Assumption
Systematic or random errors in the
chemical analysis may yield
erroneous data
'A limited number of samples were
available for background and some
potentially site-affected
environmental media
The maximum detected site
concentration was compared to two
times the maximum site-specific
background level or to the maximum
regional levels for inorganics
Magnitude of
Effect
on Risk•
Low
Low
Low
8Key: Low -~ 1 order of magnitude effect.
Direction of Effect
on Risk
May over-or under-
estimate risk
May over-or under-
estimate ris_k
May overestimate
risk
Moderate > 1 to~ 2 orders of magnitude effect.
High -> 2 orders of magnitude effect.
7-2
Program were qualified wit_h the letter "J", indicating the concentrations are
estimated. There is additional uncertainty associated with chemicals reported
in samples at concentrations below the reported detection limit, but still
included in data analysis. These chemicals were also qualified with a 11J 11 •
For some environmental media, a small number of samples were collected. For
example, there were only nine off-site surface soil/sediment samples. The
procedure for calculating an exposure point concentrati9n tends to result in
use of the maximum detected concentration in cases of relatively few samples,
and so small sample sizes or sample sizes with large variability can result in
an overestimate of risk using the RME case. In this risk assessment, the
variability of the off-site surface soil/sediment data and the small sample
population resulted in an RME concentration equal to the maximum measured
concentration for all of the chemicals of potential concern when using USEPA's
RME guidelines.
7.2 EXPOSURE ASSESSMENT
There are several sources of uncertainty in the exposure assessment which
should be recognized. These include calculation of exposure point
concentrations, the choice of exposure models used, and the selection of input
parameters used to estimate chemical intakes (either chronic daily intakes or
inhalation exposure concentrations). Exposure point concentrations were
calculated directly from site sampling data or, in the case of ambient air
exposures, predicted using volatilization and air dispersion models. In each
case, there is some degree of uncertainty in the estimates. Examples of these
uncertainties are presented _in Tables 7-2 and 7-3.
Uncertainty in the air modeling can arise from the use of inappropriate models
or the use of simplifying assumptions in the models. While the volatilization
and dispersion models used in this assessment were considered to be
appropriate for the inhalation exposure pathways under evaluation, there are
nevertheless uncertainties associated with them. For example, the EPA
7-3
TABLE 7-2
UNCERTAINTIES IN THE BASELINE. RISK ASSESSMENT
FOR THE GEIGY CHEMICAL CORPORATION SITE
ESTIMATION OF EXPOSURE POINT CONCENTRATIONS
Magnitude of Effect Direction of Effect Assumption on Risk• on Risk
Chemical concentrations reported Low May over-or under-
as non-detected were included as
one-half the detection limit in
calculating concentrations
Concentration of chemicals in
media remain constant over time
Concentrations in air were
calculated using environmental
fate and transport models
The upper 95% confidence limit
on the population mean or
maximum (whichever was lower)
was used for the RME case
Low -High
Low -Moderate
Low -High
°Key: Low -S 1 order of magnitude effect.
estimate risk
May overestimate risk
May over-or under-
. estimate risk
May overestimate risk
Moderate > 1 to S 2 orders of magnitude effect.
High -> 2 orders of magnitude effect.
7-4
TABLE 7-3
UNCERTAINTIES IN THE BASELINE RISK ASSESSMENT
FOR THE GEIGY CHEMICAL CORPORATION SITE
ESTIMATION OF CHEMICAL INTAKES
Assumption
Exposures were .assumed to occur
on a regular basis for each
selected pathway
Frequency of exposure was based
on consideration of site-specific
conditions
Default EPA assumptions regarding
body weight, duration of
exposure, and life expectancy may
not be representative for the
site area population
Exposures were estimated assuming
no migration of residents out of
the site area for 30 years
Default reasonable maximum
exposure (RME) values were used
for soil ingestion rates
The dermal absorption of
chemicals from soils through skin
was based on USEPA Region IV,
without documentation from data
in experimental studies
For future residents and worker
scenarios, assumes all of daily
soil intake (FI) will result from
activities occurring in
potentially contam_inated areas
Chemicals in soil are completely
available from soil matrix in gut
Magnitude of Effect
on Risk•
Low -High
Low
Low
Low
Low
Low -Moderate
Low -Moderate
Low -Moderate
"Key: Low -~ 1 order of magnitude effect.
Moderate > 1 to~ 2 orders of magnitude effect.
High -> 2 orders of magnitude effect.
7-5
Direction of Effect
on Risk
May over-or under-
estimate risk
May over-or under-
estimate risk
May over-or under-
estimate risk
May over-or under-
estimate risk
May overestimate
risk
May over-or under-
estimate risk
May over-or under-
estimate risk
May over-or under-
estimate risk
volatilization model is a one dimensional model which assumes a single
mechanism of migration in the soil (i.e., air diffusion) and which does not
account for variations in climatic conditions such as·temperature and soil
moisture or other environmental processes such as biodegradation which could
reduce soil levels. The model also does not account for the resistance to
volatilization presented by stagnant boundary layer at the soil surface.
These structural simplifications of the model make the model compatible with
the amount of input data available, but add to the uncertainty of the outputs.
Additionally, simplifying boundary and initial conditions were used with the
volatilization model which would allow the model to be solved analytically.
These boundary and initial conditions were all ones that would tend to
overestimate the current and future emissions from the.site soils. Additional
uncertainties are associated with the use of the ISCLT air dispersion. This
model is designed to overpredict air concentrations to compensate for their
inability to model exactly the complex dispersion process.
The parameter values used to describe the extent, frequency and duration of
exposure are also associated with some uncertainty. In addition, risks for
certain individuals within an exposed population may be higher or lower than
those predicted depending upon their actual intake rates (e.g., inhalation and
soil ingestion rates), nutritional status, body weights, etc. In general,
however, the exposure assumptions were selected to produce a reasonable upper
bound estimate of exposure in accordance with USEPA guidelines regarding
Superfund site risk assessments.
In particular, the use of the RME approach to estimate exposure point
concentrations may overestimate potential exposures and thus risks. The
exposure point concentration statistics used to calculate CDis (i.e., the 95%
upper confidence limit on the mean, or maximum, whichever is less) are
strongly influenced by the sample size and variance or geometric standard
deviation (GSD) of the chemical concentrations being evaluated. CDis can
contribute to an ovrestimation of risk, particularly when maximum
concentrations are used as part of the RME exposure point concentration.
7-6
When calculating exposure point concentrations in soil from sampling data, 1/2
of the reported non-detected concentrations were included in the calculation
of the 95% upper confidence limit of the population mean if 1/2 of the
detection limit was not greater than the maximum measured value. Any approach
dealing with non-detected chemical concentrations is associated with some
uncertainty. This is because chemicals in such a situation may be absent from
the medium or may be present at a concentration which ranges from
infinitesimal to a concentration just below the detection limit.
Uncertainties are inherent in the selection of pathways for evaluation. In
•particular, it was assumed that individuals in the site area would engage in
certain activities that would result in exposures for each selected pathway.
Further, even if an individual were to engage in an activity, it is not
necessarily true that an exposure would be experienced. For example, it is
unlikely that every time an individual trespasses on the site (assuming this
were to occur), he or she will contact and incidentally ingest surface soils.
The
0
exposure parameter values used for the RME scenario are also associated
with some uncertainty. In most cases, values for the RME.case were specified
by USEPA guidance documents (USEPA 1989, 1991a). Many of these values are
conservative and are based on risk management interpretations of limited data.
An example is soil ingestion rates. Current USEPA guidance recommends default
soil ingestion rates of 200 mg/day for young children and 100 mg/day for older
individuals including adults. Data from the Calabrese et al. (1989) soil
tracer study indicate that the average soil ingestion rate for the study
population was 26 mg/day for the three most reliable tracer elements, with a
95th percentile ingestion rate of 202 mg/day (which correlates well with
USEPA's default value). In contrast, the available data on incidental soil
ingestion for adults is almost nonexistent. The Calabrese et al. (1990) adult
study shows an average adult soil ingestion rate of 41 mg/day for the three
most reliable tracer elements (higher than the mean observed for the much
larger study population of children).
(1991) reanalysis of the Binder et al.
Further, Thompson and Burmaster's ~
(1986) estimated average soil ingestion
7-7
rates of 62 and 24 mg/kg for a child (1-6) and adult, respectively. This
indicates that the USEPA default soil ingestion rate of 100· mg/day is likely
to overestimate adult exposures and risks. These results additionally
highlight the uncertainties associated with using soil ingestion tracer
studies, a topic which Stanek and Calabrese (1991) have discussed in some
detail.
There is additional uncertainty associated with the dermal absorption factor
used in this risk assessment. USEPA Region IV has directed that an absorption
factor of 1% for all organic chemicals (including chlorinated pesticides) be
used to assess the risks associated with dermal contact of soil. Wester et
al. (1990) performed in vitro studies in which DDT bound to soil was applied
to human skin in tissue culture. They found that only 0.04% was transferred
into the plasma receptor fluid after a 24-hour exposure. Absorption into
plasma is necessary as a first step in transporting DDT to its target organs.
Additionally, these investigators noted that 96% of the DDT was washed off the
skin indicating that usual hygiene practices can reduce dermal exposure. The
' authors of this study conclude "This data suggest that chemicals do partition
from soil and penetrate skin and become systemically available. Henceforth,
exposure to hazardous chemicals in soil must be considered important." Other
studies also show that while pure DDT can partition into skin, less than 1% is
actually absorbed into receptor fluid, even after 120 hours (Hawkins and
Reifenrath 1984, Bronaugh and Steward 1986).
Similar in vitro or in vivo studies with other pesticides using a soil matrix
are not available. Data from Feldman and Maibach (1974), however, also show a
similar trend of little actual absorption during short-term exposures to
pesticides applied in pure form or using solvents as vehicles. In this study,
pesticides in an acetone solution were applied to the forearms of human
subjects; the skin sites were not covered or washed for 24 hours. Absorption
was determined by urinary excretion analysis. For aldrin the results showed
that after four, eight and 12 hours, 0.3%, 0.6% an~ 0.9%, respectively, of the
applied chemical was absorbed. For dieldrin, after f,ur, eight and 12 hours,
0.6%, 1.1% and 1.6%, respectively, was absorbed. Similarly, for lindane,
7-8
0.6%, 1.1% and 1.6%, respectively, was absorbed. Similarly, for lindane,
0.3%, 0.8% and 1.8%, respectively, was absorbed. Further, the effect of a
soil matrix will greatly reduce the absorption of these chemicals (Wester et
al. 1990). The in vitro Wester et al. (1990) study showed that the percent
absorption of both DDT and BaP from an applied acetone vehicle· was
approximately 17 times higher than from an applied soil vehicle. Data from
Poiger and Schlatter (1980) using 2,3,7,8-TCDD show that absorption from non-
soil matrices (methanol, polyethylene glycol) was approximately six times
higher that from a soil matrix. Since the exposure pathway of interest in
this assessment is soil contact, the effect of the soil matrix needs to be
considered in determining the extent of dermal absorption. Feldman and
Maibach's results show that, when adjusted for a soil matrix, the absorption
of the tested pesticides will be negligible due to matrix inhibition and the
fact that the remaining organochlorines are more hydrophobic and volatile than
DDT.
7.3 TOXICOLOGICAL DATA
In most risk assessments, one of the largest sources of uncertainty is in
health criteria values. Health criteria for evaluating long-term exposures
such as risk reference doses or cancer slope factors are based on concepts and
assumptions which bias an evaluation in the direction .of over-estimation of
health risk. As USEPA notes in its Guidelines for Carcinogenic Risk
Assessment (USEPA 1986a):
There are major uncertainties in extrapolating both from animals to
humans and from high to low doses. There are important species
differences in uptake, metabolism, and organ distribution of
carcinogens, as well as species and strain differences in target site
susceptibility. Human populations are variable with respect to genetic
constitution, diet, occupational and home environment, activity patterns
and other cultural factors.
Table 7-4 presents the uncertainties associated with the toxicity assessment.
The most significant chemicals of concern at the site belong to the chemical
7-9
TABLE 7'4
UNCERTAINTIES IN THE BASELINE RISK ASSESSMENT
FOR THE GEIGY CHEMICAL CORPORATION SITE
TOXICITY ASSESSMENT
Assumption
Conservatively derived cancer slope
factors and reference doses were used to
assess risks
Cancer slope factors derived from animal
studies are based on upper 95% confidence
limits derived from the linearized multi-
stage model
Risks were assumed to be additive
although they may potentially be
synergistic or antagonistic
Cancer risks were added across chemicals
with different EPA weight-of-evidence
classifications (e.g., adding risks for a
Group A and Group B2 carcinogen)
The dermal exposure pathway was evaluated
using oral toxicity criteria and
adjusting CDis by a default oral
absorption modifying factor of one
8Key: Low -$ 1 order of.magnitude effect.
Magnitude of
Effect
on Riska
Low -Moderate
Moderate -High
Moderate
Moderate
Low -High
Moderate > 1 to$ 2 orders of magnitude effect.
High -> 2 orders of magnitude effect.
7-10
Direction of Effect
on Risk
May overestimate
risk
May overestimate
risk
May over-or under-
estimate risk
May overestimate
risk
May underestimate
risk
class of chlorinated pesticides. These chemicals have numerous structural
similarities and, therefore, are expecte4 to exhibit similar mechanisms of
biological action including carcinogenicity and are amenable to discussion as
a class. The risk manager should keep in mind that, despite the relatively
high cancer slope factors which have been calculated for these chemicals, the
qualitative evidence supporting the hypothesis of human carcinogenicity is
weak. In this section, the evidence for human and animal carcinogenicity of
the class and individual chemicals will be discussed in the interests of
presenting risk managers with sufficient toxicological evidence to arrive at
an informed decision for the site.
USEPA has classified all of these chemicals (with the exception of beta-BHC)
as Group B2 carcinogens. As noted above, group B2 carcinogens have sufficient
evidence for carcinogenicity from animal studies but inadequate evidence fro~
human studies. USEPA (1991c) has classified beta-BHC as a Group C carcinogen
for which there is limited evidence in animals. USEPA has also classified
gamma-BHC as a B2/C carcinogen meaning that there is insufficient evidence to
support either classification. Risk managers in some USEPA programs (e.g.
Office of Drinking Water and Office of Solid Waste) have regulated Group C
carcinogens on a less stringent basis than Group A or B carcinogens due to the
lesser weight of evidence.
The Agency follows conservative guidelines when evaluating toxicity studies in
order to be health productive. However, it is prudent to discuss the
uncertainties surrounding the toxicity studies in order to provide risk
managers with information. With the exception of DDT1, USEPA's oral cancer
slope factors for the chlorinated pesticides are all based on studies where
liver tumors were induced in mice. A review of the bioassays conducted by the
National Toxicology Program (Popp 1985) shows that aldrin, chlordane, p,p'-
DDE, dicofol (a DDT derivative), heptachlor (a component of chlordane), ~nd
toxaphene all have induced liver tumors in B6C3Fl mice, however, none of these
1The term DDT refers to any or all of DDT, DDD, or DDE.
7-11
have induced liver tumors .in Osborne Mendel rats (aldrin, chlordane, and
toxaphene have been associated with non-statistically significant increases in
tumors at other sites in rats). DDT has been the most studied of the
chlorinated pesticides. The detailed review of the toxicology of DDT produced
by ATSDR (1989) reveals that, of 18 studies, DDT was found to·be carcinogenic
in nine. Of these nine, rnoUse liver tumors were the carcinogenic endpoint in
five studies. In addition to the preponderance of mouse liver tumors, with a
few exceptions, the evidence for the genotoxicity of the organochlorines is
either negative or weak. Those chemicals which do exhibit genotoxicity (e.g.
aldrin) do not do so by reacting with DNA (ATSDR 1991), therefore, they are
considered to be non-genotoxic or epigenetic carcinogens. Of all the
chemicals found at the Geigy site, the evidence is strongest for
carcinogenicity of DDT.
One of the chemicals of potential concern, delta-BHC could not be
quantitatively evaluated because insufficient toxicity information is
available to derive carcinogenic and noncarcinogenic toxicity criteria.
However, based on the limited toxicity information that is available, this
isomer is less toxic than the other isomers of BHC (alpha-, beta-and gamma-)
for which health effects criteria are available and which were present at
greater concentrations at the site. In fact, USEPA (1991b) has classified
deltacBHC in group D, not classifiable as to human carcinogenicity.
Furthermore, no noncarcinogenic inhalation health effects criteria have been
developed for some of the selected chlorinated pesticides (e.g., gamma-BHC,
4,4'-DDD, 4,4'-DDE, etc). Therefore, noncarcinogenic effects could not be
quantitatively evaluated for the inhalation pathways. The absence of
noncarcinogenic inhalation information will serve to suggest that the risk
quantification may be underestimated as inhalation pathway quantification are
incomplete.
There is also uncertainty in assessing the toxicity of a mixture of
chemicals. In this assessment, the effects of exposure to each contaminant
present has initially been considered separately. However, these substances
7-12
J
'
occur together at the site_, and individuals may be exposed to mixtures of the
chemicals. Prediction of how these mixt~res of toxicants will interact must
be based on an understanding of the mechanisms of such interactions. The
interactions of the individual components of chemical mixtures may occur
during absorption, distribution, metabolism, excretion, or activity at the
receptor site. Individual compounds may interact chemically, yielding a new
toxic component or causing a change in the biological availability of an
existing component, or may interact by causing different effects at different
receptor sites; Suitable data are not currently available to rigorously
characterize the effects of chemical mixtures similar to those present at the
site. Consequently, as recommended by USEPA (1986b, 1989), chemicals present
at the site were assumed to act additively, and potential health risks were
evaluated by summing excess lifetime cancer risks and calculating hazard
indices for noncarcinogenic effects. This approach to assessing risk
associated with mixtures of chemicals assumes that there are no synergistic or
antagonistic interactions among the chemicals considered (USEPA 1989). To the
extent that these assumptions are incorrect, the actual risk could be under-
or over-estimated.
7.4 SENSITIVITY ANALYSIS
As discussed above, there are a number of major sources of uncertainty
inherent in this assessment. The single risk estimates for the RME case
presented in Section 5.0 are highly conservative, in some cases likely to
predict exposures and risks at the upper 99th percentile or higher of the
possible range of actual exposures and risks. To provide additional
information on the uncertainty inherent in these risk estimates, this section
presents the results of a sensitivity analysis which exposures an average case
exposure scenario. While toxicological data is also a critical source of
uncertainty, in the conservative direction, in this risk assessment
alternative toxicity criteria (such as maximum likelihood estimates for cancer
slope factors) are not investigated.
7-13
The exposure parameters wh.ich were tested in this ·analysis are discussed below
and summarized in Table 7-5 and 7-6 (current and future conditions,
respectively). Only parameter values that varied from the RME case are shown
in these tables; otherwise the values presented in Section 4.4 were used.
First, as noted above, the current (USEPA 1989, 199la).recommended approach
for calculating RME exposure point concentrations is one of the most important
and conservative sources of uncertainty in this assessment. Thus, for the
sensitivity analysis, the arithmetic mean concentrations were used to
calculate risks. For the child/teenage soil ingestion pathway, a conservative
average case soil ingestion rate of 24 mg/kg was based on Thompson and
Burmaster's (1991) reanalysis of the Binder et al. (1986) study. The soil-to-
skin was evaluated using an average value of 0.5 mg/cm2 (Driver et al. 1989,
Clement 1988). Additionally, age-specific surface area information (USEPA
1985, 1989) was used for the dermal pathways. For example, for the older
child/teenager a skin surface area of 1,372 cm2/day was used for the average
case. This is the 50th percentile values from USEPA (1985, 1989), assuming
for the average case that the surface area of the hand and one-half of the
arms (12% of the total surface area) is uncovered and exposed.
For residential exposure scenarios, an average case exposure duration of nine
years based on the average time an individual spends at one residence (USEPA
1989) was used. The average soil ingestion rates of 62 and 24 mg/day for
child (1-6 years) and adult residents, respectively were based upon Thompson
and Burmaster' s (1991) reanalysis of the Binder et al. (1986) .study. An
average groundwater ingestion rate based on USEPA· (1989) was also used.
Finally, an average inhalation rate for a hypothetical future on-site resident
of 14 m3/day was used, based on data provided by USEPA (1985).
For the future merchant scenario, an average time at one job was assumed to be
8.4 years, which is two times the median tenure of employees with their.
current employer (4.2 years) (Bureau of Labor Statistics 1991).
7-14
' I
I
TABLE 7-5
SUMMARY OF POTENT !AL· HEAL TH RISKS: RME AND CONSER VAT IVE AVERAGE EXPOSURE CASES
EXPOSURE PATHWAY
Ingestion of On-Site
Surface Soil/Sediment by an
Older Child Trespasser
Ingestion of Off-Site
Surface Soil/Sediment by an
Older Child Trespasser
Dermal Contact with On-Site
Surface Soil/Sediment by an
Older Child Trespasser
Dermal Contact with Off-Site
Surface Soil/Sediment by an
Older Child Trespasser
Inhalation of Chemicals
Volatilized from On-Site
Surface Soil/Sediment by an
Older Child Trespasser
CURRENT LANO USE CONDITIONS
PARAMETERS
RME Case
·95th UCL/Max -soil ingestion rate 100 mg/kg
Average Case
·Arithmetic Mean
-soil ingestion rate 24 mg/kg
RME Case
-95th UCL/Max
·soil ingestion rate 100 mg/kg
Average Case
-Arithmetic Mean
•soil ingestion rate 24 mg/kg
RME Case
·95th UCL/Max
·skin surface area available for
contact 3086 cm2/day
-soil-to-skin adherence
factor 1.0 mg/cm2
Average Case
-Arithmetic Mean
-skin surface area available for
contact 1372 cm2/day
-soil-to-skin adherence
factor 0.5 mg/cm2
RME Case
·95th UCL/Max
-skin surface area available for
contact 3086 cm2/day
-soil-to-skin adherence factor 1.0 mg/cm2
Average Case
·Arithmetic Mean
·skin surface area available for
contact 13n cm2/day
-soil-to-skin adherence
factor 0.5 mg/cm2
RME Case
·95th UCL/Max
-exposure time 4 hours/day
Average Case
·Arithmetic Mean
·exposure time 2 hours/day
UPPER BOUND
EXCESS LI FET !ME
CANCER RISK (a)
7E-O7
7E-O8
?E-O6
2E·O7
4E·O7
5E-O8
2E-O6
1E·O7
2E·O8
1E·OB
= This pathway could not be evaluated due to the absence of EPA toxicity criteria.
HAZARD INDEX
FOR NONCARCINOGENIC
EFFECTS (b)
< 1
< 1
< 1
< 1
< 1
< 1
< 1
< 1
(a) The upperbound individual excess lifetime cancer·risk represents the additional probability that an
individual may develop cancer over a 70-year lifetime as a result of exposure conditions evaluated.
(b) The hazard index indicates whether of not exposure to mixtures of noncarcinogenic chemicals may result
in adverse health effects. A hazard index less than one indicates that adverse hunan health effects are unlikely to occur.
7-15
TABLE 7-5 (Continued)
SUMMARY OF POTENTJAl HEALTH RISKS: RME AND CONSERVATIVE AVERAGE EXPOSURE CASES
CURRENT LAND USE CONDITIONS
EXPOSURE PATH~AY
Inhalation of Chemicals
Volatilized from On-Site
Surface Soil/Sediment by a
Nearby Merchant
Inhalation of Chemicals
Volatilized from On-Site Surface Soil/Sediment by a Young Child (1-6 years) Resident
Inhalation of Chemicals
Volatilized from on-Site Surface Soil/Sediment by an
Adult Resident
Inhalation of Chemicals
in dust particulates from
On-site surface Soil/Sediment
by a Young Child (1·6 years)
Resident
PARAMETERS
RME Case
·95th UCL/Max -exposure duration 25 years
Average Case
•Arithmetic Mean
-exposure duration 8.4 years
RME Case -95th UCL/Max
-exposure frequency 350 days/year
RME Case
. -95th UCL/Max
-exposure duration 30 years
Average Case
·Arithmetic Mean
-exposure duration 9 years
RME Case
·95th UCL/Max
-exposure frequency 350 days/year
Inhalation of Chemicals RME Case
in dust particulates from ·95th UCL/Max
On-Site Surface Soil/Sediment ·exposure duration 30 years
by en Adult Resident
Average Case
·Arithmetic Mean -exposure duration 9 years
Inhalation of Chemicals RME Case
in dust particulates from ·95th UCL/Max
on-Site Surface Soil/Sediment ·exposure duration 25 years
by an Adult Merchant
Average Case
·Arithmetic Mean
-exposure duration 8.4 years
UPPERBOUND
EXCESS LIFETIME
CANCER RISK (a)
6E·07
3E·07
1E-07
9E-08
SE-08
BE-11
1E-10
3E-11
6E-10
2E·10
= This pathway could not be evaluated due to the absence of EPA toxicity criteria.
HAZARD INDEX
FOR NONCARCINOGENJC
EFFECTS (bl
(a)
(bl
The upperbound individual excess lifetime cancer risk represents the additional probability that an
individual may develop cancer over a 70-year lifetime as a result of exposure conditions evaluated. The hazard index indicates whether of not exposure to mixtures of noncarcinogenic chemicals may result in adverse health effects. A hazard index less then one indicates that adverse hi.nan health effects are unlikely to occur.
7-16
TABLE 7·6
SUMMARY OF POTENTIAL ·HEALTH RISKS: RME AND CONSERVATIVE AVERAGE EXPOSURE CASES
FUTURE LAND USE CONDITIONS
EXPOSURE PATHWAY
Ingestion of On-Site
Surface Soil/Sediment by a
Hypothetical Future Merchant
Ingestion of On-Site
Surface Soil/Sediment by a
Hypothetical Future Child
(1-6 yrs) Resident
Ingestion of On-Site
Surface Soil/Sediment by a
Hypothetical Future Adult
Resident
Dermal Contact with On-Site
Surface Soil/Sediment by a
Hypothetical Future Merchant
Dermal Contact with On-Site
Surface Soil/Sediment by a
Hypothetical Future Child
(1-6 yrs) Resident
Dermal Contact with On-Site
Surface Soil/Sediment by a
Hypothetical Future Adult
Resident
UPPER BOUND EXCESS LIFETIME
PARAMETERS CANCER RISK (a)
RME Case 4E·06
·95th UCL/Max
-exposure duration 25 years
-soil ingestion rate 100 mg/day
Average Case
-Arithmetic Mean
-exposure duration 8.4 years
·soil ingestion rate of 24 mg/day
RME Case
·95th UCL/Max
·soil ingestion rate 200 mg/day
Average Case
·Arithmetic Mean
-soil ingestion ra_te 62 mg/day
RME Case
·95th UCL/Max
-exposure duration 30 years
-soil ingestion rate 100 mg/day
Average Case
-Arithmetic Mean
-exposure duration 9 years
-soil ingestion rate 24 mg/day
RME Case
·95th UCL/Max
·exposure duration 25 years
-soil-to-skin adherence
factor 1.0 mg/cm2
Average Case
-Arithmetic Mean
•exposure duration 8.4 years
-soil-to-skin adherence
factor 0.5 mg/cm2
RME Case
·95th UCL/Max
-soil-to-skin adherence
factor 1.0 mg/cm2
-skin surface area 3140 cm2
Average Case -Arithmetic Mean
-soil-to-skin adherence
factor 0.5 mg/cm2
-skin surface area 1789 cm2
RME Case
-95th UCL/Max
•exposure duration 30 years
•soil-to-skin adherence
factor 1.0 mg/cm2
Average Case
-Arithmetic Mean
-exposure duration 9 years
-soil-to-skin adherence
factor 0.5 mg/cm2
3E·07
3E·OS
4E·06
1E·OS
5E·07
6E·07
5E·08
4E·06
SE-07
1E·06
SE-08
= This pathway could not be evaluated due to the absence of EPA toxicity criteria.
HAZARD INDEX FOR NONCARCINOGENIC
EFFECTS (b)
< 1
< 1
< 1
< 1
< 1
< 1
< 1
< 1
< 1
< 1
< 1
< 1
(a)
Cb)
The upperbound individual excess lifetime cancer risk represents the additional probability that an
individual may develop cancer over a 70-year lifetime as a result of exposure conditions evaluated.
The hazard index indicates whether of not exposure to mixtures of noncarcinogenic chemicals may result
in adverse health effects. A hazard index less than one indicates that adverse hunan health effects
are unlikely to occur.
7-17
TABLE 7-6 (continued)
SUMMARY OF POTENTIAL·HEALTH RISKS: RME AND CONSERVATIVE AVERAGE EXPOSURE CASES FUTURE LAND USE CONDITIONS
EXPOSURE PATHWAY
Ingestion of Surficial Groundwater by a Hypothethcal Future Child (1-6 years)
Resident
Ingestion of Surficial
Groundwater by a Hypothethcal
Future Adult Resident
Ingestion of Surficial Groundwater by a Hypothethcal Future Merchant
Ingestion of MW-11D Groundwater by a Hypothethcal Future Child (1·6 years)
Resident
Ingestion of Well MW-11D Groundwater by a Hypothethcal
Future Adult Resident
Inhalation of Volatiles While Showering with Surficial
Groundwater by a Future Child (1·6 years) Resident
Inhalation of Volatiles While Showering with Surficial Groundwater by a Future Adult Resident
PARAMETERS
RME Case
-95th UCL/Max
Average Case ·Arithmetic Mean
RME Case
-95th UCL/Max
-exposure duration 30 years
-ingestion rate 2 liters/day
Average Case
·Arithmetic Mean •exposure duration 9 years
-ingestion rate 1.4 liters/day
RME Case
-95th UCL/Max
·exposure duration 25 years
Average Case
·Arithmetic Mean ·exposure duration 8.4 years
RME Case
-Maxirrun concentration
RME Case
-95th UCL/Max
·exposure duration 30 years
·ingestion rate 2 liters/day
Average Case
·exposure duration 9 years ·ingestion rate 1.4 liters/day
RME Case
-95th UCL/Max
Average Case
·Arithmetic Mean
RME Case
-95th UCL/Max
·exposure duration 30 years
Average Case
·Arithmetic Mean
·exposure duration 9 years
UPPERBOUND
EXCESS LI FET !ME
CANCER RISK (a)
2E-03
lE-04
4E-03
6E-05
lE-03
3E-05
7E-04
2E-03
3E-04
3E-08
6E-09
4E-08
7E-09
= This pathway could not be evaluated due to the absence of EPA toxicity criteria.
HAZARD INDEX
FOR NONCARC!NOGEN!C
EFFECTS (b)
> 1 (10)
> 1 (2)
>, (4)
< 1 (0.6)
> 1 (1.4)
< 1
> 1 (2.4)
> , (1.2)
< 1
< 1
< 1
< 1
< 1
(a)
Cb)
The upperbound individual excess lifetime cancer risk represents the additional probability that an individual may develop cancer over a 70·yeer lifetime as a result of exposure conditions evaluated. The hazard index indicates whether of not exposure to mixtures of noncarcinogenic chemicals may result in adverse health effects. A hazard index less than one indicates that adverse htinan health effects are unlikely to occur.
7-18
TABLE 7-6 (continued)
SUMMARY OF POTENT JAL ·HEAL TH RISKS: RME AND CONSERVATIVE AVERAGE EXPOSURE CASES
EXPOSURE PATHWAY
Dermal Exposures While
Showering with Surficial
Groundwater by a Future Child
(1-6 years) Resident
Dermal Exposures While
Showering with Surficial
Groundwater by a Future Adult Resident
Inhalation of Chemicals
From On-Site Surface Soil/
Sediment by a Hypothetical
Future Child (1·6 years)
Resident
Inhalation of Chemicals
From On-Site Surface Soil/
Sediment by a Hypothetical
Future Adult Resident
Inhalation of Chemicals From On-Site Surface Soil/
Sediment by a Hypothetical
Future Adult Merchant
FUTURE LAND USE CONDITIONS
PARAMETERS
RME Case
-95th UCL/Max
Average Case
-Arithmetic Mean
RME Case
-95th UCL/Max
-exposure duration 30 years
Average Case
-Arithmetic Mean
-exposure duration 9 years
RME Case
-95th UCL/Max
RME Case
-95th UCL/Max
-exposure duration 30 years
Average Case
-Arithmetic Mean
-exposure duration 9 years
RME Case
-95th UCL/Max
·exposure duration 25 years
Average Case
•Arithmetic Mean
-exposure duration 8.4 years
UPPERBOUND
EXCESS LIFETIME
CANCER RISK (a)
2E-O6
2E-D7
6E-O6
1E-O7
1E-D6
9E-O7
SE-O7
6E-O7
3E-O7
= This pathway could not be evaluated due to the absence of EPA toxicity criteria.
HAZARD I NOEX
FOR NONCARCINOGENIC
EFFECTS (b)
<1
<1
<1
<1
(a) The upperbound individual excess lifetime cancer risk represents the additional probability that an
individual may develop cancer over a 70-year lifetime as a result of exposure conditions evaluated.
(b) The hazard index indicates whether of not exposure to mixtures of noncarcinogenic chemicals may result
in adverse health effects. A hazard index less than one indicates that adverse hl.lllan health effects are unlikely to occur.
7-19
The resulting risks for the average case .exposure scenarios are compared with
the RME estimates in Tables 7-5 and 7-6. Both excess·lifetime cancer risks
and hazard index values are shown. As can be seen from this table, the RME
exposure scenarios provide conservative estimates of potential risks which
exceed the conservative average case by up to two orders of magnitude. This
should be kept in mind when evaluating the results of this Baseline Risk
Assessment.
This Baseline Risk Assessment should not be construed as presenting an
absolute evaluation of risks to persons exposed to soil from the Geigy
Chemical Corporation site. Rather, it is a conservative analysis intended to
indicate the potential for adverse impacts to occur.
7-20
8.0 SUMMARY AND CONCLUSIONS
Clement International Corporation evaluated the human ·health and ecological
risks associated with past operations at the Geigy Chemical Corporation Site,
a former pesticide formulation facility. This Baseline Risk Assessment was
performed for the Potentially Responsible Parties (PRPs) under an
Administrative Order on Consent with the United States Environmental
Protection Agency (USEPA) Region IV. The primary data used in this evaluation
was collected during the Remedial Investigation conducted by Environmental
Resources Management-Southeast, and the Feasibility Study conducted by Sirrine
Environmental.
The Geigy Chemical Corporation site is located in Aberdeen, North Carolina.
From 1947 until 1967 the site was used as a pesticide formulation facility.
Subsequent to 1968, the site had been used for retail distribution of
agricultural chemicals and fertilizers. Extensive remedial activities have
already occurred at the site; soil has been excavated and removed to hazardous
waste treatment, storage and disposal facilities, and areas of the site have
been covered with geotextile, clean fill and an indigenous species of grass.
Thus, this Baseline RA addresses a no-further action alternative. The no-
further action alternative was evaluated in accordance with the National
Contingency Plan and USEPA guidance for risk assessments at Superfund sites.
Based upon USEPA guidance, all of the organic chemicals measured in the
environmental media selected for evaluation were considered to be chemicals of
potential concern. The chemicals associated with past site activities,
however, are organochlorine pesticides. Inorganic chemicals in_groundwater
were selected as chemicals of potential concern because of the limited
background data which was available. The predominant chemicals in on-site
soil are toxaphene, and DDT and· its metabolites DDE, and DDD while in
groundwater, toxaphene and the BHC isomers are predominant.
8-1
For each chemical of poten~ial concern, toxicity information was then
compiled. This included brief descriptions of the potential toxicity of each
chemical to human health and quantitative toxicity criteria used to calculate
risks. The toxicity criteria were primarily obtained from USEPA's Integrated
Risk Information System (IRIS) and Health Effects Assessment Summary Tables
(HEASTs).
Potential exposure pathways were reviewed and selected for quantitative
evaluation in the risk assessment. The following exposure pathways were
selected for detailed evaluation under current and surrounding land-use
conditions:
• Incidental ingestion of chemicals in on-site surface soil/sediment
by an older child trespasser (8-13 years),
• Dermal absorption of chemicals in on-site surface soil/sediment by
an older child (8-13 years),
• Incidental ingestion of chemicals in off-site surface
soil/sediment by an older child (8-13 years),
• Dermal absorption of chemicals in off-site surface soil/sediment
by an older child (8-13 years),
• Inhalation of volatilized surface soil/sediment chemicals by an
older child trespasser (8-13 years),
• Inhalation of volatilized surface soil/sediment chemicals by a
merchant north of the site,
• Inhalation of volatilized surface soil/sediment chemicals by a
nearby adult and young child resident (1-6 years) northeast of the
site,
• Inhalation of wind blown dust particulates by a merchant north of
the site, and
• Inhalation of wind blown dust particulates by a nearby adult and
young child resident (1-6 years) northeast of the site. ·
8-2
Under future land-use conditions, the following exposure pathways were
selected for evaluation:
• Incidental ingestion of chemicals in on-site surface soil/sediment
by a hypothetical future adult and child (1-6 years) resident,
• Incidental ingestion of chemicals in on-site surface soil/sediment
by a hypothetical future merchant,
• Dermal absorption of chemicals in on-site surface soil/sediment by
a hypothetical future adult and child (1-6 years) resident,
• Dermal absorption of chemicals in on-site surface soil/sediment by
a hypothetical future merchant,
• Ingestion of groundwater from the surficial aquifer by
hypothetical future on-site adult and child (1-6 years) residents,
• Ingestion of groundwater from the surficial aquifer by a
hypothetical future on-site merchant,
• Ingestion of groundwater from the second uppermost aquifer within
property boundaries by hypothetical future on-site adult and child
(1-6 years) residents,
• Ingestion of groundwater from the off-site second uppermost
aquifer (MW-llD) by hypothetical future adult and child (1-6
years) residents,
• Inhalation of volatile organic chemicals while showering with
groundwater from the surficial aquifer by hypothetical future on-
site adult and child (1-6 years) residents,
• Inhalation of volatile organic chemicals while showering with
groundwater from the second uppermost aquifer within property
boundaries by hypothetical future on-site adult and child (1-6
years) residents,
• Dermal absorption of chemicals while showering with groundwater
from the surficial aquifer by hypothetical future on-site adult
and child (1-6 years) residents,
• Inhalation of volatilized surface soil/sediment chemicals by.
hypothetical future adult and child (1-6 years) residents, and
• Inhalation of volatilized surface soil/sediment chemicals by a
hypothetical future merchant.
8-3
Human exposure and risk were thus considered under both current and future
land-use conditions for the chemicals of potential concern at the site,
Cumulative risks across pathways and for all chemicals were also presented.
Under current land-use conditions, the cumulative risk for an on-site older
child trespasser in contact with surface soil and air on the site was equal to
USEPA's point of departure risk of lx10·6 . The cumulative risk for an older
child contacting off-site sediment was 9x10·6 • None of these risks exceed
USEPA's remedial risk range of lxl0"4 to lx10·6 , and they are far below USEPA's
criterion of lxlo-4 for cumulative risk. In addition, noncarcinogenic effects
were well below the level of concern.
Off-site exposures to merchants north of the site and to young child and adult
residents northeast of the site were also evaluated under current land-use
conditions for the inhalation of on-site dust and volatilized chemicals.
The cumulative inhalation risks to these receptors, ranging from 9xlo-8 to
6xl0"7, were well below USEPA's remedial risk range of lxl0"4 to lx10·6 .
Noncarcinogenic effects were also well below the level of concern.
Under future land-use conditions, the cumulative risk for a residential young
child (1-6 years) exposed to the chemicals of potential concern in soil, air
and surficial groundwater was 2xl0"3, while for an adult the cumulative risk
was 4xlo·3. These risks were dominated by the consumption of pesticides in
groundwater from the surficial aquifer over a period of 6 years (child) and 30
years (adult). Inhalation and dermal exposures while showering accounted for
far less risk than exposure through ingestion. If exposure to surficial
groundwater was not to occur in the future, the cumulative risks for a young
child and an adult resident exposed to chemicals in surface soil and air would
be reduced to 4x1o·S and 2xl0"5. These risks are well within USEPA's risk
range of lx10·4 to lxl0"6 used for the selection of remedial alternatives. The
incidental ingestion of surface soil containing toxaphene was most responsible
for these risks.
8-4
Noncancer risks to hypothetical young child (1-6 years) and adult residents
are similarly dominated by the ingestion of groundwater from the surficial
aquifer. The presence of pesticides in surficial groundwater resulted in a
hazard index greater than 1.0 for liver and kidney effects for both a young
child and adult resident.
The cumulative risks for a merchant contacting soil, air and surficial
groundwater under future land-use conditions was estimated to be lxlo-3-These
risks were also dominated by the ingestion of groundwater from the surficial
aquifer over a period of 25 years. The cumulative risk associated with the
contact of on-site surface soil and air was 5x10-6. This risk is within
USEPA's risk range of lxlo-4 to lxl0"6 used for the selection of remedial
alternatives. Of the air and soil pathways, risks are highest for the
incidental ingestion of chemicals in surface soil, and are primarily
attributed to toxaphene. In addition, the hazard index was greater than 1.0
for liver effects due to the hypothetical consumption of surficial
groundwater. Again, pesticides were responsible for potential noncarcinogenic
effects.
The risks associated with domestic use of groundwater from the second
uppermost aquifer within the property boundary was evaluated for hypothetical
adult and child residents. The estimated risks for ingestion ranged from
lxlo-5 to 2xl0"5 for a young child (1-6 years) and an adult, respectively.
These risks are associated with trichloroethene and are within USEPA's risk
range of lx10·6 and lxl0"4 • The hazard indices were calculated for the
noncarcinogenic effects of trichloroethene on the liver for both receptors.
The hazard index was less than 1.0 for adults and greater than 1.0 for young
children. Risks associated with inhalation of volatilized chemicals from the
second uppermost aquifer while showering are 3xl0"6 and 4xl0"6 for a child and
adult resident, respectively. These risks are within USEPA's risk range. of
lxl0"4 to lx10·6 used for the selection of remedial alternatives.
Risk was also estimated for a future resident who might consume groundwater
8-5
from the second uppermost aquifer in the vicinity of off-site monitoring well
MW-11D. Pesticides were not detected in .the second uppermost aquifer within
property boundaries. The risk associated with this hypothetical future
exposure was estimated to be 7xlo-4 for a young child (1-6 years) resident,
and 2xlo·3 for an adult resident. Risks associated with inhalation and dermal
exposure while showering we.re either less than USEPA' s point of departure risk
of lx10·6 (inhalation) or were within USEPA's remedial risk range of lx10·4 to
lxlo-6 (dermal). The hazard index for liver effects was greater than 1.0 for
a future adult resident ingesting groundwater in the vicinity of MW-11D, while
for a young child, the hazard index was greater than 1.0 for liver and kidney
effects.
Adverse ecological impacts associated with the site are not expected to occur.
No aquatic life impacts are expected, as the two drainage ditches that occur
at the site do not contain enough water to sustain aqua.tic life. No impacts
on the vegetative community are expected given the probable low phytotoxicity
of the insecticides of concern in soil. Adverse terrestrial wildlife impacts
also are not expected. The site is not expected to support extensive wildlife
populations, given its small size, the limited diversity of the vegetative
community (which limits food and cover resources), and the availability of
higher quality habitat in adjacent areas. Some impacts are possible for soil
invertebrates living in limited areas of the site, although these impacts
could not be evaluated with any degree of certainty given the available
toxicological and exposure database. Even if toxic effects in soil
invertebrates are possible in localized areas, extensive impacts are
considered unlikely because the sandy and low-organic content soil present
naturally at the site is unlikely to support an abundant and diverse soil
invertebrate community.
A soil remediation goal for the risk-limiting chemical, toxaphene, was derived
in accordance with EPA guidance for the direct contact pathway of greatest
concern, i.e. the incidental ingestion of soil under future residential
conditions (Appendix E). Not-to-exceed surface soil concentrations of 5 mg/kg
8-6
toxaphene, 50 mg/kg toxaphene, and 500 mg/kg toxaphene were found to represent
lx10·6 , lx10·5, and lx10·4 excess upperbound lifetime residual cancer risks
respectively, for site-wide exposure to all of the pesticides combined.
8-7
9.0 REFERENCES
EXECUTIVE SUMMARY
SIRRINE ENVIRONMENTAL. 1991. Draft Report of the Feasibility Study: Geigy
Chemical Corporation Site, Aberdeen, North Carolina
U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA). 1991. Role of Baseline Risk
Assessment in Superfund Remedy Selection Decisions. OWSER Directive
9355.0-30 Memo from Don R. Clay. April 22, 1991
SECTION 1.0
COWHERD, C., MULESKI, G.E., ENGLEHART, P.J., and GILLETTE, D.A. 1985. Rapid
Assessment of Exposure to Particulate Emissions from Surface
Contamination Sites. Midwest Research Inst., Kansas City, MO. PB85-
192219
ERM -Southeast, Inc. 1991. Draft Report Remedial Investigation Study
.Geigy Chemical Corporation Site, Aberdeen, North Carolina
FOSTER, S.A. and CHROSTOWSKI, P.C. 1987.
Organic Contaminants in the Shower.
Meeting of APCA, New York, New York.
Inhalation Exposures to Volatile
For Presentation at the 80th Annual
June 21-26, 1987
U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA). 1986a. Guidelines for
Carcinogenic Risk Assessment. Federal Register 51:33992-34003
U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA). 1986b. Guidelines for
Estimating Exposures. Federal Register 51:34042-34054.
U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA). 1986c. Guidelines for the
Health Risk Assessment of Chemical Mixtures. Federal Register 51:34014-
34023.
U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA). 1989a.
Guidance for Superfund. Volume I: Human Health
A). Interim Final. EPA/540/1-89/002. December
Risk Assessment
Evaluation Manual.
1989
(Part
U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA). 1989b. Exposure Factors
Handbook. Office of Health and Environmental Assessment, Washington,
D.C. July
U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA). 1990a.
hazardous substances pollution contingency ~lan.
(March 8, 1990)
9-1
National oil and'
Fed. Reg. 55:8666-8865
U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA). 1990b. Superfund: Guidance for
Data Useability in Risk Assessment. Interim Final.· Office of Emergency
and Remedial Response. EPA/540/G-90/008. Directive: 9285.7-05.
(October 1990)
U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA). 1991a. Risk Assessment
Guidance for Superfund. Volume I: Human Health Evaluation
Supplemental Guidance. Standard Default Exposure Factors.
Final. Washington, D.C. OSWER Directive 9285.6-03. March
Manual
Interim
25, 1991
U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA). 1991b. Revised EPA Region IV
Supplemental Risk Assessment Guidance. March 26, 1991 ·
SECTION 2.0
BODEK, I, LYMAN, W.J., REEHL, W.F. and ROSENBLATT, D.H. 1988. Environmental
Inorganic Chemistry: Properties, Processes, and Estimation Methods.
Pergamon Press, New York
BOERNGEN, J.G. and SHACKLETTE, H.T. 1981. Chemical Analyses of Soils and
Other Surficial Materials of the Conterminous United States. United
States Department of the Interior. Geological Survey. Open File Report
81-197
ERM -Southeast, Inc. 1991. Draft Report Remedial Investigation Study
Geigy Chemical Corporation Site, Aberdeen, North Carolina
GILBERT, R.O. 1987. Statistical Methods for Environmental Pollution
Monitoring. Van Nostrand Reinhold, New York
SIRRINE ENVIRONMENTAL. 1991. Draft Report of the Feasibility Study: Geigy
Chemical Corporation Site, Aberdeen, North Carolina
U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA). 1988a. Statistical Methods for
Evaluating Ground-Water Monitoring Data From Hazardous Waste Facilities.
53 Fed Reg. 39720-39731. October 11, 1988
U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA). 1989a. Risk Assessment
Guidance for Superfund. Volume I: Human Health Evaluation Manual. (Part
A). Interim Final. EPA/540/1-89/002. December 1989
U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA). 1991a. Risk Assessment
Guidance for Superfund. Volume I: Human Health Evaluation Manual
Supplemental Guidance. Standard Default Exposure Factors. Inter{m
Final. Washington, D.C. OSWER Directive 9285.6-03. March 25, 1991
U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA). 199lb.~ Revised EPA Region IV
Supplemental Risk Assessment Guidance. March 26, 1991
9-2
SECTION 3. 0
U .S ENVIRONMENTAL PROTECTION AGENCY (USEPA) .. 1986. Guidelines for
Carcinogenic Risk Assessment. Federal Register 51:33992-34003.
U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA). 1991. Integrate Resource
Information Systems (IRIS). Environmental Criteria and Assessment
Office, Cincinnati, OH.
Aldrin
AGENCY FOR TOXIC SUBSTANCES AND DISEASE REGISTRY (ATSDR). 1987.
Toxicological profile for Aldrin/Dieldrin. USPHS, Atlanta, GA. Draft
AMERICAN CONFERENCE OF GOVERNMENTAL INDUSTRIAL HYGIENISTS (ACGIH). 1986.
Documentation of the Threshold Limit Values and Biological Exposure
Indices. 5th ed. Cincinnati, Oh, Pp. 17, 196 (As cited in ATSDR 1987)
BEYERMANN, K. and ECKRICH, W. 1973. Gas-chromatographische Bestimmung von
Insecticid-Spuren in Luft. Z. Anal. Chem. 265:4-7 (As cited in ATSDR
1987)
BORGMANN, A., KITSELMAN, C., DAHM, P., PANKASKIE, J., and DUTRA, F. 1952a.
Toxicological studies of aldrin on small laboratory animals.
Unpublished report of Kansas State College (As cited in ATSDR 1987)
BORGMANN, A., KITSELMAN, C., DAHM, P., PANKASKIE, J., and DUTRA, F. 1952b.
Toxicological studies of dieldrin on small laboratory animals.
Unpublished report of Kansas State College, July, 34 pp., (As cited in
ATSDR 1987)
DAVIS, L. 1965. Pathology report on mice
or heptachlor epoxide for two years.
Dr. A.J. Lehrman, July 19 (As cited
fed dieldrin, aldrin, heptachlor,
Internal FDA memorandum to
in USEPA 1988)
DEICHMANN, W. 1972. Toxicology of DDT and related chlorinated hydrocarbon
pesticides. J. Occup. Med. 14:285 (As cited in USEPA 1980)
EPSTEIN, S. 1975. The carcinogenicity of dieldrin. Part 1. Sci. Total
Environ. 4:1-52 (As cited in USEPA 1988)
FARB, R., SANDERSON, T., MOORE, B., and HAYES, A.
effect of selected mycotoxins on the tissue
of aldrin and dieldrin in the neonatal rat.
Inter-America Conference on Toxicol. Occup.
1987)
1973. Interaction: The
distribution and retention
Paper presented at the 8th
Med. (As cited in ATSDR
FELDMANN, R. and MAIBACH, H. 1974. Percutaneous penetration of some
pesticides and herbicides in man. Toxicol. Appl. Pharmacol. 28:126-132
(As cited in ATSDR 1987)
9-3
FITZHUGH, 0., NELSON, A., _and QUAIFE, M. 1964. Chronic oral toxicity of
aldrin and dieldrin in rats and dogs. Food Cosmet. Toxicol. 2:551-562
(As cited in USEPA 1988)
GEORGIAN 1974. (As cited in USEPA 1988)
HAYES, W. 1982. Pesticides Studied in Man. The Williams and Wilkins Co.,
Baltimore, MD. Pp. 234-247
HEATH, D. and VANDEKAR, M. 1964. Toxicity and metabolism of dieldrin in
rats. Br. J. Ind. Med. 21:269-279 (As cited in ATSDR 1987)
HODGE, H., BOYCE, A., DEICHMANN, W., and KRAYBILL, H. 1967. Toxicology and
no-effect levels of aldrin and dieldrin. Toxicol. Appl. Pharmacol.
10:613-675 (As cited in ATSDR 1987)
HOOGENDAM, I., VERSTEEG, J., and DEVLIEGER, M. 1962. Electroencephalograms
in insecticide toxicity. Arch. Environ. Health 4:92-100 (As cited in
ATSDR 1987)
HUNTER, C. and ROBINSON, J.
I. Ingestion by human
15:614-626 (As cited
1967. Pharmacodynamics
subjects for 18 months.
in ATSDR 1987)
of dieldrin (HEOD).
Arch. Environ. Health
HUNTER, C. and ROBINSON, J. 1969. Pharmacodynamics of dieldrin (HEOD)
ingestion by human subjects for 18 to 24 months, and post exposure for 8
months. Arch. Environ. Health 18:12-21 (As cited in ATSDR 1987)
IATROPOULOS, M., MILLING, A., MILLER, W., NOHYNEK, G., ROZMAN, K., COULSTON,
F., and KORTE, F. 1975. Absorption, transport,.and organotropism of
dichlorobiphenyl (DCB), dieldrin, and hexachlorobenzene (HCB) in rats.
Environ. Res. 10:384-389 (As cited in ATSDR 1987)
JAGER, K. 1970. Aldrin, Dieldrin, Endrin, and Telodrin: An epidemiological
and toxicological study of long-term occupational exposure. Elsevier
Puhl. Co., New York. Pp. 121-131 (As cited in ATSDR 1987)
NATIONAL CANCER INSTITUTE (NCI). 1978. Bioassay of aldrin and dieldrin for
possible carcinogenicity. DHEW Publication No. (NIH) 78-821. NCI
Carcinogenesis Tech. Rep. Ser. No. 21 NCI-C6-TR-21 (As cited in USEPA
1988)
OTTOLENGHI, A., HASEMAN, J., and SUGGS, F. 1974. Teratogenic effects of
aldrin, dieldrin, and endrin in hamsters and mice. Teratology 9:11-16
(As cited in ATSDR 1987)
PROBST, G., MCMAHON, R., HILL, L., THOMPSON, D., EPP, J., and NEAL, S. 1981.
Chemically-induced unscheduled DNA synthesis in primary rat hepatocyte
cultures; A comparison with bacterial mutagenicity using 218 chemicals.
Environ. Mutagenesis 3:11-32 (As cited in ATSDR 1987)
9-4
ROCCHI et al. 1980. (As cited in USEPA 1988)
SHELL. 1984. Review of mammalian and human toxicology, aldrin and dieldrin.
Review series HSE 84.003. Shell International' Petroleum Maatschappij.
B.V. The Hague. (As cited in ATSDR 1987)
SUMDARAM, K., DAMODARAN, V., VENKITASUBRAMANIAN, T. 1978a. Absorption of
dieldrin through monkey and dog skin. Indian J. Exp. Biol. 16:101-103
(As cited in ATSDR 1987)
SUNDARAM, K. , DAMODARAN, V. ,
dieldrin through skin.
ATSDR 1987)
and VENKITASUBRAMANIAN, T. 1978b. Absorption of
(As cited in Indian J, Exp. Biol. 16:1004-1007
TREON, J. and CLEVELAND, F. 1955. Toxicity of certain chlorinated hydrogen
insecticides for laboratory animals, with special reference to aldrin
and dieldrin. Agric. Food Chem. 3:402-408 (As cited in ATSDR 1987)
U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA). 1988. Chemical Profiles for
Extremely Hazardous Substances. Aldrin. U.S. USEPA, June 1988
U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA). 1991. Integrated Risk
Information System (IRIS). Office of Health and Environmental
Assessment Office, Cincinnati, Ohio. ~
WALKER, A., STEVENSON, D., ROBINSON, J., THORPE, E., ROBERTS, M. 1969. The
toxicology and pharmacodynamics of dieldrin (HEOD): Two-year oral
exposures of rats and dogs. Toxicol. Appl. Pharmacol. 15:345-373 (As
cited in ATSDR 1987)
BHC Isomers
ALBRO, P.W. and THOMAS, R. 1974.
and hexa chlorocyclohexane
12:378-384
Intestinal absorption of hexachlorobenzene
isomers in rats. Bull Environ Contam Toxicol
BAUMANN, K., ANGERER, J., HEINRICH, R., LEHNERT, G. 1980. Occupational
exposure to hexachlorocyclohexane. I. Body burden of HCH-isomers. Int.
Arch Occup Health 47:119-127
CZEGLEDI-JANKO, G. and AVAR, P. 1970. Occupational exposure to lindane:
Clinical and laboratory findings. Br J Indust Med 27:283-286
FITZHUGH, 0.G., NELSON, A.A., FRAWLEY, J.P. 1950. The chronic toxicities of
technical benzene hexachloride and its alpha, beta and gamma isomers. J
Pharmacol Exp Ther 100:59-66
HITACH~, M., YAMADA, K., TAKAYAMA, S. 1975. Brief communication: Cytologic
changes induced in rat liver cells by short-term exposure to chemical
substances. J Natl Cancer Inst 54:1245
9-5
HOOKER CHEMICAL CORPORATION. 1969. FBHC, Fortified Benzene Hexachloride,
Bulletin No. 480, Industrial Chemicals Division, Niagara Falls, NY, pp.
1-4
INTERNATIONAL AGENCY FOR RESEARCH ON CANCER (IARC). 1979. IARC monographs on
the evaluation of the carcinogenic risk of chemicals to humans.
Chemicals, industrial processes and industries associated with cancer.
IARC Monogr Eval Carcinog Risk Chem Hum 24:133-135
ITO, N., NAGASAKI, H., ARAI, M., SUGIHARA, S., MAKIURA, S. 1973. Histologic
and ultrastructural studies on the hepatocarcinogenicity of benzene
hexachloride in mice. JNCI 51:817-826
ITO, N. , NAGASAKI, H. , AOE, H. , SUGIHARA, S. , MIYATA, Y. , ARAI , M. , SHIRAI, T.
1975. Development of hepatocellular carcinomas in rats treated with
benzene hexachloride. JNCI 54:801-805
LAKKAD, B.C., NIGAM, S.K., KARNIK, A.B., THAKORE, K.N., ARAVINDA BABU, K.,
BHATT, D.K., KASHYAP, S.K. 1982. DominaNt-lethal study of technical-
grade hexachlorocyclohexane in Swiss mice. Mutat Res 101:315-320
KASHYAP, S.K. 1986. Health surveillance and piological monitoring of
pesticide formulators in India. Toxicol Lett 33:107-114 .
MULLER, D., KLEPEL, H., MACHOLZ, R.M., LEWERENZ, H. -J., ENGST, R. 1981.
Electroneurophysiological studies on neurotoxic effects of
hexachlorocyclohexane isomers and gamma-pentachlorocyclohexane. Bull
Environ Contam Toxicol 27:704-706
NIGAM, S.K., KARNIK, A.B., MAJUMDER, S.K., VISWESWARIAH, K., SURYANARAYANA
RAJU, G., MUKTH BAI, K., LAKKAD, B.C., THAKORE, K.N., CHATTERJEE, B.B.
1986. Serum hexachlorocyclohexane residues in workers engaged at a HCH
manufacturing plant. Int Arch Occup Environ Health 57:315-320
SAXENA, M.C., SIDDIQUI, M.K.J., BHARGAVA, A.K., SETH, T.D., KRISHNAMURTI,
C.R., KUTTY, D. 1980. Role of chlorinated hydrocarbon pesticides in
abortions and premature labor. Toxicology 17:323-331
SAXENA, M.C., SIDDIQUI, M.K.J., SETH T.D., KRISHNA MURTI, C.R. 1981a.
Organochlorine pesticides in specimens from women undergoing spontaneous
abortion, premature or full-term delivery. J Anal Toxicol 5:6-9
SAXENA, M.C., SIDDIQUI, M.K.J., BHARGAVA, A.K., KRISHNA MURTI, C.R., KUTTY, D.
1981b. Placental transfer of pesticides in humans. Atch Toxicol
48: 127 -134
SRINIVASAN, K., RAMESH, H.P., RADHAKRINAMURTY, R. 1984. Renal tubular
dysfunction caused dietary hexachlorocyclohexane (HCH) isomers. J.
Environ Sci Health 19:453-466
9-6
THORPE, E. and WALKER, A.I.T. 1973. The toxicology of dieldrin (HEOD). II.
Comparative long-term oral toxicity studies in mice with dieldrin, DDT,
phenobarbitone, beta-BHC, and gamma-BHC, Food Cosmet Toxicol 11:433-
442
U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA). 1991. Integrated Risk
Information System (IRIS). Environmental Criteria and Assessment
Office, Cincinnati, Ohio.
VAN VELSEN, F.L., DANSE, L.H.J., VAN LEEUWEN, F.X.R., DORMANS, J.A.M.A., VAN
LOGTEN, M.J. 1986. The subchronic oral toxicity of the beta-isomer of
hexachlorocyclohexane in rats. Fund Appl Toxicol.6:697-712
Gamma-BHC
DAVIES, J.E., DEDHIA, H., MORGADE, C., et al. 1983. Lindane poisonings.
Arch. Dermatol. 119:142-144
DESI, I., VARGA, L., and FARKAS, I. 1978. Studies on the immunosuppressive
effect of organochlorine and organophosphoric pesticides in subacute
experiments. J. Hyg. Epidemiol. Microbiol. Immunol (Praha) 22:115-122
DEWAN, A., GUPTA, S.K., JAIN, J.P., et al. 1980. Effect of lindane on
antibody response to typhoid vaccine in weanling rats. J. Environ. Sci.
Health. Bl5(3):395-402 .
FITZHUGH, O.G., NELSON, A.A., and FRAWLEY, J.P. 1950. The chronic toxicities
of technical benzene hexachloride and its alpha, beta, and gamma-
isomers. J. Pharmacol. Exp. Ther. 100:59-66
MATSUOKA, L.M. 1981. Convulsions following application of gamma-benzene
hexachloride (letter). J. Am. Acad. Dermatol. 5(1):98-99
MORGAN, D.P., ROBERTS, R.J., WALTER, A.W., et al. 1980. Anemia associated
with exposure to lindane. Arch. Environ. Health 35:307-310
SAMUELS, A.J., and MILBY, T.H. 1971. Human exposure to lindane: Clinical,
hematological, and biochemical effects. J. Occup. Med 13:147-151
SHIVANANDAPPA, T., and KRISHNAKUMARI, M.K. 1983. Hexachlorocyclohexane-
induced testicular dysfunction in rats. Acta. Pharmacol. Toxicol.
52:12-17
THORPE, E., and WALKER, A.I.T. 1973. Toxicology of dieldrin (HEDD). II.
Comparative long-term oral toxicity studies in mice with dieldrin,' DDT,
phenobarbitone, beta-HCH and gamma-HCH. Food Cosmet. Toxicol. 11:433-
442
~
TILSON, H.A., SHAW, S., MCLAMB, and R.L. 1987. The effects of lindane, DDT
and chlordane on avoidance responding and seizure activity. Toxicol.
Appl. Pharmacol. 88(1):57-65
9-7
TURNER, J.C., and SHANKS, V. 1980. Absorption of some organochlorine
compounds by the rat small intestine-in vivo. Bull. Environ. Contam.
Toxicol. 24(5):652-655
U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA). 1984. Health Effects
Assessment for Lindane. Office of Emergency and Remedial Response.
Washington, D.C. EPA 540/1-8-056. September 1984
U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA). 1985. Drinking Water Criteria
Document for Lindane. Final Draft. Environmental Criteria and
Assessment Office. ECAO-CIN-402. March 1984
U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA). 1991a. Integrated Risk
Information System (IRIS). Environmental Criteria and Assessment
Office, Cincinnati, Ohio.
U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA). 1991b. 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. FY-1991
VODOPICK, H. 1975. Erythropoietic hypoplasia after exposure to gamma-benzene
hexachloride. JAMA 24:850-851
WOLFF, G., ROBERTS, D.,
lindane in mice:
8:1889-1897
MORRISSEY, R., et al. 1987. Tumorigenic responses to
Potentiation by a dominant mutation. Carcinogenesis
ZOECON CORPORATION. 1983. MRID No. 00128356. (As cited in EPA 1991a).
Available from EPA
Barium
BRENNIMAN GR, AND LEVY PS. 1984. High barium levels in public drinking water
and its association with elevated blood pressure. In: Advances in
Modern Toxicology IX, E.J., Calabrese, Ed. Princeton Scientific
Publication, Princeton, NJ. p 231-249.
GOYER, R.A. 1986. Toxic effects of metals. In Klaasen, G.D., Amdur, M.D.,
and Doull, J., eds. Casarett and Doull's Toxicology: The Basic Science
of Poisons. 3rd ed. Macmillan Publishing Co., New York. Pp. 623-624
PERRY, H.M., KOPP, S.J., ERLANGER, M.W., and PERRY, E.G. 1983.
XVII. Cardiovascular effects of chronic barium ingestion. In Hemphill,
D.D., ed. Proceedings of he University of Missouri's 17th·Annual
Conference of Trace Substances in Environmental~Health. University of
Missouri Press, Columbia, Missouri (As cited in EPA 1984)
9-8
TARASENKO, M., PROMIN, 0., and SILAYEV, A. 1977.
industrial poisons (an experimental study).
Immunol. 21:361 (As cited in EPA 1984)
Barium Compounds as
J. Hyg. Epiderm. Microbial.
U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA). 1984. Health Effects
Assessment for Barium. Environmental Criteria and Assessment Office,
Cincinnati, Ohio. September 1984. EPA 540/1-86-021
U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA). 1991a. Integrated Risk
Information System (IRIS). Environmental Criteria and Assessment
Office. Cincinnati, Ohio.
U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA). 1991b. Health Effects
Assessment Summary Tables. Prepared by Office of Health and
Environmental Assessment, Environmental Assessment and Criteria Office,
Cincinnati, OH, for the Office of Solid Waste and Emergency Response,
Office of Emergency and Remedial Response, Washington, D.C. FY-1991
WONES, R.G., STADLER, B.L. and FROHMAN, L.A. 1990. Lack of effect of
drinking water barium on cardiovascular risk factor. Environ Health
Perspective. 85:1-13.
Benzoic Acid
GOSSELIN, R.E., SMITH, R.P., and HODGE,
of Commercial Products. 5th ed.
Maryland. P. 203
H.C., eds. 1984. Clinical Toxicology
Williams and Wilkins, Baltimore,
OPDYKE, D.L.J. 1979. Benzoic acid. Monographs on fragrance raw materials.
Food Cosmet. Toxicol. 17(Supplement):715-722
JOINT FAO/WHO EXPERT COMMITTEE ON FOOD ADDITIVES. 1974. Toxicological
Evaluation of Some Food Additives Including Anticaking Agents,
Antimicrobials, Antioxidants, Emulsifiers, and Thickening Agents. FAO
Nutr. Rep. Ser. No. 53A, Rome. WHO/Food Add./74.5. (As cited in Opdyke
1979)
SAX, N.I. 1984. Dangerous Properties of Industrial Materials. 6th ed. Van
Nostrand Reinhold Co., New York. P. 378
U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA). 1991. Integrated Risk
Information System (IRIS). Environmental Criteria and Assessment
Office, Cincinnati, Ohio.
Bis(2-ethylhexyl)phthalate
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
9-9
NATIONAL TOXICOLOGY PROGRAM (NTP). 1982. Carcinogenesis Bioassay of Di(2-
ethylhexyl)phthalate in F344 Rats and B6C3F1 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
U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA). 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
U.S ENVIRONMENTAL PROTECTION AGENCY (USEPA). 1986. Superfund Public Health
Evaluation Manual. Office of Emergency and Remedial Response,
Washington, D.C. EPA 540/1-86-060
U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA). 1991a. Integrated Risk
Information System (IRIS). Environmental Criteria and Assessment
Office, Cincinnati, Ohio.
U. S. ENVIRONMENTAL PROTECTION AGENCY (USEPA). 1991b. 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. FY-1991
Chlordane
INFANTE, P.E., EPSTEIN, S.S, and NEWTON, W.A. 1978. Blood dyscrasias and
childhood tumors and exposure to chlordane and heptachlor. Scand. J.
Work Environ. Health 4:137-150
NATIONAL CANCER INSTITUTE (NCI). 1977. Bioassay of Chlordane for Possible
Carcinogenicity. NCI Carcinogenesis Tech. Rep. Ser. No. 8
U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA). 1985. Draft Health Advisory
for Chlordane. Office of Drinking Water, Washington, D.C.
U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA). 1991. Integrated Risk
Information System (IRIS). Environmental Criteria and Assessment
Office, Cincinnati, Ohio.
VELSICOL CHEMICAL CORPORATION. 1973. Available from EPA. Write to FOI, EPA,
Washington, D.C. 20460
VELSICOL CHEMICAL CORPORATION. 1983. MRID No. 00138591, 00144313. Available
from EPA. Write to FOI, EPA, Washington, D.C. 20460
DDT, DDE, DDD
JENSON, J.A., et al. 1957. DDT metabolites in feces and bile of rats.
Agric. Food Chem. 5:919
9-10
LAUG, E.P., NELSON, A.A., _FITZHUGH, 0.G., and KUNZE, F.M. 1950. Liver cell
alteration and DDT storage in the rat of the rat induced by dietary
levels of 1-50 ppm DDT. J. Pharmacol. Exp. Ther. 98:268-273
MCLACHLAN, J.A., and DIXON, R.L. 1972. Gonadal function in mice exposed
prenatally to p,p'-DDT. Toxicol. Appl. Pharmacol. 22:327
NATIONAL INSTITUTE FOR OCCUPATIONAL SAFETY AND HEALTH (NIOSH). 1978. Special
Occupational Hazard Review: DDT. DHEW Publication No. 78-200
NATIONAL CANCER INSTITUTE (NCI). 1978. Bioassays of DDT, TDE, and p,p'-DDE
for Possible Carcinogenicity. NCI-CG-TR-1321
ROSSI, L., BARBIERI, 0., SANGUINETI, M., CABRAL, J., BRUZZI, P., and SANTI, L.
1983. Carcinogenicity study with technical-grade DDT and DDE in
hamsters. Cancer Res 43:776-781
GOSSELIN R.E., SMITH R.P, AND HODGE H.C. 1984. Clinical Toxicology of
Commercial Products. 5th ed. Williams and Wilkins. Baltimore.
REGISTRY OF TOXIC EFFECTS OF CHEMICAL SUBSTANCES (RTECS). 1987.
Volume 5. U.S. Department of Health and Human Services.
SCHMIDT, R. 1973.
(DDT) on the
317 (German)
[Effects of 1,1,1-trichloro-2,2-bis(p-chlorophenol)-ethane
prenatal development of the mouse.] Biol. Rundsch. 11:316-
TOMATIS, L., TURUSOV, V., CHARLES, R.T., BIOCCHI, M., and GATI, E. 1974.
Liver tumors in CF-1 mice exposed for limited periods to technical DDT.
Z. Krebsforsch. 82:25-35
U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA). 1980. Ambient Water Quality
Criteria Document for DDT. Office of Water Regulations and Standards,
Washington, D.C. EPA 440/5-80-038
U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA). 1984. Health Effects
Assessment Document for DDT. Office of Emergency and Remedial Response,
Washington, D.C.
U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA). 1991. Integrated Risk.
Information System (IRIS). Environmental Criteria and Assessment
Office, Cincinnati, Ohio.
WEISS G. 1986. Hazardous Chemicals Data Book. Noyes Data Corporation. Park
Ridge, New Jersey. 2nd ed.
Dieldrin
DAVIS, K.J., and FITZHUGH, 0.G. 1962. Tumorigenic potential of aldrin and
dieldrin for mice. Toxicol. Appl. Pharmacol. 4:187-189
9-11
DEICHMANN, W.R. 1972. Toxicology of DDT and related chlorinated hydrocarbon pesticides. J. Occup. Med. 14:285-292
FELDMANN, R.J., and MAIBACH, H.I. 1974.
pesticides and herbicides in man.
Percutaneou·s penetration of some
Toxicol. Appl. Pharmacol. 28:126-132
HEALTH, D.F., and VANDEKAR, M. 1964. Toxicity and metabolism of dieldrin in rats. Br. J. Ind. Med. 21:269-279 _,
MURPHY,D.A., and KORSCHGEN, L.F. 1970. Reproduction growth and tissue residues of deer fed dieldrin. Wildlife Mgmt. 34:887-903
NATIONAL CANCER INSTITUTE (NCI). 1978. Bioassays of Aldrin and Dieldrin for Possible Carcinogenicity. DHEW Publication No. (NIH) 78-821. · National Cancer Institute Carcinogenesis Technical Report Series No. 21. NCI-CG-TR-21. 184 pp.
NATIONAL INSTITUTE FOR OCCUPATIONAL SAFETY AND HEALTH (NIOSH). 1978. Special Occupational Hazard Review. Aldrin/Dieldrin. U.S. DHEP Publication No. 78-201
NATIONAL RESEARCH COUNCIL (NRG). 1982. An Assessment of the Health Risks of Seven Pesticides Used for Termite Control. August 1982. NRC-P901. NTIS Publication PB83-136374
OTTOLENGHI, A.D., HASEMAN, J.K., and SUGGS, F. 1974. Teratogenic effects of aldrin, dieldrin, and endrin in hamsters and mice. Teratology 9:11-16
TENNEKES, H.A., WRIGHT, A.S., DIX, K.M., KOEMAN, J.H. 1981. Effects of dieldrin, diet and bedding on enzyme function and tumor incidence in livers of male CF-1 mice. Cancer Res. 41:3615-3620
THORPE, E., WALKER, A.I.T. 1973. The toxicology of _dieldrin
Part II. Comparative long-term oral toxicology studies
dieldrin, DDT, phenobarbitone, beta-BHC and gamma-BHC.
Toxicol. 11:433-441
(HEOD).
in mice with
Food Cosmet.
TREON, J., and CLEVELAND, F.D.
hydrocarbon insecticides
to aldrin and dieldrin.
1955. Toxicity of certain
for laboratory animals with
Agric. Food Chem. J. 3:402
chlorinated
special reference
U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA). 1980. Ambient Water Quality Criteria for Aldrin/Dieldrin. Office of Water Regulations and Standards. October 1980. NTIS Publication No. PB81-117301
U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA). 1991. Integrated Risk Information System (IRIS). Environmental Criteria and Assessment Office, Cincinnati, Ohio
9-12
WALKER, A.I.T., STEVENSON, D.E., ROBINSON, J., THORPE, E., and ROBERTS,
M. 1969. The toxicology and pharmacodynamics of dieldrin (HEOD):
Two-year oral exposures of rats and dogs. Toxicol. Appl.
Pharmacol. 15:345-373
WALKER, A.I.T., THORPE, E., STEVENSON, D.E. 1972. The toxicology of dieldrin
(HEOD). I. Long-term oral toxicity studies in mice. Food. Cosmet.
Toxicol. 11:415-432
Endrin Ketone
APSIMON, J.W., YAMASAKE, K., FRUCHIER, A., CHAU, A.S., and HUBER, C.P., 1982.
Apparent carbon-carcon bond cleavage in an expoxide. 2,J,4,4,5,6-
hexachloro-12-oxopentacyclo(5.4.l.l.011,03,10,05,9)tridecane: A minor
product from the acid treatment of endrin. Can. J. Chem. 60:501-508
WHETSTONE, R.R. 1964. Chlorocarbons and chlorohydrocarbons: chlorinated
derivatives of cyclopentadiene. In Kirk, R.E., and Othmer, D.F., eds.
Encyclopedia of Chemical Technology, Volume 5, 2nd edition, John Wiley
and Sons, New York, pp. 240-252
Manganese
KAWAMURA, R., IKUTA, H., FUKUZUMI, S., et al. 1941. Intoxication by
manganese in well water .. Kitasato Arch. Exp. Med. 18:145-149
LAI, J.C.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
LEUNG, r.K.C., LAI, J.C.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
NRG (NATIONAL RESEARCH COUNCIL). 1989. Recommended Dietary Allowances, 10th
ed. Food and Nutrition Board, National Research Council, National
Academy Press, Washington, D.C. 230-235.
ROELS, H., LAUWERYS, R., BUCHET J-P., ET AL. 1987.
among workers exposed to manganese: Effects
nervous system, and some biological indices.
11:307-327.
Epidemiological
on lung, central
Am. J. Ind. Med.
survey
SARIC, M., MARKICEVIC, S., and HRUSTIC, 0. 1977. Occupational exposure to
manganese. Br. J. Ind. Med. 34:114-118
SCHROEDER, H.A., BALASSA, D.D., AND TIPTON, I.H. 1966. Essential trace
metals in man: Manganese, a study in homeostasis. J. Chron. Dis.
19:545-571.
9-13
U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA). 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
U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA). 1984b. Health Effects
Assessment for Manganese (and compounds). Environmental Criteria and
Assessment Office, Washington, D.C. EPA 540/1-86-057
U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA). 1986. Guidelines for
carcinogen risk assessment. Fed. Reg. 51:33992-34003 (September 24,
1986)
U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA). 1991a. Integrated Risk
Information System (IRIS). Environmental Criteria and Assessment
Office, Cincinnati, Ohio.
U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA). 1991b. 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. FY-1991
WHO (WORLD HEALTH ORGANIZATION). 1973. Trace elements in human nutrition:
Manganese. Report of a WHO Expert Committee. Technical Report Service,
532, WHO, Geneva, Switzerland. 34-36.
Mercury
BERNAUDIN, J.F., DRUET, E., DRUET, P., and MASSE, R. 1981. Inhalation or
ingestion of organic or inorganic mercurials produces auto•imrnune
disease in rats. Clin. Immunol. Immunopathol. 20: 488-494.
DRUET, P., DRUET, E., POTDEVIN, F., and SAPIN, C. 1978. Immune type
glomerulonephritis induced by HgC12 in the brown Norway rat. Ann.
Immunol. 129C:777-792
FAWER, R.F., DERIBAUPIERRE, B., GUILLEMIN, M.P., BERODE, M. and LOBE, M.
1983. Measurement.of hand tremor induced by industrial exposure to
metallic mercury. J. Ind Med. 40: 204-208.
FITZHUGH, O.G., 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.
C.D., and Amdur, M.O., eds.
Science of Poisons. 2nd ed.
Pp. 421-428
1980. Metals. In Doull, J., Klaassen,
Casarett and Doull's Toxicology: The Basic
Macmillan Publishing c·o. , New York.
9-14
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. Mu_tagenicity, Carcinogenicity and
Teratogenicity of Industrial Pollutants. Plenum Press, New York.
Pp. 59-126
PIIKIVI, L. 1989. Cardiovascular reflexes and low long-term exposure to
mercury vapor. Int Arch Occup Environ Health 61:391-395.
PIIKIVI, L. and HANNINEN, H. 1989. Subjective symptoms and psychological
performance of chlorine-alkali workers. Scand J Work Environ Health.
15:69-74.
PIIKIVI, L. and TOLONEN, V. 1989. EEG findings in chloro-alkali workers
subjected to low long-term exposure to mercury vapor. Br J. Ind MEd.
46:370-375.
RAHOLA, T., HATTULA, T., KORLAINEN, A., and MIETTINEN, J.K. 1971. The
biological halftime of inorganic mercury (Hg2+) 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
U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA). 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
U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA). 1984. Health Effects
Assessment for Mercury. Environmental Criteria and Assessment Office,
Cincinnati, Ohio. EPA 540/1-86-042
U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA). 1991. 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. FY-1991
WORLD HEALTH ORGANIZATION (WHO). 1976. Environmental Health Criteria,.
Mercury. Geneva
4-Methyl-2-pentanone
AMERICAN CONFERENCE OF GOVERNMENTAL INDUSTRIAL HYGIENISTS (ACGIH). 1986.
Documentation of the Threshold Limit Values and Biological Exposure
Indices. 5th ed. Cincinnati, Ohio. P. 402
9-15
ELKINS, H. 1959. The Chemistry of Industrial Toxicology. 2nd ed. John Wiley and Sons, New York. P. 121.
MACEWEN, J.D., VERNOT, E.H., and HAUN, C.C.
Continuous Exposure to Methyl Isobutyl
National Technical Information Service.
1971. Effect of 90-Day
Ketone on Dogs, Monkeys
AD Rep. ISS-730291
and Rats.
MICROBIOLOGICAL ASSOCIATES. 1986. Subchronic Toxicity of Methyl Isobutyl Ketone in Sprague-Dawley Rats. Preliminary report of Research Triangle Institute, Research Triangle Park, North Carolina. Study No. 5221.04. January 1986
UNION CARBIDE CORPORATION. 1983. Ninety-Day Inhalation Study in Rats and Mice Sponsored by CMA. U.S. EPA/OTS public files 0757577469
U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA). 1986. Methyl Isobutyl Ketone in Sprague-Dawley Rats.
Washington, D.C. (As cited in EPA 1989a)
Subchronic Toxicity of
Office of Solid Waste,
U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA). 1991a. Integrated Risk Information System (IRIS). Environmental Criteria and Assessment
Office, Cincinnati, Ohio.
U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA). 1991b. 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. FY-1991
Toxaphene
ALLEN, A.L., KOLLER, L.D., POLLOCK, G.A. 1983. Effect of toxaphene exposure on immune responses in mice. J Toxicol Environ Health 11:61-69
BOOTS HERCULES AGROCHEMICALS INC. n.d. Boots Hercules toxaphene insecticide summary of toxicological investigations. Bulletin T-105d
BOYD, E.M. and TAYLOR, F.I. 1971.
rats. Toxicol Appl Pharmacol
Toxaphene toxicity in protein-deficient
18:158-167
CHANDURKAR, P.S. and MATSUHARA, F. 1979. Metabolism of toxaphene components in rats. Arch Environ Contam Toxicol 8:1-24
CHU, I., VILLENEUVE, D.C., SUN, C.W., SECOURS, V., PROCTER, B., ARNOLD, _E., CLEGG, D., REYNOLDS, L., VALLI, V.E. 1986. Toxicity of toxaphene in the rat and beagle dog. Fund Appl Toxicol 7 :·406-418
CHU, I., SECOURS, V, VILLENEUVE, D.C., VALLI, V.E., NAKAMURA, A., COLIN, D., CLEGG, D.J., ARNOLD, E.P. 1988. Reproduction study of toxaphene in the rat. J Environ Sci Health (B) 23:1010-126
9-16
CROWDER, L.A. and DINDAL, .E.F. 1974. Fate of chlorine-36-labeled toxaphene
in rats. Bull Environ Contam Toxicol 12:320-327
DiPIETRO, J .A., HALIBURTON, J.C. 1979. Toxaphene· toxicosis in swine. J Am
Vet Med Assoc 175:452-453
FITZHUGH, O.G. and NELSON, A.A. 1951. Comparison of chronic effects produced
in rats by several chlorinated hydrocarbon insecticides. Fed. Proc.
10:295
KOLLER, L.D., EXON, J.H., NORBURY, K.C. 1983. Induction of humoral immunity·
to protein antigen without adjuvant in rats exposed to immunosuppressive
chemicals. J Toxicol Environ Health 12:173-181
LITTON BIONETICS. 1978. Carcinogenic evaluation in mice. Toxaphene. Final
report. Wilmington, DE: Sponsored by Hercules, Inc. Submitted to US
Environmental Protection Agency, Office of Special Pesticide Review
Division, Washington, DC. LBI Project No. 20602, Kensington, MD
McGEE, L.C., REED, H.L., FLEMING, J.P. 1952. Accidental poisoning by
toxaphene: Review of toxicology and case reports. JAMA 149:1124-1126
MEHENDALE, H.M.
function:
16:19-25
1978. Pesticide-induced modification of hepatobiliary
Hexachlorobenzene, DDT, and toxaphene. Food Cosmet Toxicol
MOHAMMED, A., HALLBERG, E., RYDSTROM, J., SLANINA, P. 1985. Toxaphene:
Accumulation in the adrenal cortex and effect on ACTH-stimulated
corticosteroid synthesis in the rat. Toxicol Lett 24:137-143
NCI. 1977. Bioassay of toxaphene for possible carcinogenicity. Bethesda,
MD: National Cancer Institute, Division of Cancer Cause and Prevention,
Carcinogenesis Testing Program. DHEW/PUB/NIH-79-837; NCI-CG-TR-37; PB-
292290, 105
OLSON, K.L., MATSUMURA, F., BOUSH, G.M. 1980. Behavioral effects on juvenile
rats from perinatal exposure to low levels. Arch Environ Contam Toxicol
9:247-257
PARIS, D.F. and LEWIS, D.L. 1973. Chemical and microbial degradation of ten
selected pesticides in aquatic systems. Residue Rev 45:95-124
PEAKALL, D.B. 1976. Effects of toxaphene on hepatic enzyme induction and
circulating steroid levels in the rat. Environ Health Perspect 30:97-
98
SAMOSH, L.V. 1974. Chromosome aberrations and character of satellite
associations after accidental exposure of the human body to
polychlorocamphene. Cyto Genet (Engl) 8:24-27
9-17
TROTTMAN, C.H. and DESAIAH, D. 1980. Induction of rat hepatic microsomal
enzymes by toxaphene pretreatment. J Environ Sci Health B 15:121-134
U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA). 1980. Ambient Water Quality
Criteria for Toxaphene. Environmental Criteria and Assessment Office,
Cincinnati, Ohio. EPA 440/5-80-076. NTIS PB 81-117863
U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA). 1991. Integrated Risk
Information System (IRIS). Environmental Criteria and Assessment
Office, Cincinnati, Ohio.
WARRAKI, S. 1963. Respiratory hazards of chlorinated camphene. Arch.
Environ. Health 7:253-256
1,2,4-Trichlorobenzene
BLACK, W.D., VALLIE, V.E.O., RUDDICK, J.A., and VILLENEUVE, D.C. 1983. The
toxicity of three trichlorobenzene isomers in pregnant rats. The
Toxicologist 3:30
BROWN, V.K.H., MUIR, C., and THORPE, E. 1969. The acute toxicity and skin
irritant properties of 1,2,4-trichlorobenzene. Ann. Occup. Hyg.
12:209-212
CARLSON, G.P. 1977. Chlorinated benzene induction of hepatic porphyria.
Experientia 33:1627-1629
CARLSON, G.P., and TARDIFF, R.G. 1976.
the metabolism of foreign organic
36:383-394
Effect of the chlorinated benzenes on
compounds. Toxicol. Appl. Pharmacol.
COATE, W.B., SCHOEFISCH, W.H., LEWIS, T.R., and BUSEY, W.M. 1977. Chronic
inhalation exposure of rats, rabbits, and monkeys to 1,2,4-trichloro-
benzene. Arch. Environ. Health 32:249-255
KITCHIN, K.T., and EBRON, M.T. 1983. Maternal hepatic and embryonic effects
of 1,2,4-trichlorobenzene in the rat. Environ. Res. 31:362-373
KOC IBA, R.J., LEONG, B .K., and HEFNER, R. E., Jr.
study of 1,2,4-trichlorobenzene in the rat,
Drug Chem. Toxicol. 4:229-249
1981. Subchronic toxicity
rabbit, and beagle dog.
POWERS, M.B., COATE, W.B., and LEWIS, T.R. 1975. Repeated topical
applications of 1,2,4-trichlorobenzene: Effects on rabbit ears. Arch.
Environ. Health 30:165-167
SMITH, C.C., CRAGG, S.T., and WOLFE, G.F. 1978. Subacute toxicity of
1,2,4-trichlorobenzene (TCB) in subhuman primates. Fed. Proc. 37:248
9-18
U.S ENVIRONMENTAL PROTECTION AGENCY (USEPA). 1985.
Document for Chlorinated Benzenes. Office of
Assessment. Washington, D.C. January .1985.
Health Assessment
Health and Environmental
EPA/600/8-84/0lSF
U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA). 1991. 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. FY-1991
WATANABE, P.G., KOCIBA, R.J., HEFNER, R.E., Jr., YAKEL, H.O., and LEONG,
B.K.J. 1978. Subchronic toxicity studies of 1,2,4-trichlorobenzene in
experimental animals. Toxicol. Appl. Pharmacol. 45:322-333
YAMAMOTO, H. , OHNO, Y. , NAKAMORI, K. , OKUYAMA, T. , IMAI, S. , and ISUBURA, Y.
1957. [Chronic toxicity and carcinogenicity test of 1,2,4-trichloro-
benzene on mice by dermal painting.] J. Nara. Med. Assoc. 33:132-145
(Japanese)
Trichloroethene
AMERICAN CONFERENCE OF GOVERNMENTAL 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.
Cincinnati, Ohio.
Environmental Criteria and Assessment Office,
EPA 540/1-86-046
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). 1991. 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. FY-1991
FUKUDA, K., TAKEMOTO, K., and TSURUTA, H. 1983. Inhalation carcinogenicity
of trichloroethylene in mice and rats. Ind. Health 21:243-254 ·
GREIM, H., BIMBOES, D., EGERT, G., GIGGELMANN, W., and KRAMER, M. 1977.
Mutagenicity and chromosomal aberrations as an analytical tool for in
vitro detection of mammalian enzyme-mediated formation of reactive
metabolites. Arch. Toxicol. 39:159
9-19
KIMMERLE, G., 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)
MALTONI, C., LEFEMINE, G., COTTI, G. 1986. Experimental Research on
Trichloroethylene. Carcinogenesis Arch. Res. Industrial Carcinogenesis
Series. Maltoni, C., Mehlman, M, A., Eds. Vol. V. Princeton
Scientific Publishing Co., Inc., Princeton, NJ. p. 393
NATIONAL CANCER INSTITUTE (NCI).
Trichloroethylene. GAS No.
Series No. 2. PB-264 122
1976. Carcinogenesis Bioassay of
79-01-6. Carcinogenesis Technical Report
NATIONAL TOXICOLOGY PROGRAM (NTP). 1983. Carcinogenesis Studies of
Trichloroethylene (Without Epichlorohydrin), GAS No. 79-01-6,
rats and B6C3F1 mice (Gavage Studies). Draft. August 1983.
NTP TR 243.
in F344/N
NTP 81-84,
STEPHENS, C. 1945. Poisoning by accidental drinking of trichloroethylene.
Br. Med. J. 2:218
TORKELSON, T.R., and ROWE, V.K. 1981. Halogenated aliphatic hydrocarbons.
In Clayton, G.D., and Clayton, P.B., eds. Patty's Industrial Hygiene
and Toxicology. 3rd ed. John Wiley and Sons, New York. Vol. 2B,
pp. 3553-3559
Vanadium
BROWNING, E. 1969. Toxicity of Industrial Metal. 2nd ed. Appleton-Century-
Crofts, New York
NATIONAL ACADEMY OF SCIENCES (NAS). 1974. Vanadium. Committee on Biological
Effects of Atmospheric Pollutants, Division of Medical Sciences,
National Research Council, Washington, D.C.
NATIONAL INSTITUTE OF OCCUPATIONAL SAFETY AND HEALTH (NIOSH). 1977.
for a Recommended Standard--Occupational Exposure to Vanadium.
(NIOSH) Publication No. 77-222
Criteria
DHEW
SCHROEDER, J.A., MITCHNER, M., and NASON, A.P. 1970. Zirconium, niobium,
antium, antimony, vanadium and lead in rats: Life term studies.
J. Nutr. 100(1):59-68
9-20
STOKINGER, H.E., WAGNER, W.E., MOUTAIN, J.T., STACKSILL, F.R., DOBROGORSKI,
O.J., and KEENAN, R.G. 1953. Unpublished Results. National Institute
for Occupational Safety and Health, Div.ision of Occupational Health,
Cincinnati~ Ohio
U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA). 1991a. Integrated Risk
Information System (IRIS). Health Criteria and Assessment Office,
Cincinnati, Ohio
U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA). 1991b. 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. FY-1991
Zinc
HAMMOND, P.B., and BELILES, R.P. 1980. Metals. In Doull, J., Klaassen,
Casarett and Doull's Toxicology: The Basic
Macmillan Publishing Co., New York.
G.D., and Amdur, M.O., eds.
Science of Poisons. 2nd ed.
Pp. 409-467
PORIES, W.J., HENZEL, J.H., ROB, C.G., and STRAIN, W.H. 1967.
of wound healing in man with zinc sulfate given by mouth.
1:121-124
Acceleration
Lancet.
PRASAD, A.S., SCHOOMAKER, E.B., ORTEGA, J., et al. 1975. Zinc deficiency in
sickle cell disease. Clin. Chem. 21:582-587
U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA). 1984.
Assessment for Zinc (and Compounds). Office of
Response,.Washington, D.C. EPA 540/1-86-048.
Health Effects
Emergency and Remedial
September 1984
·u.s. ENVIRONMENTAL PROTECTION AGENCY (USEPA). 1990. 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. September
1990
SECTION 4.0
AGENCY FOR TOXIC SUBSTANCES AND DISEASE REGISTRY (ATSDR). 1989. Toxicity
Profile for Alpha-, Beta-, Gamma-and Del ta-Hexachlorocyclohexane·, U.S.
Public Health Service, ATSDR #205-88-0608
AGENCY FOR TOXIC SUBSTANCES AND DISEASE REGISTRY (ATSDR). 1989. Toxicity
Profile for Chlordane, U.S. Public Health Service, ATSDR #205-88-0608
9-21
AGENCY FOR TOXIC SUBSTANCES AND DISEASE REGISTRY (ATSDR). 1989. Toxicity
Profile for DDT, DDE and DDD, U.S. Public Health Service, ATSDR #205-88-
0608
AGENCY FOR TOXIC SUBSTANCES AND DISEASE REGISTRY (ATSDR). 1990. Toxicity
Profile for Toxaphene, U.S. Public Health Service, ATSDR #205-88-Q608
AGENCY FOR TOXIC SUBSTANCES AND DISEASE REGISTRY (ATSDR). 1991. Toxicity
Profile for Aldrin/Dieldrin, U.S. Public Health Service, ATSDR #205-88-
0608
BLANK, I.H., MOLONEY, J., ALFRED, B.S., SIMON, I., and APT.," C. 1984. The
Diffusion of Water Across the Stratum Corneum as a.Function of its Water
Content. J. Invest. Derm. 82:188-194
BOMBERGER, D.C., GWINN, J.L., MABEY, W.R., TUSE, D. and CHOU, T.W. 1983.
Environmental Fate and Transport at the Terrestrial-Atmospheric
Interface. In: Fate of Chemicals in the Environment. Compartment and
Multimedia Models for Predictions. American Chemical Society.
Washington, D.C. 1983
BROOKS, G.T. 1977. Chlorinated Insecticides:
Pesticide Chemistry in the 20th Century.
Washington, D.C.
Retrospect and Prospect.
ACS Symposium Series 37.
BRONAUGH, R.L., and STEWART, R.F. 1986. Methods for in vitro percutaneous
absorption studies. VI. Preparation of the barrier layer. J. Pharm.
Sci. 75, 487-491.
BUREAU OF LABOR STATISTICS (BLS). 1991. Statistical Summary: Tenure· with
Current Employer as of January 1987. (Transmitted via facsimile July 1,
1991)
CACI MARKETING SYSTEMS. 1991. Geigy Chemical Corporation Site 0-1 mile
radius. 1990 Census Detailed Age Profile.
CALABRESE, E.J., BARNES, R., STANEK, E.J., PASTIDES, H., GILBERT, C.E.,
VENEMAN, P., WANG, S., LASZTITY, A., and KOSTECK, P.T. 1989. How much
soil do young children ingest: An epidemiologic study. Reg. Tox. and
Pharma. 10:123-137
COWHERD, C., MULESKI, G.E., ENGLEHART, P.J., and GILLETTE, D.A. 1985. Rapid
Assessment of Exposure to Particulate Emissions from Surface
Contamination Sites. Midwest Research Inst., Kansas City, MO. PB85-
192219
DRIVER, J.H., KONZ, J.J. and WHITMYRE, G.K. 1989. Soil Adherence to Human
Skin. Bull. Environ. Contam. Toxicol. 53:814-820
9-22
EDWARDS, C.A. 1966. Insecticide residues in soils. Residue Reviews. 13:83-
132
ERM -Southeast, Inc. 1991. Draft Report Remedial ·I'nvestigation Study.
Geigy Chemical Corporation Site, Aberdeen, North Carolina.
FELDMAN, R.J. AND MAIBACH, H.I.
through the skin in man.
1970. Absorption of some or·ganic compounds
J. Invest. Derm. 54:399-404
FELDMAN, R.J. AND MAIBACH, H.I. 1974. Percutaneous Penetration of Some
Pesticides and Herbicides in Man. Tox. and Appl. Pharm. 28:126-132
FOSTER, S.A., and CHROSTOWSKI, P.C. 1986. Integrated Household Exposure
Model for Use of Tap Water Contaminated with Volatile Organic Chemicals.
Presented at the 79th Annual Meeting of the Air Pollution Control
Association. Minneapolis, Minnesota. June 22-27, 1986.
FOSTER, S.A. and CHROSTOWSKI, P.C. 1987.
Organic Contaminants in the Shower.
Meeting of APCA, New York, New York.
Inhalation Exposures to Volatile
For Presentation at the 80th Annual
June 21-26, 1987
FRASER, J.L. and LUM, K.R. 1983. Availability of elements of environmental
importance in incinerated sludge ash. Environ. Sci. Technol. 17:52-54
GILBERT, R.O. 1987. Statistical Methods for Environmental Pollution
Monitoring. Van Nostrand Reinhold, New York
GOTFELTY, D.E., TAYLOR, A.W., and ZOLLER, W.H. 1984. Volatilization of
Surface-Applied Pesticides from Fallow Soil. J. Agric. Food Chem.
32:638-643
HAWKINS, G.S., Jr., AND REIFENRATH, W.G. 1984. Development of an in vitro
model for determining the fate of chemicals applied to skin. Fundam.
Appl. Toxicol. 28, 126-131.
JAQUESS, A.B., WINTERLIN, W. and PETERSON, D. 1989. Feasibility of Toxaphene
Transport through Sandy Soil. Bull. Environ. Contam. Toxicol. 42:417-
423
JURY, W.A., SPENCER, W.F. and FARMER, W.J. 1983. Behavior Assessment Model
for Organics in Soil: I. Model Description. J. Environ. Qual., Vol.
12, No. 4.
JURY, W.A., SPENCER, W.F. and FARMER, W.J. 1984. Behavior Assessment Model
for Trace Organics in Soil: Ch. II through IV. J. Environ. Qual; Vol.
13, No. 4
JURY, W.A., WINTER, A.M., SPENCER, W.F. et al.
transformation of organic chemicals in the
Rev. Environ. Contam. Toxicol. 99:119-164
9-23
1987. Transport and
soil-air-water ecosystem.
KLAASSEN, G.D., AMOUR, M.0., DOULL, J., 1986.
Toxicology The Basic Science of Poisons.
3rd Edition.
Casarett and Coull's
Macmillan Publishing Company,
LAND, C.E. 1975. Table of confidence limits for linear functions of the
normal mean and variance. Math. Stat. Vol. III. Pp. 385-419
LUCIER, G.W., RUMBAUGH, R.C., McCOY, Z., HASS, R., HARVAN, D., and ALBRO, K.
1986. Ingestion of soil contaminated with 2,3,7,8-tetrachlorodibenzo-p-
dioxin (TCDD) alters hepatic enzyme activities in rats. Fund. and Appl.
Toxicol. 6:364-481
McCONNEL, E.E., LUCIER, G.W., RUMBAUGH, R.C., ALBRO, P.W., HARVAN, D.J., HASS,
J.R., and HARRIS, M.W. 1984. Dioxin in Soil: Bioavailability after
Ingestion by Rats and Guinea Pigs. Science. 223:1077-1079
McLAUGHLIN, T. 1984. Review of Dermal Absorption. Office of Health and
Environmental Assessment. USEPA, Washington, D.C. EPA/600/8-84/033.
MICHAELS, A.S., CHANDRASEKARAN, S.K., and SHAW, J.E. 1975. Drug permeation
through human skin: Theory and in vitro experimental measurements.
AIChE J. 21:985-996
MILLINGTON, R.J. and QUIRK, J.P. 1961. Permeability of porous solids.
Trans. Faraday Soc. 57:1200-1207
NASH, R.G. 1983. Comparative volatilization and dissipation rates of several
pesticides from soil. J. Agric. Food Chem. 31:210-217
NATIONAL OCEANIC ATMOSPHERIC ADMINISTRATION (NOM). 1989. Local
Climatological Data. Annual Summary with Comparative Data. Raleigh, NC
NATIONAL COUNCIL ON RADIATION PROTECTION AND MEASUREMENT (NCRP). 1985.
Radiological Assessment: predicting the transport, bioaccumulation, and
uptake by man of radionuclides released to the environment. NCRP Report
No. 76. Bethesda, MD Pp. 210
NUS Corporation Superfund Division. 1988. Analytical Results, Sample
Locations· and Descriptions, Site Investigation, Geigy Chemical
Corporation Site, Aberdeen, North Carolina. Prepared under TDD No. 54-
8702-51 Contract No. 68-61-7346, for the Waste Management Division,
USEPA, March 1988,
POIGER, H. and SCHLATTER, C. 1980, Influence of solvents and adsorbents on
dermal and intestinal absorption of TCDD. Fd. Cosmet. Toxicol. 17:477-
481
ROSCOE, G.A. 1987.
Assessments.
1987.
Analysis of Risk Distribution in Superfund Risk
Memo to EPA Region I Risk Assessment Workgroup. May 12,
9-24
SEDMAN, R.M. 1989. The development of applied levels for soil contact: A
scenario for the exposure of humans to soil in a residential setting.
Env. Health Perspec. 79, 291-313
SIRRINE ENVIRONMENTAL. 1991. Draft Report of the Feasibility Study: Geigy
Chemical Corporation Site, Aberdeen, North Carolina
U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA). 1979. Water-Related
Environmental Fate of 129 Priority Pollutants. EPA Contract No. 68-01-
3852 and 68-01-3867
U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA). 1985. Development of
Statistical Distribution or Ranges of Standard Factors Used in Exposure
Assessments. Office of Health and Environmental Assessment, Washington,
D.C. March 1985. Final Report. OHEA-E-161
U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA). 1986. Developments of Advisory
Levels for Polychlorinated Biphenyls (PCBs) Cleanup. EPA, Office of
Health and Environmental Assessment. Washington, D.C. OHEA-E-187
U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA). 1987. Industrial Source
Complex (ISC) Dispersion Model User's Guide-Second Edition (Revised).
Vol. I. EPA, Office of Air Quality Planning and Standards, Research
Triangle Park, North Carolina. EPA-450/4-88-002a.
U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA). 1988. Superfund Exposure
Assessment Manual. Office of Emergency and Remedial Response.
EPA/540/1-88/001. OSWER Directive 9285.1
U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA). 1989a. Risk Assessment
Guidance for Superfund. Volume I: Human Health Evaluation Manual. (Part
A). Interim Final. EPA/540/1-89/002. December 1989
U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA). 1989b. Exposure Factors
Handbook. Office of Health and Environmental Assessment, Washington,
D.C. July
U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA). 1990a.
hazardous substances pollution contingency plan.
(March 8, 1990).
National oil and
Fed. Reg. 55:8666-8865
U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA). 1991a. Risk Assessment
Guidance for Superfund. Volume I: Human Health Evaluation Manual
Supplemental Guidance. Standard Default Exposure Factors. Interim
Final. Washington, D.C. OSWER Directive 9285.6-03. March 25, 1991
VAN DEN BERG, M., SINKE, M., and WEVER, H. 1987. Vehicle Dependent
Bioavailability of Polychlorinated Dibenzo-p-Dioxins (PCDDs) and
Dibenzofurans (PCDFs) in the Rat. Chemosphere, Vol. 16, pp. 1193-1203.
9-25
WENDLING, J. , HILEMEAN, F_. , ORTH, R. , UMBREIT, T. , HESSE, E. , and GALLO, M.
1989. An analytical assessment of the bioavailability of dioxin
contaminated soils to animals. Chemosphere. 18:925-932
\JESTER, R.C., MAIBACH, H.I., BUCKS, D.A.IJ., SEDIK, L., MELENDRES, J., LIAO, . . and DIZIO, S. 1990. Percutaneous Absorption of Benzo[a]pyrene from
Soil. Fundamental and Applied Toxicol. 15:510-516.
YANG, J.J., ROY, T.A., KRUGER, A.J. NEIL, IJ. and MACKERER, C.R. 1989. In
vitro and In vivo percutaneous absorption of benzo[a]pyrene from
petroleum crude-fortified soil in the rat. Bull. Environ. Contam.
Toxicol. 43:207-2142
9-26
_c
SECTION 5.0
SIRRINE ENVIRONMENTAL. 1991. Draft Report of the Feasibility Study: Geigy
Chemical Corporation Site, Aberdeen, North Caro1ina
U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA). 1989. Risk Assessment Guidance
for Superfund. Volume I: Human Health Evaluation Manual. (Part A).
Interim Final. EPA/540/1-89/002. December 1989
U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA). 1990. National oil and
hazardous substances pollution contingency plan. Fed. Reg.
555:8666-8865 (March 8, 1990)
SECTION 6,0
CATHEY, B. 1982. Comparative Toxicities of Five Insecticides to the
Earthworm, Lumbricus tenestris. Agric. and Env. 7:73-81
EDWARDS, C.A. and LOFTY, J.R. 1972. Biology of Earthworms. Bookworm
Publishing Company
ENO, C.F. and EVERETT, P.H. 1958. Effects of Soil Applications of 10
Chlorinated Hydrocarbon Insecticides on Soil Microorganisms and the
Growth of Stringless Black Valentine Beans. Soil. Sci. Soc. Am. Proc.
22:235-238
FOX, C.J.S. 1967. Effects of Several Chlorinated Hydrocarbon Insecticides on
the Springtails and Mites of Grassland Soil. J. Econ. Ent. 60(1):77-79
HOPKINS, A. and KIRK, V.M. 1957. Effect of Several Insecticides on the
English Redworm. J. Econ. Ent. 50(5):699-700
REINECKE, A.J. and VENTER, J.M. 1985. Influence of dieldrin on the
reproduction of the earthworm Eisenia fetida (Oligochaeta). Biol.
Fertil. Soils 1:39-44
U.S. DEPARTMENT OF AGRICULTURE (USDA). 1974. Rare and Endangered Birds of
the Southern National Forests. USDA Forest Service. Southern Region.
van GESTEL, C.A.M. and MA, W-C. 1988. Toxicity and Bioaccumulation of
Chlorophenols in Earthworms, in Relation to Bioavailability in Soil.
Ecotox. Environ. Safety. 15:289-297
SECTION 7 .0
AGENCY FOR TOXIC SUBSTANCES AND DISEASE REGISTRY (ATSDR). 1989. Toxicity
Profile for DDT, DDE and DDD, U.S. Public Health Service, ATSDR #205-88-
0608
9-27
AGENCY FOR TOXIC SUBSTANCES AND DISEASE REGISTRY (ATSDR). 1991. Toxicity Profile for Aldrin/Dieldrin, U.S. Public Health Service, ATSDR #205-88-0608
BINDER, S., SOKAL, D. and MAUGHAN, D. 1986. Estimating Soil Ingestion: The Use of Tracer Elements in Estimating the Amount of Soil Ingested by Young Children. Arch. Env. Hlth. (41)341-345
BUREAU OF LABOR STATISTICS (BLS). 1991. Statistical Summary: Tenure with Current Employer as of January 1987. (Transmitted via facsimile July 1, 1991)
BUTLER, W.H. and NEWBERNE, P,M. 1975. Mouse Hepatic Neoplasia. Proceedings of a Workshop held at the H.T.S. Management Centre, Lane End, High Wycombe (Great Britain) 12-17 May 1974
CALABRESE, E.J., BARNES, R., STANEK, E.J., PASTIDES, H., GILBERT, C.E., VENEMAN, P., WANG, S., LASZTITY, A., and KOSTECK, P.T. 1989. How much ·soil do young children ingest: An epidemiologic study. Reg. Tax. and Pharma. 10:123-137
CALABRESE, E.J., STANEK, E.J., GILBERT, C.E. and BARNES, R.M. 1990. Preliminary Adult Soil Ingestion Estimates: Results of a Pilot Study. Regulatory Toxicology and Pharm. 12:88-95
CHROSTOWSKI, P.C., FOSTER, S.A. and DOLAN, D. 1991. Monte Carlo Analysis of the Reasonable Maximum Exposure (RME) Concept. Proceedings of the
Hazardous Materials Control '91 Conference. December 3-5, 1991
CHROSTOWSKI, P.C. and WHEELER, J.K. 1991. Actual vs. Predicted Chemical Exposures at Superfund Sites. For presentation at the Hazardous
Materials Control '91 Conference. December 3-5, 1991
CLEMENT INTERNATIONAL CORPORATION. 1990. Estimation of Exposure and Risk for Superfund Baseline Risk Assessments. Fairfax, VA
INTERNATIONAL AGENCY FOR RESEARCH ON CANCER (IARC). 1987. Overall Evaluations of Carcinogenicity: An Updating of IARC Monographs. Volume 1 to 42. IARC Monographs on the Evaluation of Carcinogenic Risks to Humans. Supplement 7
NATIONAL CANCER INSTITUTE (NCI). 1978. Bioassays of DDT, TDE, and p,p'-DDE for possible carcinogenicity. NCI Carcinogenesis Technical Report Series. No. 131
NEWBERNE, P.M., SUPHAKARN, V., PUNYARIT, P. and DeCAMARGO, J. 1987.
Nongenotoxic Mouse Liver Carcinogens. Banbury Report 25: Nongenotoxic
Mechanisms in Carcinogenesis.
POPP, J.A. 1984. Mouse Liver Neoplasia, Current Perspectives. Hemisphere Publishing Corporation, Washington
9-28
SHINDELL, S. and ULRICH, S. 1986. Mortalities of workers employed in the
manufacture of chlordane: an update. J. Occup. Med. 28:497-501
SMITH, A.G. 1991. Chapter 15: Chlorinated Hydrocarbon Insecticides.
Handbook of Pesticide Toxicol. 2:731-740
STANEK, E.J. and CALABRESE, E.J. 1991. A guide to interpreting soil
ingestion studies. Reg. Tox. and Pharma. 13:263-277
THOMPSON, K.M and BURMASTER, D.E. 1991. Parametric Distributions for Soil
Ingestion by Children. Risk Analysis. (11)2: 339-342
U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA). 1986a. Guidelines for
Carcinogenic Risk Assessment. Federal Register 51:33992-34003
U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA). 1986b. Guidelines for the
Health Risk Assessment of Chemical Mixtures .. Federal Register 51:34014-
34023.
U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA). 1989. Risk Assessment Guidance
for Superfund. Volume I: Human Health Evaluation Manual. (Part A).
Interim Final. EPA/540/1-89/002. December 1989
U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA). 1991a. Risk Assessment
Guidance for Superfund. Volume I: Human Health Evaluation Manual
Supplemental Guidance. Standard Default Exposure Factors. Interim
Final. Washington, D.C. OSWER Directive 9285.6-03. March 25, 1991
U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA). 1991b. Integrated Resource
Information Systems (IRIS). Environmental Criteria and Assessment
Office, Cincinnati, OH.
U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA). 1991c. Health Effects
Assessment Summary Tables. Prepared by Office of Health and
Environmental Assessment, Environmental Assessment and Criteria Office,
Cincinnati, OH, for the Office of Solid Waste and Emergency Response,
Office of Emergency and Remedial Response, Washington, D.C. FY-1991.
WANG, H. and MACMAHON, B. 1979. Mortality of workers employed in the
manufacture of chlordane and heptachlor. J. of Occupational Med. 21:
745-748
9-29
APPENDIX A
EPA REGION IV GUIDANCE FOR DATA SUMMARY
The arithmetic mean presented in these tables was calculated using detected
values only as per USEPA Region IV guidance (USEPA 1991b) and differs from the
one used in the human health assessment for the average case scenario.
A-1
TABLE A-1
SUMMARY OF CHEMICALS IN SURFACE SOIL/SEDIMENT
(Organics: ug/kg, Inorganics: mg/kg)
Mean Site-Specifc Range of Frequency of Sample Arithmetic Range of Detected Background Background
Chemical Detection (c) Size Cd) Mean (e) Concentrations Concentrations(f) Concentrations(g)
ON-SITE (a)
Organics: --------* Aldrin 2 I 80 2 5.9 5.9 ND (<8.5 to <9.2) * alpha-BHC 6 / 80 6 390 13 1,500 ND (<8.5 to <9.2) * beta-BHC 28 I 80 28 250 4.4 2,000 ND (<8.5 to <9.2) * delta-BHC 3 / 80 3 340 33 · 840 ND (<B.5 to <9.2) * garrrna-BHC 3 / 80 3 240 41 • 620 ND (<8.5 to <9.2) * Benzoic acid 3 I 3 3 1,400 200 · 3,600 ND (<3,200) * alpha-Chlordane 1 / 80 1 45 45 ND (<85 to <92) * garrma-Chlordane 1 / 80 1 49 49 NO (<85 to <92) * 4,4'-000 73 I 80 73 1,400 7.7 · 15,000 9.2 · 32 * 4,4'-DOE 80 I 80 80 1,100 3.7 · 11,000 11 · 76 * 4,4' -DOT 80 I 80 80 3,700 9.4 · 54,000 33 · 110 * Dieldrin 7 I 80 7 390 11 · 1,500 ND (<17 to <18) * Toxaphene 66 / 80 66 19,000 340 · 220,000 180 • 260
lnorganics:
----------Alllllim.1n 3 / 3 3 6,400 1,820 · 9,630 2,140 · 2,660 50,000 100,000 Arsenic 3 / 3 3 1.7 0.8 · 2.4 0.7 1 .2 7.6 BarilJJI 3 / 3 3 20 14.3 • 22.7 8.9 300 700 Beryllium 1 / 3 1 0. 1 0. 1 ND 0.01 40
Calcitin 3 / 3 3 2,200 687 • 4,750 105 · 907 4,000 8,50D Chromil.111 3 / 3 3 5. 1 2.8 · 6.8 2.1 · 2.7 15 70 Copper 71 / 74 71 13 2.6 • 37.7 2.7 · 5.6 30 Iron 3 / 3 3 5,300 2,810 • 7,080 1,380 • 1,640 20,0DO · 70,000 Lead 80 I 80 80 55 1.4 · 336 7.6 • 90.2 Magnesillll 2 I 2 2 1,100 208 · 2,000 158 5,000 7,000 Manganese 3 I 3 3 26 13. 7 · 33.9 12.7 • 20.2 200 • 3,000 PotassillJl 3 I 3 3 260 221 314 ND 5,000 · 26,0DD Vanadi1.n 2 I 3 2 9.7 9.6 9.7 3.2 7D · 150 Zinc 78 / 78 78 55 1.6 · 732 15.3 · 26.4
OFF-SITE Cb)
Organics: --------* beta-BHC 1 / 9 1 540 540 ND (<8.5 to <9.2) * 4,4'-000 7 I 9 7 7,600 13 · 25,000 9.2 · 32 * 4,4' -ODE 8 I 9 8 1,400 29 • 6,600 11 · 76 * 4,4'-DDT 9 I 9 9 13,000 73 • 52,000 33 • 110 * Dieldrin 1 /.9 1 12 12 NO (<17 to <18) * Toxaphene 8 I 9 8 57,000 200 · 190,000 180 • 260
Jnorganics:
----------Copper 8 I 9 8 5.0 1. 1 9.6 2.7 · 5.6 30 Lead 9 I 9 9 17 6.5 35.3 7.6 90.2 Zinc 7 I 7 7 21 6.8 68.3 15.2 • 26.4
*=Chemical of potential concern.
ND= Not detected (range of detection limits reported in parentheses).
(a) S-le results from SD·1·1 through SD·4·1, SD-6·1, SD-7·1, SD-13·1, SD-19·1, SD·20·1, SD-21·1, S0·22·1
(duplicate of SD-6·1), S0-41, SS-01, SS-04, S5·09, SS·20·0 through SS-47·0, SS-49·0 through SS-63·0, SS·103·0 through SS-107·0 SS·110·0 SS·58·20S SS·61·20S SS·62·20S SS·63·20S SS·64·20S SS·66·20S SS-71·0
ss-67-o, ss-82-0: ss-83-o,'ss-84-0, sS-92-10N, sS-93-o thro~gh ss-97-o: ss-33 cdllplicate of Ss-27), sS-ss
(duplicate of SS·44J, SS·93·10N·0.5, and SS-168·0.5 (duplicate of SS·93·10N·0.5J. The following sa..,les
were not included in the sainnary because they are under at least 6 inches of clean fill: SD-8, SD-18, SS·65, SS-85, SS·87 to SS-90 and SS-92.
(b) Safl1)le results from OSD-22-1 through OSD-28-1, OSD-30-1 (duplicate of OSD-22-1), OSD-42, and OSD-43.
Cc) The nUTDer of.samples in which the chemical was detected divided by the.total nllnber of sarrples analyzed.
Cd) Mean sarrple size includes detected values which were used to calculate the arithmetic mean.
(e) Arithmetic mean concentrations were calculated using only detected values according to USEPA Region IV · Guidance (1991b).
Cf) Background consists of surface soil/sediment sarrples SS-121, SS-122 and OSD-21.
(g) Regional Background levels from Hoke, Chatham, and Randolf Counties, North Carolina (Boerngen and Shacklette
1981) and national background levels from Bodek et al. (1988).
A-2
Chemical
1.5-2.5 FEET Cd)
Organics:
Aldrin
Alpha·BHC
beta·BHC
delta·BHC
garrrna-BHC
4 4'·DDD
4 14'-DDE
4'4•-DDT
oieldrin
Endrin ketone
Heptachlor
Heptachlor epoxide
Toxaphene
Jnorganics:
Copper
Lead
Zinc
TABLE A-2
SUMMARY OF CHEMICALS IN ON-SITE SUBSURFACE SOIL
(Organics: ug/kg, lnorganics: mg/kg)
Frequency of
Detection (a)
1/62
9/62
22/62
8/52
9/62
9/62
17/62
29/62
9/62 2/62
2/62
1/62 35/62
57/57
52/52
49/49
Mean
Sample
Size Cb)
1
9
22
8
9
9
17
29
9 2
2
1
35
57
52
49
Arithmetic
Mean Cc)
130
470
250
170 130
690
330
2,100 290 150
260
15 14,000
7.7 13
27
Range of Detected
Concentrations
130 24 1,600
10 1,600
12 · 890
11 • 510 44 · 1,400 27 · 2,500
23 · 14,000
32 • 1,600
29 · 280
48 • 470 15 180 130,000
1.5 17.7
2 202
3.2 269
(8)
(bl
(c)
(d)
The nlll'lber of SBl'l'4)les in which the chemical was de~~cted divided by the total nllllber
of S8°"les analyzed.
Mean s~le size includes only detected values which were used to calculate the
arithmetic mean.
The arithmetic mean concentrations were calculated using detected values only according
to USEPA Region JV Guidance (1991b).
sa""le results from SD-1-1.5, SD·1·2.5, SD·2·1.5, so-2-2.5, so-3-1.5, so-3-2.5,
S0-6·1.5, S0-8·1.5, SD·8·2.5, SD·9·2.5, SD-10-1.5, S0-10·2.5, SD-11·1.5, SD·11·2.5,
S0-12·1.5, SD-12·2.5, SD·13·1.5, SD·13·2.5, SD·19·1.5, SD-19·2.5, SD·21·1.5, SD·21·2.5,
SD-10-2, SD-11,2, s0-12-2, and SD-14-2.
Salll)le results also from SS-46·2, SS-48·2, SS-49-2, SS-51-2, SS-57-2 through
SS-59-2, SS-61·2 throueh SS-67·2, ss-69·2, SS-71-2, SS-82·2, SS-90·2 through SS-93-D2, SS-98·2 through SS-101·2 ss-103·2 SS-105·2 SS-106·2 SS-109·2 ss-110-2 SS-112-2 ss-116-2 throueh SS-119·2, ss-132·2, ss-131·2 (blind split of ss'.101-2,, .;..i ss-133·2
(blind split of SS·63·2).
A-3
I
_[}
12-Mar-92 ONSUB1
Chemical
· 4-10 FEET Cd)
Organics:
Alddn
alpha-BHC
beta-BHC
delta-BHC
garrma-BHC
4,4'-000
4,4'-0DE
4,4'-00T
Dieldrin
TABLE A-3
SUMMARY OF CHEMICALS IN ON-SITE SUBSURFACE SOIL
(Organics: ug/kg, Jnorganics: mg/kg)
Mean
Frequency of Sample Arithmetic
Detection (a) Size (b) Mean (c)
1/63 1 1,600
3/63 3 4,000 12/63 12 200 4/63 4 500
2/63 2 760
3/63 3 200
4/63 4 64
9/63 9 780 3/63 3 1,200
bis(2-Ethylhexyl)phthelate 3/9 3 62
Heptachlor epoxide 1/63 1 16
Methoxych l or 2/63 2 145
Toxaphene 13/63 13 24,000
lnorganics:
Aliinim.lTI 9/9 9 13,000
Arsenic 8/9 8 6.7
Baril.JTI 8/9 8 6.6
Beryl l iun 3/9 3 0.4
Calcilln 2/2 2 150
Chromiun 9/9 9 13
Cobalt 1/9 1 4_ 1
Copper 63/63 63 7
Iron. 8/8 8 13,000
Lead 53/53 53 4.7
Magnesillll 8/8 8 130
Manganese 9/9 9 3.5
Nick.el 5/9 5 2.5
Selenit.Jn 2/9 2 1
Silver 3/9 3 25
Sodiun 2/2 2 180
Thalli...n 1/9 1 3.3
Vanadil.111 8/9 8 25
Zinc 40/40 40 9.4
Range of Detected
Concentrations
1,600
11 12,000 11 2,100
18 1,900
21 1,500
92 270
32 100
43 3,300 32 3,400
59 68
16
110 180
200 280,000
3.4 27,700
0.8 -22.6
2.7 -14.9
0.2 -0.5
135 -160
0.5 -35.8
4. 1
0.5 -27.5
515 -74,800
1.8 -7.5
51.9 -225
0.2 -6.7 1 .8 3
0.5 -1.5
1.1 -69.5
173 -186
3.3
4.8 63.4
1.2 -32.9
(a)
(bl
(C)
Cd)
The nllTlber of sarrples in which the contaminant was detected divided by the total nllTlber
of sarrples analyzed.
Mean sarrple size includes only detected values which were used to calculate the arithmetic-mean.
The arithmetic mean concentrations were calculated using detected values only according
to USEPA Region IV Guidance.
S"""les include• surface soil -SS-46-5 SS-48-5 SS-48-10 SS-49-5 SS-51-5 SS-57-5
SS-58·5, SS-59-5, SS-61·5 through SS-67-5, SS-63-iO through 1SS-66-10: SS-69•5: SS-69-16, SS-71-5 through SS-73-5, SS-72-10, SS-73-10, SS-76-5 through SS-79-5, SS-76-10,
SS-81-5, SS-82-5, ss-90-5 through SS-93-5, SS-91-10, SS-98-5 through ss-101-5, SS-98-10,
SS-103-5 SS-105-5 SS-106-5 ss-108-5 through SS-110-5 SS-108-10 ss-110-10 SS-112-5
SS-113-10, SS-116-5 through ss-119-5, SS-130-5 (blind split of ss-io9-5) and ss-135-5 '
(blind split of SS-71-5); sediment -SD-10-5, so-10-10, SD-11-5, SD-12-5, S0-14-10,
and SD-14-5. The following sarrples were not included in the sunnary because they are
under et least 3 feet of clean fill: ss-3, SS-6, SS-114, SS-115, SS-117, and SS-119.
A-4
TABLE A-4
SUMMARY OF CHEMICALS IN OFF-SITE SUBSURFACE SOIL (Organics: ug/kg, Inorganics: mg/kg)
Mean Frequency·of Sample Arithmetic Range of Detected Chefllical Detection (a) Size Cb) Mean (c) Concentrations
1.5-3 FEET (d)
Organics:
4,4'-DDD 2/7 2 2,400 230 • 4,600 4,4'-DOE 3/7 3 620 45 · 1,700 4,4'-DDT 5/7 5 3,700 140 · 13,000 Dieldrin 2/7 2 220 110 · 320 Enc:lrin 1/7 1 140 140 Toxaphene 717 7 10,000 790 • 36,000
Inorganics:
Copper 717 7 5.1 1.6 • 8 Lead 7/7 7 6.9 1.6 • 31.8 Zinc 7/7 7 8.1 3.8 • 12.2
3-10 FEET (e)
Organics:
alpha-BHC 1/2 1 12 12 beta·BHC 2/2 2 21 15.3 -26 4,4'-D0D 2/2 2 86 75.S • 97 4,4'·DDE 1/2 1 so so 4,4'·DDT 2/2 2 450 330 560 Toxaphene 2/2 2 2,900 1,610 4,200
Inorganics:
Copper 2/2 2 4.3 2.9 5.7 Lead 2/2 2 15 12.s -11.8
(a) The nl.l?Der of serrples in which the chemical was detected divided by the total ru.rt>er of sarrples analyzed. (b) Mean s·arrple size includes only detected values which were used to calculate the arithmetic mean. (c) The arithmetic mean concentrations were calculated using detected values only according to USEPA Region IV Guidance. (d) S-le results from OSD-24·1.S, OSD·24·2.S, OS0-27·1.5, OSD-27-2.5, OSD-30·1.5, OSD-30·2.S, and OSD·29. (el Sample results from OS0-28-4, OSD·28-5 and OS0-45·3 (blind split of OSD-28-4).
A-5
TABLE A-5
SUMMARY OF CHEMICALS IN WATER FROM SURFICIAL AQUIFER
(Organics: ug/L, Inorganics: ug/L)
Chemical
ON-SITE (a)
Organics: ---···--Aldrin
alpha-BHC
beta·BHC
del ta·BHC
ganma·BHC
Dieldrin
Endri n ketone
Mean
Frequency of Saq,le
Detection Cc) Size Cd)
2 / 5 2
5 / 5 5
5 / 5 5
5 / 5 5
5 / 5 5
2 / 5 2
4 / 5 4 bis(2-Ethylhexyl)phthalate 1 / 5 1
Toxaphene 3 I 5 3
1,2,4-Trichlorobenzene 2 / 5 2
Jnorganics:
----------Alunim.lJI 5 / 5 5
Bariun 3 I 3 3
Cactniun 2 / 5 2
Calciiin 5 / 5 5
Chromiun 2 / 5 2 Copper 1 / 5 1
Iron 3 I 5 3
Magnesiun 5 / 5 5
Manganese 3 I 3 3
Mercury 1 / 5 1
Potessiun 5 / 5 5
Seleni1.n 3 I 5 3
Sodhrn 5 / 5 5
Venadi1.1n 2 / 5 2
Zinc 5 / 5 5
OFF-SITE Cb)
Organics: --------
alpha-BHC 1 / 6
beta·BHC 1 / 6 delta·BHC 1 / 6
gerrma-BHC 1 / 6
Heptechlor epoxide 1 / 6
Dieldrin 1 / 6
4,4'-DDE 1 / 6
Endri n ketone 1 / 6
Arithmetic
Mean Ce)
0.2
9.2
6.5
10
7.6
0.3
0.4
7 5.0
4.5
5,563.7 172.9 6.5
23,493.6
5.4.
23.9 1,137
7,691
69.7
1.0
51,502 1.6
8,864
9.6
222.7
1.6
25 2.4
0.8
0.2
2
0.2
3.6
ND= Not detected (range of detection limits reported in parentheses).
(a) Sarrples include MW-2S through MW-6S.
(b) Includes phase 4 sa""les MW-7S through MW-10S, MW·12S and MW·13S.
Range of Detected Range of Background
Concentrations Concentrations Cf)
0.1 0.4 NO (<0.1 to <0.5)
1.0 36 ND (<0.5)
0.6 12 ND (<0.5)
0.1 29 ND (<0.5)
0.3 30 ND (<0.5)
0.2 0.3 ND (<0.1)
0.2 0.7 ND (<0.1)
7 ND (<10) 4.6 9.6 NO (<10)
4.0 • 5.0 NO (<10)
46.3 -17,100 171 • 172 78.6 -284 ND (g)
5.3 • 7.6 ND (<4)
918 -49,800 438
4.3 -6.5 ND (<4.8)
23.9 ND (<12) 36.7 • 3,290 550 -955
745 • 18,000 ND (g)
44 • 104 ND (g)
1.0 NO (<0.2)
1,010 160,000 706 • 744 1.2 -2.4 3.7
4,270 -12,900 7,560 • 8, 150
15.4 -38 NO (<13)
11.9 -579 15.8 -19. 7
1.6 NO (<0.05)
25 ND (<0.05) 2.4 ND (<0.05)
0.8 ND (<0.05)
0.2 ND (<0.05)
2 ND(<0.1)
0.2 NO (<0.1)
3.6 NO (<0.1)
(c) The nurber of sarrples in which the contaminant was detected divided by the total nl.llber of SBJl1)les analyzed.
Cd) Mean SBJl1)le size includes only detected values which were used to calculate the arithmetic mean.
Ce) Arithmetic mean concentrations were calculated using only detected values according to USEPA ,
Region IV Guidance.
Cf) Background consists of groundwater saq::,les MW-1S and its duplicate designated as MW-7S in phase 1.
Cg) Data rejected by QA/QC because chemical was datected in a laboratory blank at a similar concentration.
A-6
12-Mar-92 INTERWELL
SUMMARY OF
Chemical
ON-SITE (a)
Organics: --------
Trichloroethene
Inorganics:
----------AlllTiiman
CacinillTI
Calcilrn
Iron
Lead Magnesiun
Manganese
Potassiun
Sodiun
Zinc
OFF-SITE (b)
Organics:
alpha-BHC beta-BHC
delta-BHC ganma-BHC
Dieldrin
Endrin ketone 4-methyl-2-pentanone
Frequency
Detection
2 / 2
2 / 2 1 / 2
2 / 2
2 / 2
1 / 2
2 / 2
1 t 1
1 / 2
2 / 2
2 / 2
I 1
1 / 1
1 / 1
1 / 1
1 / 1
1 / 1
1 / 1
TABLE A-6
CHEMICALS IN WATER FROM SECOND UPPERMOST ACUI FER (Organics: ug/L,
of Mean Sample
(c) Size Cd)
2
2
1
2
2
1
2
1
1
2
2
Inorganics: ug/L)
Arithmetic Mean Ce)
104.5
1,932
5.9 2,710
1,128.5
9
1,015
118
869
3,930
34.8
16
6.6
4.5
11
0.3
0.4
2
Range of Detected
Concentrations
29 -180
214 -3,650
5.9 1,010 -4,410
76.9 -2,180
9.2
620 -1,410
118
869
2,780 5,070
32.4 -37. 1
16
6.6
4.5
11 ·o.3
0.4
2
ND= Not detected (detection limits reported in parentheses):
Site-Specific
Background
Concentrations· Cf)
ND ( <10)
7,620 ND (<4)
3,370
4,280
10.2
1,540
91.2
875
4,620
69.3
ND (<0.05) ND (<0.05)
ND (<0.05)
ND (<0.05)
ND (<0.1)
ND (<0.1)
ND (<0.1)
(a) Inorganics include sa~les from phase 1 (MW-4D and MW-60). Organics include additional samples from
phase 4 (MW-4D and MW-6D). (b) Sample results from MW-11D.
(c) The nl.mler of sa~les in which the chemical was detected divided by the total nl.JTlber of samples analyzed.
Cd) Mean sample size includes only detected values which were used to calculate the arithmetic mean.
(e) Arithmetic mean concentrations were calculated using only detected values according to USEPA Region IV Guidance.
Cf) Background consists of groundwater samples MW-1D, MW-14D, and MW-15D.
A-7
J]
APPENDIX A REFERENCES
BODEK, I., LYMAN, W.J., REEHL, W.F. and ROSENBLATT, D·.H. 1988. Environmental
Inorganic Chemistry: Properties, Processes, and Estimation Methods.
Pergamon Press, New York
BOERNGEN, J.G. and SHACKLETTE, H.T. 1981. Chemical Analyses of Soils and
Other Surficial Materials of the Conterminous United States. United
States Department of the Interior. Geological Survey. Open File Report
81-197
U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA). 1991b. Revised EPA Region IV
Supplemental Risk Assessment Guidance. March 26, 1991
A-8
APPENDIX B
EQUATION USED FOR STATISTICAL ANALYSIS
APPENDIX B
EQUATION USED FOR STATISTICAL ANALYSIS
The selection of the appropriate equation for statistical analysis at the
Geigy Aberdeen Site was based on USEPA's Risk Assessment Guidance for
Superfund (USEPA 1989) and personal communications between Clement
International Corporation and USEPA's Exposure Assessment Group. The first
step of the process is an evaluation of the probability distribution of
chemicals at the site. For soils, this was determined to be a log-normal
distribution which is consistent with the work of Dean (1981) and Ott (1988).
Due to the fact that the distribution was log-normal, Equation 13.13 from
Gilbert (1987) was selected for computation of the 95% upper confidence limit
(UCL) for the reasonable maximum exposure (RME) case. The equation, derived
from the work of Land (1971, 1975) yields the 95% UCL around the population
mean of a 2-parameter lognormal distribution:
where
a
y
sZ y
n
UL = exp (-+ O 5 s' + 5vH,-•) ,-. Y · Y ,ln-1
upper confidence limit
0.05
mean of the log-transformed data
variance of the log-transformed data
standard deviation of the log-transformed data
critical value of the H statistic found in Land
(1975)
number of samples in the population.
At Clement, this process is programmed into Clement's proprietary risk ·
assessment software known as the Clement Risk Information System (CRIS). Due
to this, examples of the calculation which are specific to the Geigy Aberdeen
site do not exist. The reader is referred to Example 13.3 in Gilbert (1987)
for an exact illustration of our application-of the method.
B-1
APPENDIX B REFERENCES
DEAN, R.B. 1981. Use of log-normal statistics in
Cooper, W.J., ed. Chemistry in Water Reuse.
Arbor, Michigan. Vol. 1
environmental monitoring.
Ann Arbor Science, Ann
GILBERT, R.0. 1987. Statistical Methods for Environmental Pollution
Monitoring. Van Nostrand Reinhold. New York, New York
LAND, C.E. 1971. Confidence Intervals for Linear Functions of the Normal
Mean and Variance. Annals of Mathematical Statistics .. 42:1187-1205
LAND, C.E. 1975. Table of confidence limits for linear functions of the
normal mean and variance. Math. Stat. Vol. III. Pp. 385-419
OTT, W.R. 1988. A Physical Explanation of the Lognormality of Pollutant
Concentrations. Presented at the 81st Annual Meeting of APCA, Dallas,
TX. June 14-19, 1988
U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA). 1989. Risk Assessment Guidance
for Superfund. Volume I: Human Health Evaluation Manual. (Part A).
Interim Final. EPA/540/1-89/002. December 1989
B-2
APPENDIX C
C.l SHOWER MODEL
Volatile organic chemicals (VOCs) dissolved in household water supplies can be
released into the indoor air as a result of activities such as showering,
bathing and dishwashing. Of particular concern to human health is the
potential for elevated exposures to occur in the confined space of a shower.
The shower model developed by Foster and Chrostowski (1987) was used to assess
the possible inhalation exposures to VOCs from ground water at the CIBA-GEIGY
Aberdeen site. In the shower model, inhalation exposures are modeled by
estimating the rate of chemical release into the air (generation rate), the
buildup (shower on) and decay (shower off) of VOCs in shower room air, and the
resulting time-weighted average VOC concentrations for the duration of shower
room exposure.
Estimation of the rate of VOC release into the air is based upon Liss and
Slater's adaptation of the two-layer film model of gas-liquid mass transfer.
The two-film boundary ·theory provides the basis for estimating the overall
mass transfer coefficient (Kl) for each VOC of interest according to the
following equation:
where
Kl overall mass transfer coefficient (cm/hr),
H -Henry's law constant (atm-m3/mol-K)
RT -2.4xlo-2 atm-m3/mole (gas constant of 8.2x1O-s atm-m3/mol-K times
absolute temperature of 293 K),
k9 gas-film mass transfer coefficient (cm/hr), and
kl liquid-film mass transfer coefficient (cm/hr).
Equation 1 describes the mass transfer rate of a compound at an air-water
interface where diffusion may be limited by both liquid-and gas-phase
resistances.
C-1
(1)
The chemical-specific resistances to mass transport for both the liquid and
gas phases were calculated from empirical expressions suggested by Liss and
Slater (1974). Typical values of k1 (20 cm/hr) and k9· (3,000 cm/hr), which
have been measured for CO2 and H2o, respectively, were used Co estimate
VOC-specific values for these parameters as follows:
where
20 (cm/hr) [44/MW] 1l2
kg = 3000 (cm/hr) [18/MW] 112
liquid-phase mass transfer coefficient (cm/hr),
gas-phase mass transfer coefficient (cm/hr), and
molecular weight of the chemical.
(2)
(3)
The mass transfer coefficient, KL, is adjusted Co the shower water
temperature, T5 , according to a semi-empirical equation developed to estimate
the effe·cc of temperature on oxygen mass-transfer rate:
where
KaL adjusted overall mass transfer coefficient (cm/hr),
T1 calibration water temperature of KL (K),
Ts shower water temperature (K),
m1 water viscosity at T1 (cp), and
ms water viscosity at Ts (cp).
The concentration leaving the shower droplet, Cwd, is obtained from an
integrated rate equation based on a mass-balance approach:
c"" = c.0 (1-exp[-K.Lt,/God] l
C-2
(4)
(5)
where
ewd concentration leaving shower droplet after time ts (µg/1),
ewo shower water concentration (µg/1),
KaL adjusted overall mass transfer coefficient (cm/hr),
d shower droplet diameter (mm), and
ts shower droplet drop time (sec).
The term K8L/60d combines both the rate transfer and the avai.lable interfacial
area across which volatilization can occur. The value l/60d equals the
specific interfacial area, 6/d, for a spherical shower droplet of diameter d
multiplied by conversion factors (hr/3,600 sec and 10 mm/cm).
The voe generation rate in the shower room, S, can then be calculated by the
equation:
s = c..,,(Fr)/Sv (6)
where
S indoor voe generation rate (µg/m3-min),
ewd concentration leaving shower droplet after time ts (µg/1),
Fr shower water flow rate (1/min), and
Sv shower room air volume (m3).
A simple one-compartment indoor air pollution model was used to estimate voe
air concentrations in the shower room. This model can be expressed as a
differential equation describing the rate of change of the indoor pollutant
concentration with time:
dC./dt = RC• + S (7)
where
e8 indoor voe air concentration (µg/m3),
R air exchange rate (min-1), and
S indoor voe generation rate (µg/m3-m_in).
e-3
When equation 7 is integr~ted, the time-dependent indoor concentration can be
estimated as follows:
and
where
Ds
t
(S/R) (1-exp[-Rt]) fort~ D8
(S/R(exp[RD,] -l)exp(-Rt) fort> Ds
indoor air VOC concentration at time t (µg/m3),
shower duration (min), and
time (min).
(8)
( 9)
The average shower room air concentration for the duration of the exposure can
then be calculated according to the following equation:
(10)
where
Cavg average shower room air concentration,
Dt total duration in shower room (min).
This equation can be solved as follows:
C,vg = D, -1/R + exp(-RD8 ) /R
for the duration of the shower, and as:
C,vg = D, + exp (-RD,)/ R -[R (D5 -D,)] / R
for both the duration of the shower and the duration in the room after the
shower is turned off.
Table 1 lists the input parameters to the shower model.
C-4
TABLE 1
INPUT PARAMETERS TO THE SHOWER MODEL
Parameter Value
Shower Water Temperature (Ts) 318 K
Water Viscosity at Shower Temperature (ms) 0.596 cp
Shower Droplet Drop Time (t8) 2 sec
Shower Droplet Diameter (d) 1 mm
Shower Water Flow Rate (Fr) 10 1/min
Air Exchange Rate in Shower Room (R) 8. 3xl ·2 min"1
Total Duration in Shower Room (Dt) 17 min
Shower Duration (D5) 12 min
Duration in Shower Room After Shower 5 min
Stops (Dt -D5 )
C-5
Discussion of Uncertainties
As noted in the original paper (Foster and Chrostowski 1987), the shower model
was validated by comparison to measured data (Andelman 1985). Depending on
the time, the model underestimates air-borne levels by a factor of up to about
6%. Based on a review of several shower models, McKone (1987) identified a
range of inhalation-to-ingestion doses of 0.24 to six for V0Cs, compared to
the range of 1.1 to 2.0 derived by McKone (1987) from Foster.and Chrostowski
(1987). More recently, Jo et al. (1990a) corroborated by measurements in
exhaled breath, that total chloroform exposures from showering resulted in
doses which were comparable to those calculated using the Foster and
Chrostowski (1987) model. They also found, however (Jo et al. 1990b) that
approximately one-half the total chloroform dose resulted from dermal exposure
while showering. Taking all of these results into account, the Foster and
Chrostowski (1987) model used in this assessment appears to yield reasonably
accurate predictions of exposure while showering.
C-6
APPENDIX C REFERENCES
ANDELMAN, J.B. 1985. Human exposure to·volatile halogenated organic
chemicals in indoor and outdoor air. Env. Health Persp. 62:313-318.
FOSTER, S.A. and CHROSTOWSKI, P.C. 1987. Inhalation Exposures to Volatile
Organic Contaminants in the Shower. Presented at the 80th Annual Meeting
of APCA, New York, New York. June 21-26, 1987
JO, W.K., WEISEL, C.P., AND LIOY, P.J. 1990a. Routes of chloroform exposure
and body burden from showering with chlorinated tap water. Risk Analysis
10(4):575-580.
JO, W.K_., WEISEL, C.P., AND LIOY, P.J. 1990b. Chloroform exposure and the
health risk associated with multiple uses of chlorinated tap water. Risk
Analysis 10(4):581-585.
MCKONE, T.E. 1987. Human exposure to volatile organic compounds in household
tap water: The inhalation pathway. Environ. Sci. Technol. 21(12):1194-
1201.
C-7
APPENDIX D
AIR EMISSIONS AND DISPERSION MODELING
D.l INTRODUCTION
This appendix describes the emissions and air dispersion models used to
predict air concentrations of pesticides and benzoic acid potentially
volatilized or entrained via wind erosion from the surface soils at the Ciba-
Geigy site. For the volatilization modeling, average flux rates of these
chemicals over the evaluated periods of exposure were calculated using a soil
volatilization model developed by the USEPA (1986). For the wind erosion
modeling, the annual average flux rate for respirable particles were
calculated using a Cowherd et al. (1985) emission factor. The flux rates
determined by the emissions modeling were used in conjunction with the
Industrial Source Complex Long-Term (ISCLT) computer air dispersion model
(USEPA 1987) to estimate average ambient air concentrations at various
receptor locations. Section D.2 of this appendix describes the volatilization
modeling. Section D.3 presents the details of the emissions modeling for wind
erosion. Section D.4 describes the ISCLT modeling and presents the modeled
ambient air concentrations of each of the pesticides and benzoic acid.
D.2 SOIL VOLATILIZATION
Chemical emissions from the surface soil were calculated using a soil
volatilization model based on the work of Hwang (USEPA 1986), Bomberger et al.
(1983) and Millington and Quirk (1961). Hwang developed the basic
volatilization model into which the partitioning and diffusivity models of
Bomberger and Millington and Quirk, respectively, are incorporated. The
Hwang/EPA volatilization model was originally developed for estimating air
exposures· in the EPA's development of PCB clean-up levels .. Because of the
high soil affinity of PCBs, it assumes that transport of chemical in the soil
is solely by passive diffusion in the soil gas. The, pesticides in the site
~
soils are similar to PCBs in terms of their high affinity for soil, low
volatility and general persistence, and therefore the EPA soil volatilization
D-1
model is considered appropriate for the Ciba-Geigy site when used in
conjunction with site-specific chemical .and soil parameters.
Before the EPA volatilization model was used, initial soil gas pesticide
concentrations were determined using an equilibrium partitioning approach.
Bomberger et al. (1983) established that the total amount of a specific
chemical in the soil partitions among the solid, liquid and _gas phases
according to the following equilibrium partitioning model:
where
H'
total material factor,
fraction of soil volume that is air (air-filled porosity),
fraction of soil volume that is water (water-filled
porosity) ,
Henry's law constant at 25°c (dimensionless),
soil bulk density (g/cm3),
organic carbon:water partition coefficient (cm3/g), and
fraction organ~c carbon in soil.
The soil bulk density was taken to be 1.65 g/cm3 ,. which is the midpoint in the
range of values (l.60 to 1.70) reported by the Soil Conservation Service (SGS)
for soils in the vicinity of the site. A total porosity of 0.377.was
calculated from the bulk density by assuming a particle density of 2.65 g/cm3
for the minerals that compose the soil (Mercer et al. 1982). A value of 0.067
for the water filled porosity, (8.), was determined as the average soil
moisture value measured in the on-site soil samples collected during the
remedial investigation. The air-filled porosity, (ej~, is the differen_ce
between total and water-filled porosity or 0.31. Henry's law constants (H')
D-2
and organic carbon partition coefficients (K0c) were obtained from Clement
International' s database for physicochemical parameters. (Table D-1). A
fraction of organic carbon (f0c) of 0.0043 (.43%) was·determined from the
midpoint of the range of percentages of organic matter (0.5 to 1 %) in the
site soils reported by the SGS. The fraction of total organic matter was
converted to a fraction of organic carbon using a factor of 1.72 from Lyman et
al. (1982).
In order to determine the fraction of a compound in soil gas, the soil water
phase, and the solid phase for a given sample, Bomberger et al. present the
following equations:
where
). fraction of a compound in soil gas (sg), the water phase
(w), or the solid phase (s).
The resulting soil gas concentration can then be calculated from the mass
balance equation:
where
chemical concentration in soil gas (g/cm3)
total (analytical) concentration in soil (g/g), and
soil bulk density (1.65 g/cm3).
All other variables are defined as before.
D-3
TABLE D-1
CHEMICAL-SPECIFIC PARAMETERS USED IN THE VOLATILIZATION MODEL
Calculated Analytical Soil Henry's Law Diffusivity Diffusivity Soil Gas Solubility in Concentration Koc Constant in Air in Soil COMPOUND [g/gJ [cm3/gJ (Dimensionles Concentration Water 20-25 C [cm2/sl (cm2/s] [g/cm3J [mg/LJ
Aldrin 4.40E·09 9.60E+04 (2) 3,75E·02 (3) 4,74E·02 6.73E-03 4.00E-13 1.80E-01 (2) alpha·BHC 8,30E·08 3.80E+03 (2) 3.58E·04 (3) 5.20E·02 7 .37E-03 1.81E·12 1.63E+00 (2) beta-BHC 1.20E·07 3.80E+03 (2) 4.94E-05 (3) 5,58E·02 7.91E·03 3.62E·13 1.40E+OO (2) delta-BHC 7.20E·08 6.60E+03 (2) 3.00E-05 (3) 5.58E·02 7.91E·03 7 .61E· 14 3. 14E+01 (2) ganma-BHC 6.90E·08 1. 08E+03 C 1) 5.35E·05 (3) 5.58E·02 7.91E·03 7.BBE-13 7.B0E+00 (2) Benzoic acid 1.40E·06 5.44E+03 (5) 1.63E·05 (4) 7.07E-02 1.00E-02 9.76E·13 2.90E+03 (8) Chlordanecatpha) 4.10E·08 9.50E+03 (5) 3.71E·03 (3) 4.50E·02 Chlordane(ganrna) 4.20E·08 9.50E+03 (5) 3. 71E·03 (3)
6,38E·03 3.72E·12 6.00E-03 (9) 4.50E·02 4,4' -ODO 1.30E·06 7,70E+05 (2) 2,63E·04 (3) 6.38E·03 3.81E·12 6.00E-03 (2) 4.74E·02 6.73E·03 4,4'-DDE 1.10E·06 2.97E+04 (6) 3,27E-03 (3) 1.03E·13 1.00E-01 (2) 5.34E·02 7.57E-03 4,4'-DDT 3.70E·06 2.43E+05 (1) 9,71E·04 (3) 2.82E·11 4.00E-02 (11) 4.47E-02 6.34E·03 3.44E·12 5.00E-03 (2) Dieldrin 1.50E-07 1,70E+03 (2) 4,61E·04 (3) 4.BBE-02 Toxaphene 1.60E-05 9.64E+02 (2) 1. 73E·04 (3)
6.92E·03 9.40E·12 1.95E·01 4,82E-02 6,84E·03 6.60E·10 5.00E-01
(1) Lyman, W.J., Reehl, W.F., and Rosenblatt, 0.H. 1982. Handbook of Chemical Property Estimation Methods.
McGraw-Hill, Inc., New York, and the methods presented therein. G
(2) Mabey, W.R., Smith, J.H., Podoll, R.T., Johnson, H.L., MHl, T., Chou, T.W., Gates, J., Partridge, I.W.,
Jaber, H., and Vandenberg, D. 1982. Aquatic Fate Process Data for Organic Priority Pollutants. Prepared
by SRI International. Prepared for Monitoring and Data Support Division, Office of Water Regulations and Standards. Washington, D.C. EPA Contract Nos. 68-01-3867 and 68-03-2981. c
(3) Suntio, L.R., Shir, W.Y., Mackay, D., Seiber, J.N., and Glotfelty, D. 1988. Critical Review of Henry's
Law Constants for Pesticides. Reviews of Envirormental Contamination and Toxicology, Vol. 103. Springer-Verlag New York, Inc.
(4) Calculated using Henry's Law Constant= VP/WSol, where VP= Vapor Pressure in atmospheres (atm) and WSol = Water Solubility in moles/m3. Cale
(5) Lyman, W.J., Reehl, W.F., and Rosenblatt, D.H. 1982. Calculated using Eq. 4·5: log Koc= -0.55 log
S + 3.64 (S in.mg/l). Presented in the Handbook Chemical Property Estimation Methods. McGraw-Hill, Inc., New York AC4
(6) Lyman, W.J., Reehl, W.F., and Rosenblatt, D.H. 1982. Calculated using Eq. 4-8: log Koe= 0.544 log
(2)
Kow + 1.377. Presented in Handbook Chemical Property Estimation Methods. McGraw-Hill, Jnc., New York (7) Lu, P.Y., and Metcalf, R.L. 1975. Envirormental Fate and Biodegradability of Benzene Derivatives as Stuclied in a Model Aquatic Ecosystem. Environ. Health Perspect. 10:269·84. HL 192 (8) Verschueren, K. 1983. Handbook of Envirormental Data for Organic Chemicals, Second Edition.
log KOi.'
[dimension less:
3.01 (7)
3.90 (2)
3.90 (2)
4.10 (2)
3.90 (2) 1.87 (8)
4.78 (1)
4. 78 (10)
5.99 (10)
5.69 (10)
5.98 (2) 3.50 (2)
3.30
Van Nostrand Reinhold Co., New York J
(9) National Research Council canada (NRCC). 1974. Chlordane: Its Effects in Canadian Ecosystems and its Chemistry. NRCC No. 14094 AK
(10) Chin, Y,P., Walter, J.W. and Thomas, C.V. 1986. Determination of Partition Coefficients and Aqueous
Solubilities by Reverse Phase Chromatography -II. Wat. Res. 20(11): 1443-1450 DL10
(11) US Environmental Protection Agency (USEPA). 1984. Health Effects Assessment Surmary Table. Environmental
Criteria and Assessment Office, Cincinnati, Ohio. Septenber 1984. EPA 540/1·86·008·051.
D-4
The soil gas concentrations determined as above can be used in the Hwang/EPA
(1986) volatilization model. The Hwang/EPA volatilization model is based on a
mass balance over a.vertical element of soil calculated from diffusive fluxes
across the concentration gradients above and below the element. The mass
balance equation can be written as follows:
where:
A
z
e ( acsg) acsg acs -A d -D9~ z+&z, e ;:: AAz--::: A..6.zpb-z,, at . at
cross-sectional area of interest, (cm2)
concentration of pesticides in the soil gas in soil pores,
(g/cm3)
concentration of pesticides in the solid phase, (g/g)
effective diffusivity, (cm2/s)
air-filled porosity, (dimensionless fraction)
soil bulk density, (g/cm3)
time, (sec), and
depth measured from the soil-air interface, (cm).
The effective diffusivity is determined by the chemical-specific molecular .
diffusivity and the geometry of the soil pore space. The effect of the soil
character on vapor phase diffusion was accounted for by using an empirical
model of Millington and Quirk (1961):
where
8 101, • e 2 T
air-filled porosity (unitle'ss),.
total porosity (unitless),
air diffusivity of the pesticide (at 25°G in cm2/sec), and
effective soil diffusivity of the pesticide (cm2/sec).
D-5
The values for air diffusivity were obtained from the Clement International
physicochemical parameters database.
The mass balance equation can be solved analytically using the following
simplifying boundary and initial conditions:
1. r.c. csg CSQO I at t 0, z > 0
2. B.C. csg csgo' at z -., . t > 0
3. B.C. csg 0, at z = 0, t > 0
where:
initial concentration of pesticides in the soil gas (g/cm3),
The initial condition is equivalent to assuming a uniform soil concentration.
The first boundary condition assumes a chemical distribution of unlimited
depth, and the second boundary condition assumes that soil gas concentrations
at the soil-atmosphere interface are zero and therefore do not build up as a
result of resistance due to the stagnant boundary layer at this interface.
All of these assumptions are conservative in that they likely result in
overestimates of emissions.
When the mass balance equation is solved using ·the equilibrium partitioning
relationship of Bomberger et al. (1983) and with the above initial and
boundary conditions, a flux rate is obtained which decreases as the inverse of
the square root of time. An average flux rate, NA, for a given exposure
period can also be calculated and is as follows:
N,;
Beta (P) is a variable introduced for convenience of solution which is a
combination of soil-and chemical-specific parameters and is described by the
following equation:
D-6
Table D•l summarizes the chemical·specific parameters and concentrations which
were used in the volatilization modeling calculations. The soil gas
concentrations were calculated from the average surface soil and sediment
concentrations discussed in Section 2.0. Table D-2 presents the resulting
average flux rates for the four periods of exposure evaluated in Section 4.0
of the main text of this baseline RA. The average flux rates decrease with
increasing exposure periods because of the inverse square relationship of flux
rates to time predicted by the model. Because of this expected decrease of
emissions over time, the initial condition assumption of uniform soil
concentrations (and hence very steep diffusion gradients near the surface)
would tend to result in the overprediction of flux rates. This is because the
initial condition assumption was most .likely satisfied when the chemicals were
fresh in the ·soil, while in reality twenty or more years may have passed since
the chemicals were spilled on the site soils. Therefore flux rates may have
decreased substantially from their initial values.
D.3 WIND EROSION
The flux rate of respirable particulate matter from on-site surface soils via
wind erosion was determined using a Cowherd et al. (1985) emission factor.
This emission factor predicts the annual average flux rate of respirable
material (known as PM10 , particles with an aerodynamic equivalent diameter of
10 microns.or less) due to wind erosion. According to the Cowherd method, the
first step in estimating particulate emissions through wind erosion of
unvegetated portions of the site is the classification of the surface material
as having either a "limited reservoir11 or an "unlimited reservoir" of etodible
surface particles. Surface materials composed of crusts or aggregates too
large to be eroded mixed with erodible material are representative of a
11 limited reservoir" and have low potential for wind erosion. For this
evaluation, the on·site soils were assumed to represent an "unlimited
D-7
TABLE 0·2
ANNUAL AVERAGE FLUX RATES (g/an2·S)
Exposure Periods· --------------------------------------------------------------------COMPOUND 6 years 8.4 years 9 years 25 years 30 years
Aldrin 2.02E·16 1. 71E·16 1.65E·16 9.89E·17 9.03E·17 alpha·BHC 1.95E·15 1.65E·15 1 .59E· 15 9.56E·16 8.73E·16 beta·BHC 1.09E·15 9.18E·16 8.86E·16 5.32E·16 4.86E·16 delta·BHC 3.86E·16 3.26E·16 3.15E·16 1.89E·16 1.73E·16 gmnna·BHC 1.21E·15 1.02E·15 9.89E·16 5.93E·16 5;42E•16 Benzoic acid 6.86E·15 5.80E·15 5.60E·15 3.36E·15 3.07E·15 Chlordane(alphal 1.83E·15 1.55E·15 1.49E·15 8.96E·16 8.18E·16 Chlordane(gmnnal .1 .87E·15 1.58E·15 1 .53E·15 9.18E·16 8.38E·16 4,4'·00D 1.76E·15 1.49E·15 1.44E·15 8.64E·16 7.89E·16 4,4' ·DDE 2.84E·14 2.40E·14 2.32E·14 1.39E·14 1.27E·14 4,41 -DDT 1.67E·14 1.41E·14 1 .36E·14 8.16E·15 7.45E·15 Dieldrin 5.78E·15 4.88E·15 4.72E·15 2.83E·15 2.58E·15 Toxaphene 4.96E·13 4.19E·13 4.05E·13 2.43E·13 2.22E·13
D-8
reservior11 of erodible su~face particles based on the SGS particle size
distribution for on-site soil.
Entrainment of part~cle matter is dependent on wind speed. For a given soil
type there is a threshold wind velocity which must be attained to initiate
entrainment. This threshold wind velocity was determined following the method
described by Cowherd et al. (1985). By specifying the soil aggregate particle
size distribution mode, the threshold surface friction velo~ity can be
determined from Figure 3-4. Based on the SGS particle size distribution for
on-site soils, the soil aggregate.particle size distribution mode was
estimated to be 0.3 mm. The corresponding threshold surface friction velocity
was 29 cm/s.
The threshold surface friction velocity describes the wind speed required at
the soil surface to initiate entrainment of soil particles. The Cowherd PM10
emission rate equation requires input of the lowest wind speed, measured at a
height of 7 m, which would initiate wind erosion. Frictional drag at the
earth's surface causes a deceleration of the wind. This results in a wind
speed profile that shows as increase in speed with increasing height. The
wind speed profile in the lower atmosphere can be approximated by a
logarithmic equation known as the logarithmic wind profile. This equation was
used to convert the threshold surface friction velocity to the corresponding
wind at 7 m. This conversion requires specification of the aerodynamic
roughness of the surface over which the wind is flowing. For the on-site
surface area an aerodynamic roughness of 2.0 cm was chosen based on site-
specific surface characteristics and values suggested in Cowherd et al.
(1985). The threshold friction velocity at 7 m was calculated to be 5.7 m/s.
The Cowherd PM10 emission equation also requires specification of the average
wind speed in the area and the fraction of vegetative cover on the soil.
surface. The average wind speed was obtained from meteorological data
collected approximately 25 miles from the site at Fort Bragg. The value for
the average wind speed was 2.6 m/s. The fraction of soil covered by
D-9
vegetation at the site wa~ assumed to be 50 %. This assumption was based on
observations of the surface soils while visiting the site.
The entrainment of soil particles will occur only when the wind speed is
greater than or equal the threshold wind speed.. The Cowherd PM10 emission
rate equation includes a weighting function which represents the periods when
the wind can be expected to meet or exceed the threshold wind speed. This
weighting function assumes that the wind speed distribution for a given site
can be represented by a Rayleigh distribution. Using methods described by
Cowherd et al. (1985) the value of the weighting function was calculated to be
0.35.
The values for the input parameters used to calculate the PM10 emission factor
are listed in Table D-3. Having specified the required.input parameters, the
emission factor for PM10 emissions was calculated from the following
predictive· equation developed from Gillette's (1981) field measurements of
highly erodible soil:
where:
E10 =0.036 • (1-V) • [ iJ' • F(x)
E10w annual average PM10 emission factor per unit area of
contaminated surface, (g/m2/hr)
V fraction of contaminated surface with vegetative cover (equals
0 for bare soil)
u mean annual wind speed, (m/sec)
ut threshold value of wind speed at an elevation of 7 m, (m/sec)
x 0.886(ut/u), (dimensionless ratio)
F(x) function related to the expected value of the wind
speed, (dimensionless).
The calculated value for E is given in Table D-3. ·
10w
D-10
TABLE D-3
INPUT PARAMETERS FOR WIND EROSION MODEL
V 0.50
u 2.60 m/s
u, 5. 71 m/s
X 1. 95
F(x) 0.35
E1ow 5. 95xl0"4 g/m2 -hr
D-11
To obtain the annual chemical-specific PM10 emission rate due to wind erosion,
R10 , the PM10 emission factor, E10w, is multiplied by the weight fraction of
the chemical measured in the soil in the following equation:
R10 ~ W E10w (2. 78x10·4 hr/sec)
where:
R10 emission flux of contaminant, (g/m2/sec)
E10w annual PM10 emission rate due to wind erosion, (g/m2/hr)
W mass fraction of chemical in surface soils, (g/g).
The mass fraction for each chemical used in the PM10 emission rate equation
was obtained by c9nverting the reported chemical concentrations in soil (in
ug/kg) to a unitless value of g/g by using the appropriate conversion
multipliers. It was assumed that the concentration in the PM10 particles was
equal to the chemical concentrations measured in the bulk soil. Table D-4
lists these values as well as the R10 emission rates for various contaminants.
The predicted emission rates were used to estimate the chemical-specific
ambient concentrations on-site by linking them to the air dispersion model
described in the next section.
D.3 ISCLT AIR DISPERSION MODEL
USEPA's Industrial Source Complex Long-Term (ISCLT) dispersion model was used
to estimate average annual ambient air concentrations resulting from the flux
rates estimated above. The ISCLT model is part of USEPA's UNAMAP family of
models which are considered to be USEPA's preferred group of air models. It
is a steady-state Gaussian plume model which can be used to assess pollutant
concentrations from a wide variety of sources (USEPA 1987). ISCLT estimates
annual average ground level concentrations in all directions around an
emission source out to 50 km.
The first step in the modeling process is to link the appropriate stability
array (STAR) meteorological data with the ISCLT model. Star data represents
summaries of the observed joint frequency of occurrence of wind speed and
D-12
TABLE D-4
CHEMICAL-SPECIFIC PM10 FLUX RATES FOR WIND EROSION
Compound
Aldrin
alpha-BHC
beta-BHC
delta-BHC
gamma-BHC
Benzoic Acid
alpha-Chlordane
gamma-Chlordane
4,4'-DDD
4,4'-DDE
4,4' -DDT
Dieldrin
Toxaphene
Analytical Soil
Concentration
(g/g)
4.4OE-O9
8 .. 3OE-O8
l.2OE-O7
7.2OE-O8
6.9OE-O8
1. 4OE-O6
4.lOE-O8
4.2OE-O8
1. 3OE-O6
l. lOE-O6
3.7OE-O6
1. SOE-O7
1. 6OE-O5
D-13
Annual Average
PM10 Flux Rate
(g/m2-s)
7.26E-16
l.37E-14
1.98E-14
1. 19E-14
1.14E-14
2.31E-13
6. 77E-15
6.93E-15
2.lSE-13
1. 82E-13
6.llE-13
2.48E-14
2.64E-12
direction for a range of atmospheric stabilities. The nearest national
weather service (NWS) reporting station .to the site is at Fort Bragg, North
Carolina. STAR data from Fort Bragg for the years 1966-1970 were used.
ISCLT allows selection ~f atmospheric dispersion coefficients representative
of a rural or more turbulent urban environment. Because this assessment is
limited to inhalation, no deposition rates were calculated. The emissions
from site surface soils were treated as ground-level area sources in the
model. Because ISCLT treats area sources as squares, the site was divided up
into SO-by-SO foot ·grid squares. Grid squares were included as area sources
if they were over site surface soils in the sampled areas which have not been
remediated or covered with geotextile or clean soil. In total, 33 grid
squares (equal to an area of 82,500 sq. ft.) were designated as emission
sources of fugitive dusts and volatilized chemicals.
Although the potential for volatilization from the subsurface soils in the
covered and remediated areas does exist, volatilization from these areas was
not modeled because it is expected to be insignificant relative to that from
the surface soils. The minimum of six inches of clean cover found in these
areas should significantly slow the rate of volatilization relative to that
from surface soils. In addition, the areas of clean cover and surface soil
remediation represent a small fraction of the total site area from which
volatilization from surface soil was modeled.
A unit flux rate of 1 µg/m2-sec was input into the ISCLT model as the emission
rate. Annual average 11 unit11 air concentrations were determined at two
discrete off-site receptor locations and for the area within the site property
boundary. The off-site receptor locations were selected as the closest
business and resident downwind from the site. These two receptors are located
across the road to the north and northeast, respectively, from the site, The
air concentrations associated with the unit flux were determined to be 2.53
µg/m3 at the busi~ess to the north and 0.255 µg/m3 at the residence to the
northeast. ISCLT cannot predicted ambient air concentrations directly over an
area source of emissions. The geometric configuration of the site also
D-14
obviates use of a traditional box model. In order to allow ISCLT to be used
to predict on-site air concentrations, the area source grid and a receptor
grid were designed which would minimize the effect· of· this limitation.
Specifically, on-site concentrations were determined by using a rectangular
receptor grid with SO-foot grid spacing such that each grid point was at the
center of the grid squares used to select area sources. In this way, when a
receptor location was directly over an emissions source, only emissions from
that source would not contribute to the air concentration at_ the given
receptor location. The use of a relatively small grid size ensured that the
"missing" emissions would not be significant relative to the total emissions
from all the surrounding the emissions sources. An air concentration
associated with the unit flux of 0.259 µg/m3 was calculated as the average of
the concentrations output by ISCLT for all the grid points which fell within
the site property boundary. The unit flux-based air concentrations determined
above were then multiplied by the chemical-specific flux rates (in µg/m2-sec)
calculated in Sections D.2 and D.3 of this appendix to obtain chemical-
specific air concentrations for each of the combinations of receptor locations
and exposure durations.
D-15
APPENDIX D REFERENCES
BOMBERGER, D.C., GWINN, J.L., MABEY, W.R., TUSE, D., and CHOU, T.W. 1983.
Environmental Fate and Transport at the Terrestrial-Atmospheric
Interface. In: Fate of Chemicals in the Environment. Compartment and
Multimedia Models for Predictions. American Chemical Society.
Washington, D.C. 1983
COWHERD, C., MULESKI, G.E., ENGLEHART, P.J., and GILLETTE, D.A. 1985. Rapid
Assessment of Exposure to Particulate Emissions from Surface
Contamination Sites. Midwest Research Inst., Kansas City, MO.
PB85-192219
ENVIRONMENTAL PROTECTION AGENCY (EPA). 1986. Development of Advisory Levels
for Polychlorinated Biphenyls (PCBs) Cleanup. Final. EPA, Office of
Health and Environmental Assessment. Washington, D.C. OHEA-E-187
ENVIRONMENTAL PROTECTION AGENCY (EPA). 1987. Industrial Source Complex (ISC)
Dispersion Model User's Guide -Second Edition (Revised). Vol. I. EPA,
Office of Air Quality Planning and Standards, Research Triangle Park,
North Carolina. EPA-450/4-88-002a
LYMAN,· W.J., REEHL, W.F., and ROSENBLATT, R.T. (1982). Handbook of Chemical
Property Estimation Methods. McGraw-Hill, Inc., New York, New York
MERCER, J.W., RAO, P.S.C., THOMAS, S.P., and ROSS, B. 1982. Descriptions of
Parameters and Data Useful for Evaluation of Migration Potential at
Hazardous Waste Management Facilities. EPA Contract No. 68-01-6464
MILLINGTON, R.J. and QUIRK, J.P. 1961. Permeability of porous solids.
Trans. Faraday Soc. 57:1200-1207
D-16
i
APPENDIX E
RISK-BASED SOIL REMEDIATION GOALS
Risk-based soil remediation goals for the Geigy Chemical Corporation Site were
derived for an adult ingesting on-site surface .soil under future residential
land-use conditions. Of all the media and routes of exposure considered, the
incidental ingestion of surface soil presents.the greatest risk associated
with the site. Recent EPA guidance on soil remediation (RAGS Part B) directs
that when direct contact risks are of greatest concern at a site, soil
remediation goals should be based upon the incidental ingestion pathway (USEPA
1991a).
The risks within this pathway were found to be limited by a single pesticide,
toxaphene, as can be seen on Table 5-14 of the Baseline Risk Assessment. When
considering both frequency of detection and magnitude of risk, toxaphene is"by
far the chemical of greatest potential concern at the site. Guidance in RAGS
Part B supports the limiting chemical approach for developing surface soil
remediation goals at a Superfund site (USEPA 1991a).
Table E-1 further illustrates the limiting chemical approach. In this table,
three factors are presented for each chemical of potential concern in surface
soil. One factor represents a practical frequency of detection of the
chemical in surface soil at the site under existing baseline conditions. This
frequency conservatively represents the number of times a chemical was
measured in the total number of samples with usable detection limits (i.e.
samples with elevated detection limits were not included in this statistic in
accordance with guidance in RAGS Part A [USEPA 1989]). This value may differ
from the frequency of detection shown on Table 2-1 of the risk assessment
since the mean sample size was considered here rather than the total number of
samples collected. This is a conservative, but reasonable approach when.
determining the identity of the limiting chemical associated with risk at the
site.
The second factor presented in this table represents what fraction of the
total ingestion risk each chemical was responsible for under existing baseline
E-1
TABLE E·1
LIMITING CHEMICAL DETERMINATION (a)
Chemical Frequency X Percent Risk Product
Aldrin 0.061 0.0015 0.000091 alpha·BHC 0.10 0.016 0.0016 beta-BHC 0.38 0.0095 0.0036 gamna-BHC 0.067 0.0031 0.00021 alpha-Ch tordane D.036 0.0011 0.000038 ganma-Chlordane 0.031 0.0012 0.000039 4,4' -DOE 1.0 0.017 0.017 4,4' ·ODD 0.9 0.013 0.012 4,4• ·DDT 1.0 0.060 0.060 Dieldrin 0.079 0.078 0.0062 Toxaphene 0.83 0.80 0.66
Ca) Calculated from data presented on Tables 2-1 and 5-14.
Number of Samples in Which Chemical ~as Detected
Frequency= -----------···------····------------------------Mean sarrple Size (see Table 2·1)
Individual Chemical Risk
(see Table 5·14) Total Risk
E-2
conditions. (Risk is an integrated measure that takes both toxicity and
concentration into account). This was calculated by dividing the individual
chemical risk shown on Table 5-14 in the Baseline Risk Assessment by the total
risk associated with all the chemicals for that pathway (lxl0-5).
The product of these two factors provides information regarding both the
magnitude of risk and likelihood of exposure. As can be seen by this product
presented (as the third factor) on Table E-1, toxaphene is the most
significant chemical of potential concern in surface soil when evaluating both
frequency and toxicity (i.e. the product of frequency of detection and risk
percentage is much higher than any other chemical). This means that the
presence of toxaphene will dominate surface soil ingestion risk.
In order to obtain a health protective level for the site, Clement
International calculated a not-to-exceed concentration of toxaphene in surface
soil which would provide a residual risk no greater than lx10·6 for all of the
pesticides combined. This was accomplished by successively removing the
highest concentrations measured in surface soil at the site, and calculating
the exposure point concentration, represented by the 95 percent upper
confidence limit on the arithmetic mean per RAGS Part A, on the remaining
samples. Following this, the residual risk (RAGS Part C) was calculated
assuming exposure to all remaining chemicals of potential concern
(USEPA 1991b). After several iterations, it was found that removal of surface
soil containing toxaphene concentrations greater than 5 mg/kg resulted in a
toxaphene risk of lx10·6 , with an overall risk considering all pesticides of
lx10·6. This residual site risk is presented on Table E-2, and as can be seen
from this table, toxaphene is still the risk-limiting chemical. Table E-2
also provides the toxaphene site-wide exposure point concentration of 3,200
ug/kg which corresponds to the lx10·6 risk as well as the calculated chronic
daily intake.
Because numerous (89) surface soil samples were collected over this one-acre
area containing pesticides, removal of data points containing toxaphene
greater than 5 mg/kg (presented on Table E-3)_still provides· a robust
population of. samples (51) with which to calculate a not-to-exceed
concentration. This is shown by the summary statistics on Table E-4. As can
E-3
Chemicals Exhibiting
Carcinogenic Effects
Organics:
Aldrin
alpha-BHC
beta-BHC
garrma-BHC
alpha-Chlordane
ganma-Chlordane
4,4' -ODD
4,4'-DDE
4 4'-DDT
oieldrin
Toxaphene
TOTAL
Chemicals Exhibiting
TABLE E-2
POTENTIAL RESIDUAL RISKS ASSOCIATED WITH INCIDENTAL INGESTJ.ON
OF ON-SITE SOIL/SEDIMENT BY ADULT RESIDENTS
UNDER FUTURE LAND-USE CONDITIONS (a)
RME
Exposure Point
Concentration (ug/kg) (bl
4.SOE+OO
4.80E+OO
4.40E+01 2.10E+01
4.20E+01
4.30E+01
3.00E+02
4.60E+02
1.30E+03
4.60E+01
3.20E+03 (f)
RME
Exposure Point
Concentration
USEPA RME
Chronic Daily
Intake (CDI)
(mg/kg-day) (c)
1.28E·09
1.37E-09
1.25E-08
5.99E-09
1.20E-08
1.23E-08
8.SSE-08
1.31E-07
3.71E-07
1.31E·08
9.12E·07
USEPA RME
Chronic Daily
Intake (CDI)
Slope
Factor
(mg/kg-day)-1
1. 7E+01
6.3E+OO
1.8E+OO 1.3E+OO (e)
1.3E+OO
1.3E+OO
2.4E·01
3.4E·01
3.4E·01
1.6E+01
1. 1E+OO
Reference Dose
(mg/kg-day)
[Uncertainty
Weight of
Evidence
Class (d)
B2
B2
C
B2/C
B2
B2
B2
B2
B2
B2
B2
Target Organ/
Critical Noncarcinogenic Effects (Ug/kg) (b) (mg/kg-day) Factor] (f) Effect (g)
Organics: --------
Aldrin 4.SOE+OO 2.99E-09 3.0E·OS [1,000] Liver ganma-BHC 2.10E+01 1.40E-08 3.0E-04 [100] Liver/Kidney
Benzoic acid 3.60E+03 2.40E-06 4.0E+OO [1J Malaise alpha-Chlordane 4:20E+01 2.79E-08 6.0E·OS [1,000] Liver ganma-Chlordane 4.30E+01 2.86E-08 6.0E-05 [1,000] Liver
4,4'-DDT 1.30E+03 8.65E-07 5.0E-04 [100] Liver
Dieldrin 4.60E+01 3.06E-08 5.0E-05 [100] Liver
HAZARD INDEX
USEPA RME
Upper Bound
Excess Lifetime
Cancer Risk
2.2E·08
8.6E·09
2.3E-08
7.BE-09
1.6E·08
1.6E·08 2. lE-08
4.SE-08
1.3E-07
2. lE-07
1.0E-06
---------1E-06
USEPA RME
CDI :RID
Ratio
1.0E-04
4.7E-05
6.0E-07
4. 7E-04
4.BE-04
1. 7E-03 6. 1E-04 ----·····
< 1 3E·03
(8)
(bl
(C)
(d)
Res;dual risks were calculated on the surface soil sarrples remaining on the site after areas containing
toxaphene concentrations> 5 mg/kg were removed.
(e)
( f)
(9)
RME concentration is the 95X upper confidence limit on the arithmetic mean for all chemicals except for
benzoic acid which is the maxinun concentration remaining.
See text for exposure assl.Jll)tions. USEPA Weight of Evidence for Carcinogenic Effects:
[821 Probable hunan carcinogen based on inadequate evidence from hunan studies and adequate evidence from
animal studies.
[Cl Possible hlll'lan carcinogen based on limited evidence from animal studies in the absence of
hL111an studies;
Under review by CRAVE Morkgroup.
Uncertainty factors represent the amount of uncertainty in extrapolation from the available data.
A target organ/critical effect is the most sensitive organ/effect to a chemical's toxic effect. RfDs are based
on toxic effects in the target organ or on an effect elicited by the chemical. If an RfD was based on a study
which a target organ was not identified, the organ listed is one known to be affected by the particular chemica of concern.
E-4
TABLE E-3
TOXAPHENE CONCENTRATIONS OF SAMPLES REMOVED
FROM THE ON-SITE DATA SET
(Uni ts: ug/kg)
Sarlllle ID
SS-58-2DS
SS-110-0
SS-63-0
SS-58-0
SS-93-D
SS-63-2DS
SS-62-0
SS-61-0
SS-71-0
SD-6-l(dup)
sD-6-1
SS-57-0
SS-92
sD-1-1
SS-90
SS-103-0
S0-13-1
ss-s1-o ss-1os-o
ss-106-0
SS-49-0
SS-59-0
sD-3-1
sD-8
S0-21-1
SS-46-0
SD-19-1 SD-2-1
SS-67-0
sD-2D-1
SS-6D-D
SS-88
SS-89
SS-47-0 SS-104-0
SS-50-0
SS-25-0
SS-56-0
SS-62-20S
Toxaphene
Concentration
E-5
220,000
130,000
130,000
83,000
78,000
64,000
59,000
54,000
54,000
43,000
40,000
37,000
35,000
28,000
26,000
21,000
18,000
18,000
18,000
18,000
15,000
14,000
14,000
14,000
13,000 11,000.
11,000
11,000
10,000
9,700
9,300
8,800
8,700
8,000
7,100
5,800
5,600
5,400
5,200
Chemical
Organics:
Aldrin
alpha-BHC
beta-BHC .
ganma-BHC
alpha-Chlordane
ganma-Chlordane
4,4'-00D
4 4'-DDE
414'-DDT
oieldrin
Toxaphene
TABLE E-4
SUMMARY OF CHEMICALS OF POTENTIAL CONCERN IN ON-SITE SOIL
RESIDUAL SAMPLES AT A CLEANUP LEVEL OF 5 HG/KG (5,000 UG/KG) TOXAPHENE (a)
(Organics: ug/kg}
Mean
Frequency of Sample
Detection Cb) s.ize (c)
2 / 51 32 1 / 51 32 14 / 51 51 1 / 51 49
1 / 51 27
1 / 51 29 47 / 51 51 51 / 51 51
51 / 51 51
4 / 51 50 36 I 51 49
Arithmetic
Mean (d)
4.4
4.5
31 15
41
42
160
250
650
33
1,700
Range of Detected
Concentrations
5.9
13
4.4 · 290
55
45
49
7.7 710
3.7 1,000 9.4 4,600 11 130
340 4,300
Ca) Sample results from SS-01, SS-04, sS-09, SS-20-0 through SS-24-0, SS-26-0 through SS-32-0, SS-34·0 through SS·45·0, SS-52·0 through SS-54-0, SS·61·20S, SS-64-20, SS·66·20S, SS-68,
SS-82·0 through SS-85·0 SS-87 SS·92·10N SS-93·20E SS-94·0 through SS-97·0 SS-107·0
SS-168, SD-4-1, SD-7-1, 'so-,s,'so-41, and1 the duplic~tes of SS-168, SS-27-0, ~nd SS-44-6.
(b) The n\ATlber of samples in which the contaminant was detected divided by the total nLITlber of samples analyzed.
(c) The number of samples used to calculate the mean. This number may be less than the
denominator of the frequency of detection, because non-detect samples with high detection
limits were not included in calculating the mean.
Cd) Arithmetic mean concentrations were calculated using detected values and one half the detection limit of non-detects.
;t
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be seen by the information. in this table, most of the residual pesticide
concentrations have decreased from existing baseline conditions. Only the
alpha-chlordane isomer and aldrin, detected in only 1/89 and 2/89 samples,
remain at the same (but low) RME concentration. It can be clearly seen that
the removal of soil in excess of 5 mg/kg toxaphene effectively removes most of
the other pesticides as well, resulting in a site-wide residual risk of lx10·6
for all of the pesticides combined.
Since risk is proportional to concentration, removal of surface soil
containing concentrations of toxaphene greater than 50 mg/kg would therefore
represent a site-wide residual upperbound excess lifetime cancer risk of
lx10·5 for all of the pesticides combined. A residual risk of lx10·5 would be
reasonable for this site, because it is unlikely that residential development
would occur in the future. This is because the site is currently bisected by
railroad tracks, is bordered by a highway, and most of the property consists
of either railroad or highway right-of-ways.
A not-to-exceed concentration of 500 mg/kg toxaphene would result in a lx10·4
site-wide risk; however, the maximum surface soil toxaphene concentration at
the site under current baseline conditions is 220 mg/kg.
In conclusion, a not-to-exceed surface soil concentration of 50 mg/kg
toxaphene would provide a health protective level consistent with the
potential future use of this site.
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APPENDIX E REFERENCES
U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA). · 1989 .. Risk Assessment Guidance
for Superfund. Volume I: Human Health Evaluation Manual. (Part A).
Interim Final. EPA/540/1-89/002. December 1989
U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA). 1991a. Risk Assessment
Guidance for Superfund: Volume I -Human Health Evaluation Manual (Part
B, Development of Risk-based Preliminary Remediation Goals) -Interim.
Office of Emergency and Remedial Response, USEPA, Washington, D.C.
Publication# 9285.7-0lB. December 1991
U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA). 1991b. Risk Assessment
Guidance for Superfund Volume I -Human Health Evaluation Manual (Part
C, Risk Evaluation of Remedial Alternatives) -Interim. Office of
Emergency and Remedial Response, USEPA, Washington, D.C. Publication#
9285.7-0lC. December 1991
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