NCD986175644_19970502_Davis Park Road TCE Site_FRBCERCLA RISK_Human Health Risk Assessment Rev. 0-OCR

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Document Control No. 4400-71-AGHO
Revision 0
HUMAN HEAL TH RISK ASSESSMENT
DA VIS PARK ROAD SUPERFUND SITE
GASTONIA, GASTON COUNTY, NORTH CAROLINA
Work Assignment No. 71-4LPN
MAY 1997
REGION IV
U.S. EPA CONTRACT NO. 68-W9-0057
Roy F. Weston, Inc.
1880-H Beaver Ridge Circle
Norcross, Georgia 30071
WESTON W.0. No. 04400-071-095-0008-0I
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I UNITEi>STATES ENViRoNM'EN'rAL PROTECTION AGENtY
REGION 4
ATLANTA FEDERAL CENTER
. 100 ALABAMA STREET, SW.
ATLANTA, GEORGIA 30303-3104
4WD-NSMB
Mr. David D. Nelson
Roy F. Weston, Inc~
1880-H Bi:aver Ridge Circle
Norcross, GA 30071 .·· •· ·
June 17, 1997
SUBJ: Davis Park Road TCE Site
Human Health Ri'skAssessment
Worlc Assignment 71-4LPN
Dear Mr. Nelsori:
RECEIVED
JUN 19 1997
SUPERFUND SECTION
The subject document <ia:t6d May 1997, has been reviewed by the Agency. The
following comments shall be incorporated into the revised human health risk assessment
and resubmitted for review. Please contact me after you have received this corres-
pondence and had an opportunity to formulate responses. I would like to discuss with
you the comments below and your response prior to a resubmittal of the document.
Sincerely,
Kay L. Crane
Remedial Project Manager
cc: Kevin Koporec, USEP A ./
Harry Zinn, NCDEHNR v
Recycled/Recyclable • Prtnlod with Vegetable OIi Based Inks on 100% Recycled Paper (40'¼ Postconsumer)
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MAJOR COMMENTS
I.
2.
3.
4.
5.
6.
The soil portion of the risk assessment is seriously flawed in two respects. First, the
organic soil data were reported by the laboratories in units of ug/kg, but were interpreted
as mg/kg in the risk assessment. Second, the data used in the assessment combine both :
surface and subsurface soil data ( 16 samples in all) into one data set. However, only six of
the samples (those designated with an "A") are from the surface. Codes "B,., and "C" are
from the subsurface and should not be combined with the surface soil data. The soil · '
sample coded as "D" (5-SLD) is a duplicate of 5-SLA. To illustrate the significance of .·:
this comment, except for dieldrin, PCBs and petroleum products found in 1-SLA, all soil ·
organics reported in this risk assessment were found in the subsurface.
Data collected during the October 1996 field investigation is not included in this risk
assessment. A review of Appendix A RAW DATA includes only soil sample data and
groundwater sample data collected in May 1996. Please contact EPA if you do not have :
the October 1996 data set. If you do have this data set, please confirm that it is. a
complete data set.
Since the Phase I remedial investigation did not detect any TCE or PCE at the suspected
source area, Moore's Transmission Shop, any statements to Moore's as the source area
should be qualified. Such is the case on page 1-2, Section 1.1.2, 3rd sentence. The
sentence should read: "The source of the plume of contaminated groundwater is believed
to be an area of ... " Please correct throughout the document.
Risks due to exposure to groundw~ter from private wells should be calculated individually
rather than by calculating a repre~entative concentration as was done iri this assessment.
Alternatively, the concentrations of chemicals in these wells may be compared to MCLs or
North Carolina Groundwater Standards and conclusions regarding risk made depending
on these comparisons. ·
Insufficient information is provided to duplicate the calculation of exposure point
concentrations. The mean of the transformed data, standard deviation of the transformed 1
data, and sample size are needed. Remedial goal options calculations could not he
duplicated. Please provide example calculations for these and other calculations.
The toxicity values used for manganese are not current with EPA guidance. The reference:
dose (RID) currently OD IRIS (0.14 mg/kg-d) is for the total oral intake of manganese.
The assumed dietary intake of manganese (default of 5 mg/day) must be subtracted out to . .
determine the "environmental RID" to assess exposures from non dietary sources ( drinking
water, soil) of manganese. It is also recommended in the current IRIS file for manganese
that "a modifying factor of 3 be applied if this RID is used'for assessments involving
nondietary exposures." This modifying factor (MF) is recommended based on concerns
for effects from exposure to manganese in drinking water. Of particular concern is
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7.
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:·: ?/?f {~~:. :r;::
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exposu_re of infants to elevated levels of manganese, as would occur if infant formula is
made with drinking water which contains higher levels of manganese than does human
milk. The available evidence indicates that neonates may absorb more and excrete less
manganese from the gastrointestinal tract; additionally, manganese is thought to pass the
blood brain barrier more easily in the neonate.
All these factors make the neonate a sensitive receptor for the neurological effects of
manganese. Thus, caution (in the fonn of the MF) is warranted until better toxicological
data are available from which to derive an RID .. Since neonates can in most cases be
assumed to not have significant exposure to soil, the modifying factor ordinarily does not.
need to be applied for soil exposures.· This results in a "soil RID" of 0.07 mg/kg-d. For
groundwater that is a current or potential source of drinking water, the MF of 3 should be
applied. Application of the MF of3 results in an ~nvironmental RID of0.024 mg/kg-dto:
be used for drinking water exposures. • · ' · · · · i •
Several risk-based concentrations (RBCs) pr!)vided in Tables 2-1 and 2-2 are not.correct.:
In Table,2-1, the values for TCE and PCE are off by a factor of 10 in each case; i.e., the
RBC for TCE should be 1.6 ug/1; not 0.16 ug/1. An RBC exists for dibroino-
chloromethane (reported as chlorodibromomethane in the Region III table). It is 0, 13.
ug/1. In Table 2-2, the following RBCs are incorrect: • acenaphthene, dibenzofuran, ethyl
benzene, o-xylene, arsenic, berylliwn, cadmium, mercury , nickel, and strontium. In many
of these cases, the RBC corresponding to tap water was used in place of the RBC for soil
consumption. Naphthalene has an RBC; it is 310 mg/kg. The arithmetic average
background concentrations should/be shown in Tables 2-1 and 2-2.
It appears that the soil samples w're. collected from a non-residential area. Why then is a
residential scenario considered as a current use of the site? It appears that this should ..
have been considered as a commercial/industrial area for current use and residential for
future use. Inhalation exposure to dust should have been considered a potential exposure
route.
9. A technical/editorial review of the document should be conducted prior to resubmittal. . . ; --· . . .
MINOR COMMENTS
1. Throughout the document change the site name to "Davis Park Road TCE Site."
2. P. vi -TABLE OF CONTENTS -Table 6-1 has the wrong site name.
3. P. 1-2, Section I. I. I -The second sentence should be revised to read, "The site consists V
of an area in Gastonia, Gaston County, where private wells are contarnin~ted with TCE ·
and the Moore's Transmission Shop which is belie\ied to be .the source of the groundwater·!
, . . . : . . , ' . ." . . . . . I. . ' : 1 ·.
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contamination."
4. P. 1-7, 1st par. , 1st complete sentence -This sentence refers to the "project" as having a
paint thinner-like odor. Please correct. · · ·
5. P. 1-7 -Acme Petroleum was not mentioned in the site history, Section 1.2. Please
include. · · ·
6. P. 1-7, 3rd par. -The State's 1994 investigation was an "Expanded" Site Inspection.
7. Table 1-1 -The quality of this table is poor; it would be more appropriate in an appendix:
If this table is used, the map referenced in the table is needed to illustrate the sample
locations.
8. P. 2-1, Section 2 -The fact that all but one of the surface water and sediment samples
collected revealed no detects should be mentioned in this section.
9. P. 1-6, Section 1.2.4-The passage starting with "On February 12, 1991 ... "repeats text
provided in Section 1.2.1 on page 1-4 .. The text in Section 1.2.1 should be eliminated.
10. P. 2-1, Section 2 - A map is needed showing the locations of the samples referred to in
this section and used in the risk assessment.
11. P. 2-1, Section 2.1.2 -There is a discrepancy between the number of private wells cited in
the text and the results reported i? Appendix A. The text states that 32 residential wells
were sampled; however, only 29 are reported in Appendix A. (131-PWD is a duplicate of,
131-PW, and two wells, MW-1 and MW-2, are monitoring wells). Duplicate results
should be combined, using the higher of the two detected concentrations.
12. Tables 2-1 and 2-2 -The footnote for COPCs in these tables indicates a yes/no will be
included; however, only a rationale indicator is shown. As noted in the comment above,
there is a discrepancy between the number of Residential Wells illustrated in the Frequency
of Detection column on Table 2-1 and Appendix A, Raw Data. The footnote indicated by
an "*" concerns hexavalent chromium, however, chromium does not appear in the list of
contaminants found in the residential wells. Please explain and clarify. ·
13. Table 2-1 -It is unclear to the reader how the VOCs are accounted for in this table. The
VOCs ethyl benzene, toluene, and the xylenes, are listed as SVOCs. Also, it appears as
though all the VOCs were analyzed for in all 16 samples, but the frequency of detection
reads 1/1, 2/2, or 3/3. Please reorganize and make the necessary corrections.
14. Table 2-1 -The NC 21 Standards were not used as an ARAR to screen chemicals in the
selection of COPC process. Please do so to assure that chemicals exceeding the 21
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standards are not dropped from the list of COPCs.
15. Table 2-1 (titaniwn), and Table 2-2 (titaniwn and yttriwn) -According to the
Supplemental Guidance to RAGS, Human Health Risk Assessment Bulletin No. 2, page 2-
2, a chemical should not be excluded as a COPC because ofa lack of a chronic toxicity
value. The docwnent then details how these chemicals should be handled. Please refer to
the guidance and make necessary revisions.
16. . P. 2-4, Section 2.1.3 -The text implies that all samples were analyzed for TCUT AL
parameters; however, the detection frequency in Table 2-2 shows at most three.samples
were analyzed for semi-volatiles. Please explain. . · ·
17. P. 2-4, Section 2.1.3 -The text implies there were 16 soil sample locations. This risk
assessment only addresses data gathered during May, 1996 which had only 6 soil sample
locations; multiple depths were sampled at each location. ·
'. 18. P. 2-6, Section 2.2.2 -Consistent with_ Supplemental Guidance to RAGS: Region 4
Bulletins, iron cannot be eliminated based on the fact that it is an essential nutrient.
19. P. 3-3, Section 3.2.4-Revise the current use scenario to address onsite
industrial/commercial use.
20. P. 3-4, Table 3-1 -Revise the health assessment to include the inhalation exposure route
for surficial soil.
. ;· . . . . .
21. P. 3-5, Section 3.2.4-Exposure to VOCs during showering is generally limited to
adolescents and adults. ·
22. P. 3-7, Section 3.3 -The text refers to future receptors. Previously, groundwater use was
referred to as a current use scenario. There is no question that use of groundwater, via
private wells, is a current scenario. Please explain and correct.
23. Table 3-2 -What is meant by "future soil scenario?" As presented, there is no difference ..
between current and future use with respect to soil.
24. Table 3-4 -There are two typographical errors in the last footnote.
25.
26.
P. 4-11 -Please quote the passage within the cited reference which states that PCE does
not pass through the skin to any significant extent. This conclusion differs from that
presented in the 1996 update of the toxicological profile for PCE. . .
,/'
The assessment of lead does riot correctly apply EPA' s recommended criteria. Section
5.4.3 (pg 5-15) should be edited to read:· "Since tli.e IEUBK lead model, with site data,
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27.
28.
29.
30.
31.
32.
33.
34.
predicted a probability of less than 5% exceedance of the cutoff of 10 ug/dL, lead in site
soil is not expected to pose a health threat." ·
Tables 4-1 and 4-2 -Dermal toxicity values should be shown in these tables.
Tables 5-1 through 5-6 -Too many significant figures are used in these tables and in the
text. Per Region IV guidance, one is sufficient.
Table 5-3 contains the same information as Table 5-1 and is more understandable. The
same can be said for Tables 5-6 and 5-4, For better clarity, Tables 5~ I and 5-4 could be
eliminated.
Table 5-6 -Using "0.00" for the hazard indices associated with non-ingestion uses of
groundwater implies a calculated value. It would be better to use "NA" since no
inhalation reference doses are available.
P. 5-13, Section 5.4-Lead toxicity needs to be reevaluated using swface soil data only ..
P. 6-1, Section 6.1 -Reference to ."recent months". when the s;ited reference is five years
old seems inappropriate. ·
P. 6-4, Section 6.3.1.2 -The text states that only certain wells.were used, This is not true
in this assessment.
P. 6-5, Section 6.3.1.3 -Please verify that soil samples were collected from zero - 5 ft.
The six surficial soil samples collected during May 1996 were within the top 0-6".
Appendix A
I. T The qualifier "U" for soil sample 4-SLB was omitted from the table.
Appendix D
I. Table D-1. North Carolina Groundwater Standards exist for I, 1-DCE and chloroform.
They are 0.007 mg/I and 0,00019 mg/I, respectively. TCE and PCE are also present above
their respective Groundwater Standards. Consistent with Supplemental Guidance to
RAGS: Region 4 Bulletins, chemicals that exceed ARARS are COCs. Therefore, these
chemicals are COCs and should be included in this table. The MCL for chloroform is
based on total trihalomethanes and should be footnoted as such.
2. Benzo(a)pyrene should be removed from this table.
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Prepared by:
HUMAN HEAL TH RISK ASSESSMENT
REVISION 0
,.,,,.,.
DA VIS PARK ROAD SUPERFUND S·FFE 1 2 199?
GASTONIA, GASTON COUNTY, NORTMJC..AR0OLINA
t'E:RFliND SECTION
David D. Nelson
U.S. EPA Contract No. 68-W9-0057
Work Assignment No. 71-4LPN
Document Control No. 4400-72-AGHO
MAY 1997
Date: --=S-_,(f-_L-,/f-7-'--'-l __
I I
Date: --=-SJ-i-=-f'-1---'/q_J __
WESTON Work Assignmenl Manager
-Approved by: -::-,,.,---LLle'.e".==u....:::c!..__:'=~f--f-l__ __ _
William R. Doyle
Date: ___ 5_,_~_-~Zec___-_,9_71__ __
WESTON Region IV Program
Approved by: Date: __________ _
Kay Crane
U.S. EPA Remedial Project Manager
Approved by: ______________ _ Date: _________ _
Robert P. Siem
U.S. EPA Regional Project Ofliccr
WESTON W.O. No. 04400-071-095-0008-0I
NOR/K:IWP10440010711RPMJC002.00C
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This document was prepared by Roy F. Weston, Inc., expressly for EPA. It shall not be disclosed, in whole or in part, without the-express
written permission of EPA.
Section
1
2
TABLE OF CONTENTS
Title
Human Health Risk Assessment
Davis Park Road Superfund Site
Section: Table of Contents
Revision: O
Date: May 1997
Page
INTRODUCTION ..................................................................... 1-1
Site Location and Description
I. I. I Site Location ......
1.1.2 Site Description ..
1.2 Site History/Investigations ........ .
1.2.1 Site Ownership and History ........ .
1.2.2 Process and Waste Disposal ........ .
1.2.3 Permits and Regulatory History
1.2.4 Remedial Actions to Date ..
1.3 Organization of Report
1.4 References ...... .
. .. 1-2
. 1-2
.1-4
1-4
. 1-5
. 1-5
. ...... 1-6
.. 1-10
. ........... 1-1 I
DATA EVALUATION ................................................................ 2-1
2.1
2.2
23
2.4
Introduction ..
2.1.1 Study Area Investigation ...
2. 1.2 Groundwater Investigation .......... .
2.1.3 Surface Soil Investigation
Identification of Chemicals of Potential Concern
2.2.1 Data Reduction ..... .
2.2.2 Screening Criteria ..
Chemicals of Potential Concern .......... .
References ...
............. 2-1
. ............. ,.2-1
. ..... 2-1
....... 2-4
·············2-4
. ..... 2-4
··········2-7
···························2-7
NOR/K:IWP\04400\071\RPMJC002.DOC
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This document was prepared by Roy F. Weston, Inc., expressly for EPA. lt shall not be disclosed, in whole or in part, without the express
written permission of EPA.
Section
3
4
Human Health Risk Assessment
Davis Park Road Superfund Site
Section: Table of Contents
Revision: 0
Date: May 1997
TABLE OF CONTENTS (Continued)
Title Page
EXPOSURE ASSESSMENT ........................................................ 3-1
3.1
3.2
3.3
3.4
3.5
3.6
3.7
Introduction .......... .
Characterization of Exposure Setting
3.2.1
3.2.2
3.2.3
3.2.4
Land Uses ....
Topography and Drainage ....
Geology
Potentially Exposed Populations.
·························3-]
...................... 3-1
....................... 3-1
. ... 3-2
···········••·········3-2
·································3-3
Conceptual Site Model ......................................................................... 3-5
Exposure Point Concentrations . .. . . . .. .. . . . . . . . .. . .. . ..................... 3-8
Exposure Dose Models and Assumptions ... 3-I 0
3.5.1
3.5.2
'3.5.3
3.5.4
Drinking Water Ingestion .....
Inhalation While Showering
Incidental Ingestion of Soil ...
Dermal Contact With Soil
Calculated Daily Intakes ..
References ........ .
.... 3-I I
.. 3-I I
............ 3-13
.. 3-16
. ... 3-18
. ....................... 3-18
TOXICITY ASSESSMENT ......................................................... .4-1
Introduction .......... . 4. I
4.2 Toxicity Summaries on the Chemicals of Potential Concern ..
.. .4-1
..... 4-1
4.2.1 Organics ...
4.2.2 Inorganics
4.3 Carcinogenic and Noncarcinogenic Toxicity Values ....... .
4.3. I Estimates of Carcinogenic Potency
4.3 .2 Estimates of Carcinogenicity
···················.4-I
.. .4-12
..4-19
......... 4-19
. .4-20
NOR/K:\WP\04400\071\RPMJC002.DOC II
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This document was prepared by Roy F. Weston, Inc., expressly for EPA. II shall not be disclosed, in whole or in part, without the express
written permission of EPA.
Section
5
6
4.4
Human Health Risk Assessment
Davis Park Road Superfund Site
Section: Table of Contents
Revision: 0
Date: May 1997
TABLE OF CONTENTS (Continued)
Title
4.3.3 Estimates ofNoncarcinogenic Toxicity
4.3.4 Reference Doses ..
References
Page
... .4-24
. .... 4-25
.. .4-28
RISK CHARACTERIZATION ..................................................... 5-1
5.1
5.2
5.3
5.4
5.5
Introduction ............ ..
Approaches to Evaluating Risk .....
5.2.1
5.2.2
Carcinogenic Risk .......... ..
Noncarcinogenic Risk .... ..
Risk Results
5.3. I
5.3.2
Potential Risks Associated With Current Resident .
Potential Risks Associated With Hypothetical Future Resident
Exposures
Lead Toxicity ..
54.1
54.2
54.3
Background ........
Lead Uptake/Biokinetic Model. .....
Conclusions
References .
........ 5-1
. ....... 5-2
. ....... 5-2
......... 5-4
. ... 5-5
... 5-12
. .. 5-13
....... 5-13
.... 5-15
..... 5-17
UNCERTAINTY ANALYSIS ....................................................... 6-1
6.1
6.2
6.3
Introduction
Exposure Pathways and Chemicals Associated with Significant
Cancer and Noncancer Risk
Uncertainties Associated with Exposure Assessment ..
·······6-2
.... 6-3
NOR/K:IWP\0440010711RPMJCC02.DOC Ill
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This document was prepared by Roy F. Weston, Inc., expressly for EPA. It shall not be disclosed, in whole or in part, without the express
written permission of EPA.
Section
6.4
6.5
6.6
6.3.1
Human Health Risk Assessment
Davis Park Road Superfund Site
Section: Table of Contents
Revision: O
Date: May 1997
TABLE OF CONTENTS (Continued)
Title Page
Estimation of Exposure Point Concentrations for the Groundwater
and Soil Pathways .. . .. . . . .. .. . .. . . . .. . . .. . . . . . ..... 6-4
6.3.1.l
6.3.1.2
6.4.1.3
Degradation of Volatiles ............................... .
Well Location and Contamination ................ .
Soil Depth .............................................................. .
. .. 6-4
. ..... 6-4
...... 6-5
Uncertainties Associated with Toxicity Assessment ............................... 6-5
6.4.1
6.4.2
Cancer Slope Factors ................. .
6.4.1.1
6.4. l .2
Tetrachloroethene ...... .
1, l-Dichloroethene (l, 1-DCE) ..
Reference Doses
6.4.2.1
6.4.2.2
6.4.2.3
6.4.2.4
Use of Chronic Rills in Children
2-Methyl Naphthalene
Naphthalene·.
Phenanthrene .................. .
Uncertainties Associated with Risk Characterization
References ................ .
. ...................... 6-5
·························6-6
.... 6-7
............ 6-8
............. 6-8
............... 6-8
..... 6-8
··············6-9
... 6-9
NORIK:\WP104400\071\RPMJC002.DOC IV
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This document was prepared by Roy F. Weston, Inc., expressly for EPA It shall not be disclosed, in whole or in part, without the express
written permission of EPA.
Figure
Figure 1-1
Figure 3-1
Figure 5-1
Table
Tablel-1
Table 2-1
Table 2-2
Table 2-3
Table 3-1
Table 3-2
Table 3-3
Table 3-4
Table 3-5
Table 3-6
Human Health Risk Assessment
Davis Park Road Superfund Site
Section: Table of Contents
Revision: 0
Date: May 1997
TABLE OF CONTENTS (Continued)
LIST OF FIGURES
Davis Park Road TCE site ....... .
Conceptual Site Model for David Park Road.
Bell Curve Distribution of Blood Levels ................ .
LIST OF TABLES
Title
DEM Data ....... .
Selection ofCOPCs in Groundwater Residential Wells.
Page
.. 1-3
............. 3-6
................... 5-16
Page
.. 1-8
.. 2-2
Selection ofCOPCs in Soil ......... 2-5
Chemicals of Potential Concern .............. 2-8
Exposure Scenario and Potential Exposure Routes...... .. 3-4
Exposure Point Concentrations ... 3-9
Model for Calculating Doses from Ingestion of Groundwater. . ... 3-12
Physical/Chemical Parameters for Screening VOCs in Groundwater ............. 3-14
Model for Calculating Doses from Incidental Ingestion of Soil. ........................ 3-I 5
Model for Calculating Doses from Dermal Contact with Soil. .......................... 3-17
NOR/K:\WP\04400\071\RPMJC002.DOC V
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This document was prepared by Roy F. Weston, Inc., expressly for EPA. II shall not be disclosed, in whole or in part, without the express
written permission of EPA.
Table 4-1
Table 4-2
Table 5-1
Table 5-2
Table 5-3
Table 5-4
Table 5-5
Table 5-6
Table 6-1
Human Health Risk Assessment
Davis Park Road Superfund Site
Section: Table of Contents
Revision: O
Date: May 1997
TABLE OF CONTENTS (Continued)
Carcinogenic Toxicity Data ............................................................................ 4-21
Non-Carcinogenic Toxicity Data ..................................................................... 4-26
' I
Lifetime Cancer Risk -Current and Future Scenarios Reasonable
Maximum Exposure Concentrations ................................................................. 5-6
Substances of Concern (Reasonable Maximum Concentration) That Pose
a Carcinogenic Risk Exceeding One in One Million ( 1 o·6) ................................ 5-7
Total Carcinogenic Risk by Exposure Pathway at Reasonable Maximum
Exposure Concentrations . . . . . . ...... 5-8
Total Hazard Index -Current and Future Resident Scenarios Reasonable
Maximum Exposure Concentrations .................................................................. 5-9
I
Substances:of Concern (Reasonable Maximum Concentration) Exceeding
a Hazard Iridex of 0.1 When Hazard Index for Exposure Scenario
Exceeded 11.0 ............ . .. . ................. 5-1 O
Total Hazard Index by Exposure Pathway at Reasonable Maximum
Exposure Concentrations . . . . . . . . . . .............. 5-1 I
Summary of Uncertainty Analysis North Belmont PCE Site ............. 6-10
NOR/K:\WP\04400\071\RPMJC002.DOC VI
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This document was prepared by Roy F. Weston, Inc., expressly for EPA. ti shall not be disclosed, in whole or in part. without the express
written permission or EPA. ·
Human Health Risk Assessment
Davis Park Road Superfund Site
Section: Table of Contents
Revision: O
Date: May 1 997
TABLE OF CONTENTS (Continued)
APPENDIX A -Raw Data
APPENDIX B -Exposure Doses
APPENDIX C -Risk Tables
LIST OF APPENDICES
APPENDIX D -Remediation Goal Options (RGOs)
APPENDIX E -Lead Model Results
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NOR/K:\WP\04400\071\RPMJC002.DOC VII
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This document was prepared by Roy F. Weston, Inc., expressly for EPA. It shall not be disclosed, in whole or in part, without the express
written permission of EPA.
SECTION 1
INTRODUCTION
Human Health Risk Assessment
Davis Park Road Superlund Site
Section: 1
Revision: O
Date: May 1997
This report is a human health risk assessment for the Davis Park Road Superfund site and has
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been prepared for the U.S.' Environmental Protection Agency (EPA), Region IV, Atlanta, GA, as
part of a Fund-Lead Remedial Investigation/Feasibility Study (RI/FS). In accordance with the
National Oil and Hazardous Substances Pollution Contingency Plan (NCP), the risk assessment
explains the potential human health impacts associated with a site under the no-action alternative
(i.e., in the absence of remedial or corrective action). For this risk assessment, the no-action
alternative was defined for both present and potential future uses of the site; the scope of this risk
assessment included an evaluation of both the current and potential future human health risks
associated with chemicals in various media at the site.
The human health risk assessment for the Davis Park Road site was prepared according to EPA
guidelines for risk assessments at Superfund sites. The approach and methodology used in
conducting the risk assessment followed the guidance set forth in the Risk Assessment Guidance
for Superfund (RAGS), }fuman Health Evaluation Manual (EPA, I 989), its Supplemental
Guidance "Standard Default Exposure Factors" (EPA, 199 I), the Interim Region IV 'Risk
Assessment Guidance (EPA, 1992), and the Supplemental Guidance to RAGS: Region IV
Bulletins (EPA, 1995). Where appropriate, additional guidance and information sources used in
preparing the ri~k assessmert were cited in the report.
NOR/K:IWP\04400\071\RPMJC002.00C 1-1
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This document was prepared by Roy F. Weston, lnc., expressly for _EPA. It shall not be disclosed, in whole or in part, without the express
written permission of EPA.
I.I SITE LOCATION AND DESCRfPTION
Human Health Risk Assessment
Davis Park Road Superfund Site
Section: 1
Revision: 0
Date: May 1997
The following subsections are selected from Davis Park Road TCE site, Expanded Site Inspection
(NCDEHR, 1994)
I. I. I Site Location
The Davis Park Road TC:E Site (DPR) is located between Hudson Boulevard and Dogwood
Avenue west of the City of Gastonia within the Gastonia Extra Territorial Jurisdiction (ETJ) area.
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The site consists of an area of contaminated soil behind the Moore's Transmission and Auto
Repair Shop (Moore's) and a plume of contaminated groundwater that begins at the Moore's
property at 2307 Davis Park Road and extends south along the west side of Davis Park Road to
Dogwood Avenue. The site also includes the Cedar Oak Park Subdivision located on the east side
of Davis Park Drive within the confines of Cedar Oak Circle. The site can be found on the
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Gastonia South, North Carolina USGS 7.5' Quadrangle Map at latitude 35°13'56"N and
81°13'08"W.
l. 1.2 Site Description
The site, situated on approximately 20 acres, includes private businesses and residential homes.
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The topography of the Mopre's property is slightly sloped to the west towards Crowder Creek
(Figure 1-1 ). The source of the plume of contaminated groundwater is an area of contaminated
soil located behind Moore's in the vicinity of a drain line exiting the service bay in the facility.
NOR/K:\WP\04400\0711RPMJC002.DOC 1-2
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<{
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w _J c.::
u U1
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[)._
MOORE TRANSMISSION
SHOP
ARCS/DAVIS PARK ROAD
GASTONIA, SOUTH CAROLINA
SITE LOCATION MAP
FIGURE 1-1
CHARLOTTE
DRA\JN
WRS
CHECKED
HUDSON BL VO.
D,,4 YTS P.tR.X RD.
APPROVED ATE
\J. □. NO.
04400-071
D\JG, 'NO.
P-DAVIS
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This document was prepared by Roy F. Weston, Inc., expressly for EPA. It shall not be disclosed, in whole or in part, without the express
written permission of EPA.
1.2 SITE HISTORY /INVESTIGATIONS
Human Health Risk Assessment
Davis Park Road Superfund Site
Section: 1
Revision; O
Date: May 1997
The following information was selected from the Site Inspection Report (GM!, 1992).
Prior to 1960, the site was owned by Mr. John Birch of Gastonia, who operated a service station
on site. Mr. Carl Bell, 2916 Burnt Mill Road, Charlotte, purchased the property in about ·I 960
and operated a service station on site until about 1979 or 1980, when he leased the property to
Mr. Roy Moore, who currently operates a transmission rebuild and repair facility on site.
1.2.1 Site Ownership and History
Moore's Transmission Shop, located at 2307 Davis Park Road, has been identified as one of the
possible sources of contamination.
ln July 1990, the Moo,resville Regional Office of the North Carolina Department of
Environmental Management (DEM), Groundwater Section, conducted a site inspection. During
·,he inspection, DEM personnel discovered the existence of petroleum underground storage tanks
,:usTs) on the property. 0~ February 12, I 99 I, the North Carolina Department of Environment,
Health, and Natural Resources (NCDEHNR) issued a compliance notice in accordance with 40
!:FR 280.70 Temporary Tank Closures that states, " ..... when a UST system is temporarily closed
for more than 12 months, o;_,ners and operators must permanently close the UST system if it does
not meet EPA requirements." On February 18, 1991, the USTs at Moore's Transmission Shop
were removed. At the time of removal, one tank reportedly had 5 to 7 inches of product and the I ,
other had 3 to 4 inches. The product had a paint thinner-like odor. Upon removal of the tank,
mils in the vicinity of the tanks were tested for contamination. Results showed no contamination
present in the soils.
NOR/K:IWP\04400\071\RPMJC002.DOC 1-4
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This document was prepared by Roy F. Weston, Inc., expressly for EPA. It shall not be disclosed, in whole or in part, without the express
written permission of EPf',. i
1.2.2 Process and Waste Disposal
Human Health Risk Assessment
Davis Park Road Superfund Site
Section: 1
Revision: O
Date: May 1997
In July 1990, a site inspection of the Moore's Transmission Shop was conducted by the staff from
the Mooresville Regional Office, Groundwater Section of DEM and the Gaston County Health
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Department. During the inspection, Mr. Roy Moore, owner of the transmission shop, stated the
type of work performed at the facility consisted of the repair and restoration of automobile
transmissions. Waste transmission fluid and oil are stored in 55-gallon metal drums, which are
staged on asphalt in the front part of the property. The waste material is recycled and used for
heating the building in the, winter. Mr. Moore knew nothing of the facility when it was a service
station, and he stated that Mr. Bell, the owner of the property, should be contacted concerning
the history of the property.
Mr. Moore indicated that there may be another source of contamination. He stated that there had
been a tanker truck parked in a church parking lot located approximately 1/4 mile south of the
transmission shop. The truck was from a chemical company in Charlotte. He also stated that the
parking lot showed signs of damage and speculated it may be from chemicals stored in the truck.
Mr. Moore indicated that ihe truck disappeared when news surfaced that the groundwater in the
area was contaminated. A representative of the DEM, Mooresville Office, said that other sources
confirmed this as well. DEM also inspected the parking lot and concluded that the lot was
damaged due to the weight'ofthe truck rather than a chemical spill.
1.2.3 Permits and Regulatory Historv
On March 31, 1990, Mr. Grady Russ, certified well operator of the Cedar Oak Park Subdivision,
collected a water sample 1in accordance with "Community Well Rules" and had the sample
NOR/K.\WP\04400\0711RPMJC002.DOC 1-5
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This document was prepared by Roy F. Weston, Inc., expressly for EPA. It shalt not be disclosed, in whole or in part, without the express
written permission of EPA.
Human Health Risk Assessment
Davis Park Road Superfund Site
Section: 1
Revision: 0
Date: May 1997
analyzed. The results from the sample revealed elevated levels of trichloroethylene (34.9 ppb),
tetrachloroethylene (23.7 ppb), and chloroform (9.2 ppb). A second sample was collected on
April 17, 1990, and the results closely match the first sample. As a result, the subdivision switched
to a backup well that was not contaminated. This well, however, has a much lower yield than the
primary well.
Since the first report of contaminated groundwater on May I, 1990, three private wells around
the Cedar Oak Park Subdivision have shown levels of trichloroethylene (ICE) above the North
Carolina Public Water System Maximum Contaminant Level (MCL) of 5 ppb. The highest level of
ICE measured was IO 1.4 ppb at the Charles May residence, located approximately 200 feet south
of the site. On July 6, 1990, the EPA collected samples from the contaminated wells in the Davis
Park Road/Cedar Oak Park Subdivision area. Results show the Charles May residence and Cedar
Oak Park Subdivision wells are contaminated with ICE at concentrations of 82 ppb and 81 ppb,
respectively. However, for the EPA to initiate a removal action, ICE contamination must be
either greater than or equal to the 128 ppb action level or be increasing so that it appears that the
128 ppb action level may be reached in the near fi.tture.
1.2.4 Remedial Actions to Date
On January 22, 1991, the Davis Park Road ICE site was placed on the US EPA's CERCLIS list
Federal Superfund Program with the NCDEHNR, Division of Solid Waste Management,
Superfi.tnd Section as the lead agency. On February 12, 1991, the NCDEHNR issued a
compliance notice to Mr. Carl Bell in accordance with 40 CFR 280.70 Temporary Tank Clo~ures
which states, " ..... when an UST system is temporarily closed for more than 12 months, owners
and operators must permanently close the UST system if it does not meet certain requirements ."
On February 18, 1991, the USTs at the Moore's Transmission Shop were removed. At the time of
NOR/K:IWP\0440010711RPMJC002.DOC 1-6
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This document was prepared by Roy F. Weston, Inc., expressly for EPA. It shall not be disclosed. in whole or in part, without the express
written permission of EPA.
Human Health Risk Assessment
Davis Park Road Superfund Site
Section: 1
Revision: 0
Date: May 1997
the removal, one tank reportedly had 5 to 7 inches of produce and the other had 3 to 4 inches
remaining in the tank. The project had a paint thinner-like odor. Upon tank removal, surrounding
soils were tested for contamination. Analytical results indicated that the soils were not
contaminated.
The DEM performed extensive sampling of the private wells in the vicinity of the site from. May
1990 to August 1992 (Table 1-1). Several Samples were Collected from soils behind the Moore's
operation close to a drain line which exits in the rear of the building. These soils were highly
contaminated with PCE and TCE. The drain line was installed when Acme Petroleum installed
service bays in the shop portion of the service station. A holding tank was to be installed but,
when bedrock was encountered at 2 to 3 feet, the tank was not installed.
In 1994, NCDEHNR conducted an Extended Site Inspection Investigation. They collected both
soil and groundwater samples. In soil around the drain lines, TCE and/or 1,2-dichloroethene, a
biodegradation product of TCE, was detected in all of the soil samples. Toluene and total xylenes
were also detected in the soil samples: however, they were not above any health-based
benchmarks. Groundwater was sampled via private residential wells which showed contamination
with PCE and/or TCE at levels above health-based benchmarks.
In I 996, the Science and Ecosystems Services Division of EPA (SESD) conducted a field
investigation as part of a Remedial Investigation. During this investigation, soil and groundwater
samples were collected. These data results are presented in Section 2.0 and used to quantify
health risks associated with the Davis Park Road site.
NOR/K:IWP\04400\0711RPMJC002.O0C 1-7
-----
s,,,np!e Luc;,tion A!,Jcr•cy
Ccd,11 Oill:. St,l.1tlivi:;io,1 Aqu;,tcch
J\quillcch
GCEH
EPA ESD
GCEH
EPA ESQ
Childes M;,y !C0-1) GCEH
2<119 Davis Park noad GCEH
EPA ESD
GCEH
EPA ESQ
GCEH
GCEH
Roy Moore (Moo,c Tumsmission) DEM
2307 O,wis Park Road DEM
DEM
DEM
DEM
DEM
DEM
DEM
DEM
DEM
Ch.ir!c s May (CO• I I GCEli
24 19 Davis P;irk no;,t/ GCEH
EPA ESQ /
·• ·'. ·, ,k ,, ,,, '.; t' GCEH
• ' ( EPA ESD
,., '·''• /,., GCeH
GCEH
S~yla11d Drive CW (CO ll GCEH sec 111.-ip
Jen\..ins CW !CO-Ji GCEH "<~e l\\,'\I)
111:.\..cfl'wit;,r, CW !CO •\I GC(:IC scu r11;1p
C11r111in{lh;,1n/J'r.n11y Pou\.. CW \C0·51 GCEH
sec rn.-ip
/h,ncll Gr.1vcs !CO·GI D(M
242'.:i Dilvis P;uk llo;,d GCEII
GCEH
--
D,11c
3/J 1/90
'1/17/90
' S/1 /90
7 /l 6/90
0/2 3/90
10/9/90
'1/2 7/90
? 5/1 5/90
7/6/90
0/2 3/90
I 0/9/90
1"/30/91
5/20/91
517/90
5/7/90
7 JI 2/90
7/12/90
8/0/91
0/0/91
8/1 2/9 2
0/12/92
0/1 J/92
8/1 J/92
4/27/90
/ ! 5/1 5/90
7 /G/90
8/23/90
10/9/90
1 /30/91
5/20/91
•1/27/90
4/27/90
4/'}. J/90
4/27/90
5/7/90
5/ 1 5/90
7 /1 2/90
---
$;111,plc Type
Table 1-1
DEM Data
D1inki11u W:it,,r /,,, I,)
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01inUn\) W;,1cr /,,, /£)
'
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Soil behind g:iraqc
Soil 18 .. deep al dump spot
Soil Jr deep at oil in ditch
Soil 12~ deep ;it oil in ditch
Soil JO" dee1> oily ;uea behind shop
Wa1e1 in hole
Soil beneath drain pipo
Soil 1' out ilnd 16" deep at pipe
W;itcr lhnt drilin pipo
Monitor Well fl\
D•ink.irm Water ,.
/
7
,
/
O,in~.inu W;;i1c1 / .. I. '
01inkinu W,11e1
O,i11ki11q Willtll
Dri11kinq Water
Orinki11!J W;,tc1
-----l!l!I!
/'CE TCE ChlorOlorrH cis, l. 2 l, 1,Qir:hloru 1.2.•l-"f,i 1,3.5• Tri .. Dicl•lo1oc1hc,u1 eth;\nc rnethyJbcn:onc IIH:lhyll,,:,
" 7 34 9 9.2 ."
2:J.7 31\.9 9.2
51.0 ' 12 JI I 20,9 56.1 (rilCC
I•\ 41
lK 101.'1 I K J.8 tr:ic.,
1 34.J
82 3.8J
t1acc I J 6.3 lfi\CC 4 --GOA"J 3.4AJ
IK 04 .2 I K J.5 -IK 66.2 l·K 2.8 trncc
Late fluting Chemicals (LECJ C 1 .J EE06
Clean
LEC..-44000
LEC .. 14000 l1nl1 ' I 370 2700 , 2400 soc JO ,2000 16 ,, 720 1500 730 SIC.
630 1300 S 2(·
26 ' 0.75 IK
IK 101.4 I K J.8 / \tilCe _;
134.J ,· /
82 J.aJ
11;,ce 116.3 trace 4 ' -·· ' 68AJ J.4AJ ' ,
IK tl4. 2 1 K · 3.5
I K, 66. 2 I K 2.8 traco
tr.ice uace
CLl;AN
CUAN
uace tfi1CO trace
0.31 8A 0.10
if.ICC 6.8
7
-------
S:.11,plc loc;,1iu1• A~cncy O;,t,i
Oilly Fran\.. /CO-/J DEM 5/7/'JO
2301 O:wis Park Road GCEH S/1 S/90 GCEH 7 /I 2/90
Debbie P.1,le1 (CO-OJ GCEH 5/15/90 2503 Dowis r,11k Ro;id
Glenda How/;md [CO• I I) GCEH 6/1/90 23'17 HcdQcwood Ci1clc
W.L. Godwin IC0· 121 GCEH GI) /90 2 2J.\_Davis.P.i11k Ro;id -
f\e5,1mplcd (C0-23) GCEH 7112/90
Shitlcy Fo,lncr {C0-13) GCEH 61 l /90 2717 Davis Park Ro.id
John Crenshaw !CO-1 l\J GCEH 6/1/'JO 20\(i Davis Park Road
Taite IC0· 15) GCEH Gil J90 2~01 fl1ia,oak
Howe (CO• I GI GCEH G/11190 2GO) D,wis Park Ho,id
WGAS R;idio (C0, 1 7] GCEH 6/1 1/90 62 7 Dav,s Par\:; Ro.id
.
C1u111lcy !C0· 1 OJ GCEH Ci/1 I /90 2.,2) 0;1v,s P;,11< flo;id
·.
Coe (C0· 191 GCEH G/1 1 /90 2 2 12 Dav•:. P;"I< Ho;11J
Moore Cw (CO· 2 21 GCEH 7 /1 2/90
~"" 111;,p
Oor,s Co,clla
2110) 0,1v,s f';1rk R(>;u! GCEH <:J/20/90
GCC:M 1 /30/'J 1
DEM 7 /2 3/92
Ja,ncs M;,y DEM 517/90 21100 Skyl.1tnJ D,ivc
Monie GCEH 0/23/90 ,
GCEH 0/23/90
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Table 1-1 Ccont.l
DEM Data
. ~·-S;unplc fypc PCE TCE
Qri11ki,11J Wah:• 0.25
trace 44.5
trace 37. I
Q,inl..inu Water
Dri11kin9 W,1tc1
Drinking Water
O,inking Water IK tr.ice
D1inkin9 Water C1c.1r,
Drinkin9 Wa1e, pace I .2
Drinkin9 W;i1c1
D1inkin9 W.:iter II~ 1 K
O,irlk.ing W;,ter Cle:u1
D,iokin<J W.:iler
Drin1<i,19 Wate1 t,aec 1 K
01i11kinu W;,tc1 \r;,•:,: 5 7 .55
Drinl:;in(J W;,11:r \r;1cc 24.3
uacc 20
17
D1inki11n W;11cr 0.05
OrinkirHJ W;,1c1 !Filtt:r,:dJ 0.1 O,inl:;in9 W;,1c1 tUnli!tcrctl) u:,cc '1•1\.1
----I!!!!!
..
Chlo,ofo1111 cis-1, 2 . I. l •Oichloro 1.2.4,T,i l,J.S•T1i Dichlorooihcnc 11th.inc mc1'1ylbcnzcnt1 mcthytl:icro
ttace 2.B
2.6
IK
lf.!Ce tr.:icc
lr,,cc
uacc 2. 2 uacc
1 K 1.6
111,ce 2-I
0.33 2. 2
1 K 1.5 .
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written permission of EPA. I
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1.3 ORGANIZATION 0F REPORT
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This risk assessment consihs of the following sections:
Human Health Risk Assessment
Davis Park Road Superfund Site
Section: 1
Revision: 0
Date: May 1997
Data Evaluation (Section 2). The purpose of this section 1s to evaluate and summarize the
chemicals detected in the sampled media at the Davis Park Road site. This characterization is
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comprised of two principal 1technical elements:
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• The evaluation of sile data to be used in the risk assessment.
• The selection of sitlreiated chemicals for which potential risks are assessed. I .
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Exposure Assessment (Section 3). This section presents the pathways by which current and future
residents (child and adult) ~ould come in contact with the chemicals of potential concern, the
exposure algorithms and inJut assumptions used, and the calculated exposure doses by medium, I
pathway and receptor. i
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Toxicity Assessment (Sectio/1 4). This section identifies carcinogenic and noncarcinogenic health
criteria for the chemicals of dot en ti al conce;n.
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Risk Characterization (Section 5). The exposure doses (Section 3) and toxicity criteria (Section
4) are integrated to calcullte carcinogenic and noncarcinogenic risk for each scenario and
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pathway.
Uncertainty Analysis (Sectiiln 6). The uncertainties related to key assumptions m the risk
assessment are discussed for kach of the sections. Uncertainties associated with those chemicals
and pathways that significantlt affected risk results are emphasized.
NOR/K:\WP\0440010711RPMJC002.DOC 1-10
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This document was prepared by Ro}' F. Weston, Inc., expressly for EPA. It shall not be disclosed, in whole or in part, without the express
written permission of EPA. I
Human Health Risk Assessment
Davis Park Road Superfund Site
Section: 1
Revision: 0
Date: May 1997
Appendices. The appendices contain documentation, detailed tables, and guidance for various
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sections of the report. They are as follows:
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• Appendix A -Raw1Data
• Appendix B -Exposure Doses
• Appendix C -Risk1Tabl~s .
• Appendix D -Rem~d1at1on Goal Options (RGOs)
• Appendix E -Leadl Model Results
1.4 REFERENCES
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EPA (U.S. Environmental I Protection Agency), I 989. Risk Assessment Guidance for Superfund
Volume I, Human Health 'Evaluation Manual, Part A. Interim Final. Office of Solid Waste and
' Emergency Response. Was,hington, DC, EPN540. l-89/002.
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EPA (U.S. Environmentl! Protection Agency), 1991. Supplemental Guidance: "Standard
' Default Exposure Factors':. OSWER Directive 9285.6-03; March, 1991.
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EPA (U.S. Environmental1 Protection Agency), 1992. New Interim Region IV Guidance, and
Supplemental Region IV Risk Assessment Guidance. U.S. EPA Region IV, Atlanta, GA 30365
(February 11, 1992a). ·
EPA (U.S. Environmental Protectio_n Agency), 1995. Supplemental Guidance to RAGS: Region
IV Bulletins, Nov. 1995.
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GM! (Greenhorne & O'Ma~a, Inc.), 1992. Davis Park Road TCE Site, Gastonia, North Carolina,
Phase I Site Screening !tive~tigation, October, 1992.
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NCDEHNR (North Carolin~ Department of Environment, Health and Natural Resources), 1994.
Extended Site l11.1pection Rq;ort, Davis Park Road 7CE PCE Site, Sept. 1994.
NOR/K:\WP\04400\071\RPMJC002.DOC 1-1 I
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This document was prepared by Ro~ F. Weston, Inc., expressly for EPA. It shall not be disclosed, in whole or in part, without the express
written permission of EPA. !
2.1 INTRODUCTION
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SECTION 2
DATA EVALUATION
Human Health Risk Assessment
Davis Park Road Superfund Sile
Section: 2
Revision: O
Date: May 1997
The objectives of this section are to review and summarize the analytical data for each medium
' sampled at the Davis Park Road site and to select the chemicals of potential concern to be
evaluated in the human hea
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lth risk assessment. '
2.1.1 Study Area Investi*3tion
SESD collected and handl1d all the media sampled according to the EPA Standard Operating :
Procedures Manual (EPA, 1996a). Appendix A presents a listing of the sampling data by medium I included in the risk assessment.
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2.1.2 Groundwater Investigation
Groundwater samples were collected from 32 residential wells identified in the contaminant
plume. The sampling event I for the residential wells included wells where the water is used for
potable water and householb uses. All samples were analyzed for volatile organic chemicals and 6 I
wells were analyzed for inorganic chemicals and semivolatile organic chemicals including '
pesticides and PCBs. The ddta summary is provided in Table 2-1.
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NORIK:IWP\04400\071 IRPMJC002. DOC 2-1
!I!!! 1!!11!1 I!!!! -l!l!9 l!l!9
This document was prepared by Roy F. Weston, Inc., expressly for EPA. It shall not be disclosed, in whole or in part, without the express written permission of EPA.
Carbon Disulfide
Table 2-1
Selection of CO PCs in Groundwater Residential Wells
FrcqucncJ
of
l / 32
Range of
Detection
1.0 -1.0
4/32 2.5-2.5
Range of
Detected
5.8
1.3 -2.4
Arithmetic Average Risk-Based
Detected CO Pc<•>
5.8 0.17 A
1.9 100 B
==
_ Chloroform --------'-1-32---1.0---1.0--40~-------·40-----0cl5--A ------
Dibromochloromethane l/ 32 1.0 -1.0 0.58 0.58 E
1, 1-Dichloroethene 3 / 22 l.0 -1.0 0.66 -3.8 A 2.0 0.044
1, 1-Dichloroethane 2 /32 1.0 -1.0 0.52 -0.57 0.54 81 B
cis-1,2-Dichloroethene 2 / 32 1.0 -1.0 1.6 -1.7 1.65 6.1 B
1.1.1-Trichloroethane 2 / 32 1.0 -1.0 1.2-7.8 4.5 79 B
Trichloroethenc 3 / 32 1.0 -1.0 0.92 -32 11.0 A
Tetrachloroethene 6 I 32 1.0 -1.0 3.1
Aluminum 2 / 5 50 -50 56 -460 258 3,700 B
Barium 6/6 14 -81 37 260 B
Calcium 6/6 6,200 -11,000 8,366 D
Copper 2/6 2.5 -2.5 3.4 -12 7.7 150 B
Iron 4/6 12 -12 14 -170 64.7 1,100 C,D
Magnesium 6/6 1,100 -3,700 2,417 D
Manganese 6 /13 2.5 -2.5 22 -24 23 84 B
Potassium GIG 1,400 -2,700 2, 133 D
NOR/K\WP\04400\071\DPRTBLES XLS Ti!ble 2-1 2-2
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This document was prepared by Roy F. Weston, Inc., expressly for EPA. It shall not be disclosed, in whole or in part, without the express written permission of EPA.
Tahlc 2-1
Selection of CO PCs in Groundwater Residential \Veils
Frequency Range of Range of Arithmetic Average
of Detection Detected Detected
Detection Limits Concentrations Concentrations
Sodium 6/6 --8,300 -16,000 11,366
Strontium 6/G --130-200 173.3
Titanium I / 6 2.5 -2.5 8.8 8.8
Vanadium 2/6 2.5 -2.5 4.2 -5.9 5.0
Zinc G/6 --4.~ -70 -_17,8 -·
Notes:
(I) COPC = Chemical of Potential Concern (yes/no).
(!) A= >Risk-based concentration (i.e., lxl0-6 for carcinogens and HQ= 0. l for non-carcinogens).
B = <Risk-based concentration (i.e., lx!0'6 for carcinogens and HQ= 0.1 for non-carcinogens).
C = No RBC m·ailablc to quantify risk.
Risk-Based
Screening COPC(I)
Value Basis'2>
--D
2,200 B
--C
26 B
---1,100-----B~
D = The chemical is an essential nutrient and professional judgement was used before the chemical was eliminated as a COPC.
E = The chemical is a member of a chemical class which contains other CO PCs.
* Based on toxicity information for hcxavalcnt chromium.
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Human Health Risk Assessment
Davis Park Road Superfund Site
Section: 2
Revision: O
Date: May 1997
The 16 soil sample locations were chosen to determine if PCE or any degradation products
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associated with PCE weie present. Soil samples were collected at several depth intervals and
analyzed for all target coJpound list and. target analyte list (T AL/TCL) constituents. The da,ta are
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summarized in Table 2-2. 1
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2.2 IDENTIFICATIONIOF CHEMICALS OF POTENTIAL CONCERN
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2.2.1 Data Reduction f
The quantitative assessme~t of exposure and potential risk for a site is based on the chemicals of
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potential concern. Chemic11s of potential concern are a subset of the list of all chemicals positively
identified at the site. The risks associated with the chemicals of potential concern are expected to ' I
be more significant than I the risks associated with other less toxic, less prevalent, or less
concentrated chemicals at )he site that are not evaluated qu,antitatively. The data are summarized
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by frequency of detection for each medium, the range of analytical quantitation limits, the range of '
detected concentrations, ahd the arithmetic mean of the detected concentrations. These criteria
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adhere to those set forth b; EPA Region IV in its current risk assessment guidance (EPA, 1995). I
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2.2.2 Screening Criteria I
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The screemng criteria that were used to eliminate detected inorganic or organic chemicals as
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chemicals of potential concbrn in each respective medium are briefly summarized below: I .
• Inorganic chemicals' were eliminated if the maximum chemical concentration was less than
two times the background concentration.
NORJK:IWP\04400\0711RPMJC002.00C 2-4
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Tublc 2-2
Selection of COPCs in Soil D Range of Range of Arithmetic A vcrage Risk-Based
Detected Detected Screl"ning COPc'''
0 Concentrations Vnluc Basis'2>
0
a I/, I 1,200 1,200 570 A
I/ I 2,000 2,000 15 A
I I, I I 1.0 I 1.0 130 B
I /,I 350 350 16,000 13 0 2 /,2 600 -10,000 5,330 E
O-Xvlcnc I /,I 31.0 31.0 1,400 13
Phenanthrcne 2 /12 600 -600 600 E
0 Pvrcnc I iii 380 380 230 A
Toluene I /,I 420 420 1,600 13
D
I Aluminum !6/116 2,900 -52,000 33,306 7,800 A
Arsenic 12 /116 5.0 · 10.0 4.7 -15.0 8.7 I.I A
Barium 16/!!6 52 - I IO 33.8 550 13
Bcrvllium I I 16 1.5-3.0 I. I I. I 0.016 A 0 Cadmium 3 I 16 1.5 -3.0 1.4 -3.2 2.4 39 13
Calcium 13 /116 200 -300 370 -28,000 5586 D
Chromium 16 /i16 6.4 -32 15 39• 13
I Cobalt 13 /116 4.0 -6.0 4.8 -11 6.6 470 B
Co er 16 iil6 5.7 -56 27.6 310 13
Iron 16116 16,000 -51.000 24,562 2.300 I)
I Lead 16 /;16 20 -630 156 400 A,
Magnesium 16/116 1.800 -IO ,000 3,575 I)
Manganese 16 ill6 87 -360 168 180 A
Mercurv 4 I 16 0.05 -0.05 0.03 -0.08 0.058 I. I 13 a Nickel 6 I 16 8.0 -12.0 9.3-27.0 15.7 73 13
Potassium 16 /•16 1,600 -4,500. 2.53 I D
Strontium 16/'16 4.0-38.0 18.4 2200 13
I Titanium 16 /116 5.0 -1,600 898 C
Vanadium 16 /116 38 -120 55 55 A
Yttrium 15 I ;16 5.0 -5.0 5.0-17.0 10.5 C
Zinc 16/-16 37 -300 111 2.300 13 g Notes: I
(iJ COPC = Chemical of Potential Conccrr~ (yes/no).
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(1) A= >Risk-based concentration (i.e., lx!0"6 for carcinogens and HQ= 0.1 for non-carcinogens). u B = <Risk-based concentration (i.e., I x1! o·6 for carcinogens and HQ= 0.1 for non-carcinogens).
C ""No RBC available to quantify risk.I
D = The chemical is an essential nutrient and professional judgement was used before the chemical was eliminated as a COPC.
E = The chemical is a member ofa chc\nica[ class which contains other COPCs. I • Based on toxicity information for hcxavdlent chromium.
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This document was prepared by Roy F. Weston, Inc., expressly for EPA. II shall not be disclosed, in whole or in part, without the express
written permission of EPA.
Human Health Risk Assessment
Davis Park Road Superfund Site
Section: 2
Revision: 0
Date: May 1997
• Inorganic 'chemicals were eliminated if the chemical was considered to be a natural or an
essential nutrient and had relatively low toxicity ( e.g., calcium, magnesium, iron,
potassium, and sodium).
Organic chemicals which had at least one laboratory detection were evaluated as chemicals of
potential concern, as organic chemicals are not naturally occurring in the environment and are
assumed to be anthropomorphically derived. Organic chemicals were eliminated if the maximum
chemical concentration was less than the risk-based concentration (RBC) provided by EPA
Region III (EPA, 1996b ).
2.2.2. l Groundwater
In the residential well samples, 11 organic and 13 inorganic chemicals were detected (Table 2-1 ).
Of these, 5 organic and no inorganic chemicals were retained for the risk assessment.
All the chemicals retained for the risk assessment exceeded the risk-based concentration. The
remaining chemicals were eliminated because their concentrations were less than the risk-based
concentration; an essential nutrient or toxicity values were not available to determine risk.
2.2.2.2 Soil
In the results of the soil sampling presented in Table 2-2, 21 inorganic elements and 11 org·anic
compounds were detected. Of these chemicals, 6 inorganic and 7 organic chemicals were selected
as chemicals of potential concern.
All the chemicals retained for the risk assessment either exceeded the risk-based concentration
(RBC) or were structurally similar to a COPC which exceeded the RBC. The remaining chemicals
NOR/K:\WP\04400\071\RPMJC002.DOC 2-6
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This document Was prepared by Roy F. Weston, Inc., expressly for EPA. It shall not be disclosed, in whole or in part, without the express
written permission of EPA.
Human Health Risk Assessment
Davis Park Road Superfund Site
Section: 2
Revision: 0
Date: May 1997
were eliminated because their concentrations were less than the risk-based concentration; an
essential nutrient or toxicity values were not available to determine risk.
2.3 CHEMICALS OF POTENTIAL CONCERN
A number of organic and inorganic chemicals were detected in the media sampled at the Davis
Park Road site. The list of site-related chemicals of potential concern (COPCs) was developed
based on the established screening criteria (Subsection 2.2.2). Table 2-3 presents the summary of
chemicals of potential concern by media that will be quantitatively evaluated in the risk
assessment.
2.4 REFERENCES
EPA (U.S. Environmental Protection Agency), 1989. Risk Assessment Guidance for Superfund,
Human Health Evaluation Manucil -Volume I, Part A. Interim Final. Office of Solid Waste and
Emergency Response. Washington', D.C. OSWER Directive 9285-7-0!a, EPA/540H-89/002.
EPA (U.S. Environmental Protection Agency), 1995. Supplemental Guidance to RAGS: Region
IV Bulletins, Nov. 1995.
EPA (U.S. Environmental Protection Agency), 1996a. Standard Operating Procedures and
Quality Assurance Manual, Athens, Georgia, May 1996.
EPA (U.S. Environmental Protection Agency), 1996b. Risk Based Concentration Table, January-
June I 996. Roy L. Smith, Ph.D. Office of RCRA Technical & Program Support Branch. April I 9,
1996.
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This document was prepared by Roy F. Weston, Inc., o.:xpn:ssly for EPA
It shall not be disclosed, in whole or in part, without the express v.rrith:n pem1ission of EPA.
Table 2-3
Chemicals of Potential Concern
Groundwater
I, 1-Dichloroethene 0.66 -3.8
Bromodichloromethanc 5.8
Chlorofom1 40
Dibromochloromethane 0.58
Tetrachloroethene 0.52 -10
Trichloroethene 0.92 -32
2,000
1,900 -94.000
660 -10,000
Phenanthrenc 600
380
Aluminum 2,900 -52,000
Arsenic 4.7 -15
Bcl)'llium I.I
Lead 20 -630
Manganese 37 -360
Vanadium 38 -120
NOR/K.IWP\04400\071\DPRTBLES XLS Table 2-3 2-8 512/97
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written permission of EPA.
3.1 INTRODUCTION
SECTION 3
EXPOSURE ASSESSMENT
Human Health Risk Assessment
Davis Park Road Superfund Site ,
Section: 3
Revision: 0
Date: May 1997
The purpose of the exposure assessment is to estimate the magnitude of potential human exposure
to the chemicals of potential concern at the Davis Park Road site. The results of the exposure
assessment are subsequently combined with chemical-specific toxicity information to
quantitatively estimate the potential human health risks associated with chemical exposure.
3.2 CHARACTERIZATION OF EXPOSURE SETTING
This step of the assessment discusses the physical environment and the land and water, uses
associated with the current and potential future uses of the site and the surface soils, groundwater
and the stream/sediment bodies in the immediate vicinity which have been impacted by the site.
3.2.l Land Uses
Land use in the vicinity of the site is largely residential with some industrial facilities. The nearest ,
residence is located less than 50 feet north-northwest of the site and the nearest school is 3,300
feet to the east. These distances were determined from USGS Quadrangle Maps and other
reference maps.
Gaston County has a mean annual precipitation of approximately 46 inches and a mean annual
lake evaporation of approximately 40 inches. Therefore, the net annual precipitation is 6 inches.
The 2-year 24-hour rainfall in this area is approximately 3. 0 inches.
NQR/K:\WP\04400\071\RPMJC002.DOC 3-1
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written permission of EPA.
3.2.2 Topography and Drainage
Human Health Risk Assessment
Davis Park Road Superfund Site
Section: 3
Revision: 0
Date: May 1997
The topography of the Davis Park Road site is relatively flat around the site but slopes westerly
towards Crowder Creek. Elevations on the site range from approximately 770 feet National
Geodetic Vertical Datum (NGVD) around the site, to approximately 660 feet at Crowder Creek.
The distance to the nearest downstream surface water body, Crowder Creek, is approximately
3,500 feet. The change in elevation over this horizontal distance is approximately 110 feet;
therefore, the slope of the intervening terrain is estimated to be 3. 7 percent. Crowder Creek flows
south-southeast into South Carolina. Approximately 15 miles downstream, Crowder Creek flows
into Lake Wylie. Crowder Creek in the Gastonia area has no recreational use except for very
limited bridge fishing several miles downstream of the site. However, once Crowder Creek nears
Lake Wylie, some recrea6onal activities such as fishing, canoeing, and swimming are possible.
The State of North Carolina has designated Crowder Creek as being suitable for Class C uses,
which include fish and wildlife propagation, secondary recreation, and agriculture. There are no
public water supply surface water intakes within 15 miles of the Davis Park site.
3.2.3 Geology
The Davis Park Road site is located within the Piedmont Physiographic Province and is further
characterized as Foliated to Massive Granitic rock unit of the King Mountain Belt. The formation
is described as a coarse grain, porphyritic, well-foliated biotite granite. Others have described this
formation to have several intrusion phases exhibiting cross-cutting relationships and differing in
texture and degree of foliation. The rocks are megacrystic to equigranular granite to quartz
monzonite.
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written permission of EPA.
Human Health Risk Assessment
Davis Park Road Superfund Site
Section: 3
Revision: 0
Dale: May 1997
Most of the domestic water supplies, industrial supplies, and several municipal supplies in Gaston
County are obtained from wells. The wells used in rural sections are dug type wells that derive
water from the weathered and disintegrated zone between the soil and the underlying
unweathered rock. Drilled wells used for higher yield for industrial and municipal use obtain water
from either granite or schist formations These wells have an average depth of 180 feet for schist
wells and 165 feet for granite wells. Average yields for these formations range from 150 and 100
gallons per minute, respectively. The closest domestic well to the site is the May residence, which
is located approximately 250 feet south of the site. The closest community well is the Cedar Oak
Development located approximately 1/4 mile south of the site.
Most residents living within a 1/2-mile-radius of the Davis Park Road site are connected to ,either
the Cedar Oak Park Subdivision community well or private drinking water wells. The remaining
residents, between 1/2 and 4 miles from the site are connected to the Gaston Water District or
private/community wells .. The Gaston Water District draws its water from the South Fork
Catawba River located northeast of the City.
3.2.4 Potentially Exposed Populations
The potential exposure pathways for the residents are listed in Table 3-1. The potential human
receptors are described in· the conceptual site model (Subsection 3 .3 ). The following narrative
discusses the rationale for pathways and routes of exposure for the residential scenarios.
• Current Resident - A child (age 1-6 years) and an adult are proposed for evaluation in the
current resident exposure scenario. Residents are proposed for evaluation because
residential developments currently exist immediately surrounding the site. The age groups
are proposed because of different types of exposure io the affected media depending on
NOR/K:\WP\04400\0711RPMJC002.DOC 3-3
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NOR/K: \WP\04400\071 \TBMJCOOl . DOC
Table 3-1
Human Health Risk Assessment
Davos Park Road Superfund Site
Section: 3
Revision: 0
Date: May 1997
Exposure Scenario and Potential Exposure Routes
Adult and Child Residents
•
•
' •
•
Ingestion of groundwater
Inhalation of VOCs while showering
Ingestion of soil
Dcmrnl contact with soil
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written permission of EPA.
Human Health Risk Assessment
Davis Park Road Superfund Site ,
Section: 3
Revision: O
Date: May 1997
activity of the receptors. Media to which there may be exposure include groundwater and
soil.
Exposure dose calculations for the groundwater pathways will be based on chemical data from the
residential wells currently used by some residents. The routes of exposure evaluated for
groundwater for all age groups include ingestion and inhalation of VOCs while showering.
Ingestion and dermal contact with soil is evaluated for both age groups.
• Future Resident -' For the future use scenario it is proposed that the same pathways be
evaluated as in the current use scenario. It is a conservative assumption that
concentrations will remain the same and not reduce through natural degradation
processes.
3.3 CONCEPTUAL SITE MODEL
The conceptual site model for the Davis Park Road site (Figure 3-1) incorporates information on
the potential chemical sources, affected media, release mechanisms, routes of migration, and
known or potential human receptors. The purpose of the conceptual site model is to provide a
framework in which to identify potential exposure pathways occurring at the site, and to aid in
identifying data gaps. Information presented in previous reports on the site history, demography,
and local land and water uses is used to identify potential exposure pathways at the site.
An exposure pathway consists of four elements (EPA, 1989) and includes:
NOR/K:\WP\04400\071\RPMJC002.D0C 3-5
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PRIMARY SECONDARY
PRIMARY RELEASE SECONDARY RELEASE PATHWAY EXPOSURE RECEPTORS
SOURCE MECHANISM SOURCE MECHANISM ROUTE
MOORE'S
TRANSMISSION
SHOP
;!~
. ;~~: 1A1
SUR;ACE f----1%'ii®ll ____ ~
'°~ i
SUBSURFACE
SOIL
FIGURE 3-1 CONCEPTUAL SITE MODEL FOR DAVIS PARK ROAD
Fll..E: E:IDAVIS-P.CDR
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written permission of EPA.
• A source and mechanism of chemical release.
• A retention or transport medium.
Human Health Risk Assessment
Davis Park Road Superfund Site
Section: 3
Revision: O
Date: May 1997
• A point of potential human contact with the contaminated medium.
• A route of exposure (inhalation, ingestion, dermal absorption) at the contact point.
When all of these elements are present, the pathway is considered complete. The assessment of
pathways by which potential human receptors may be exposed to contaminants includes an
examination of existing migration pathways (e.g., water, soil) and exposure routes (e.g.,
inhalation, ingestion, dermal absorption) as well as those that may be reasonably expected in the
future.
After the sources of contaminants: are identified, the next step in the development of the
conceptual model is to determine mechanisms of release to environmental media. The primary
release mechanism for the Davis Park Road site is the suspected disposal of solvents on the soil.
The secondary source of chemicals is contaminated subsurface soil. The secondary release
mechanism is infiltration to groundwater.
The following paragraphs describe the potential pathways to which human receptors may be
exposed.
• Groundwater -Contaminated groundwater is believed to be the major source of potential I exposure for future human receptors. Groundwater became contaminated through the
release of chemicals from improper disposal of waste solvent to the surface and subsurface
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soils. The subsequent infiltration of precipitation resulted in the movement of
contaminants from subsurface soil to groundwater. Groundwater-related pathways
evaluated for the current and future adult and child residents include ingestion and
inhalation of VO Cs while showering.
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This document was prepared by Roy F. Weston, Inc., expressly for EPA. It shall not be disclosed, in whole or in part, without the express
written permission of EPA.
Human Health Risk Assessment
Davis Park Road Superfund Site
Section: 3
Revision: O
Date: May 1997
• Soils -Soil was sampled in the area suspected of past disposal. Direct routes of exposure
evaluated for soil include incidental ingestion of soil and dermal contact while working
outside (i.e., children playing, gardening, etc.).
3.4 EXPOSURE POINT CONCENTRATIONS
The 95 percent upper confidence limit (UCL) on the arithmetic mean of organic and inorganic
chemicals in soil and groundwater were used as the exposure concentration unless it exceeded the
maximum concentration. ,Where this occurred, the maximum concentration was used as the
exposure point concentration for that chemical. The exposure concentrations used to evaluate the
potential receptors are listed in Table 3-2. The following formula was used to determine the 95
percent UCL on the arithmetic mean assuming the samples are log-normally distributed (EPA,
1992a):
( , sH ) X; +0.5s· + ,--:
UCL= e vo-i
Where:
e = constant (natural log)
x, = arithmetic mean of the log-transformed data for contaminant i.
s = standard deviation of the log-transformed data
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This document was prepared by Roy F. Weston, Inc., expressly for EPA. It shall not be disclosed, in whole or in part, without the express
written permission of EPA.
Chemicals of
Potential Concern
Groundwater Sce11ario µg/L
I, 1-Dichloroethene '
Bromodichloromethane '
Chloroform
Dibromochloromethane
Tetrachloroethene
Trichloroethene
Future Soil Scenario mg/kg
2-Methyl naphthalene
Acenaphthene
Aluminum
Arsenic
Beryllium
Dibenzofuran
Dieldrin
Lead
Manganese
Naphthalene
Pl~enanthrcnc
Pyrene
Vanadium
Table 3-2
Ex)Josurc Point Concentrations
Human Health Risk Assessment
Davis Park Road Superfund Site
Section: 3
Revision: 0
Date: May 1997
Maximum UJJJJCr Confidence Ex11osu re Point
Detection Limit* Concentration
3.8 0.69 0.69
5.8 0.69 0.69
40.0 1.05 1.05
0.58 0.51 0.51
10.0 1.0 1.0
32.0 3.9 3.9
94,000 > IE+6 94,000
1,200 --1,200
52,000 55,208 52,000 I
15 10.12 10.12
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2,000 --2,000
18 26.1 18
630 ----
360 205 205
10,000 > IE+6 10,000
600 600 600
380 --380
120 63.5 63.5
• In the event the sample size is small and the variability is great, a very large UCL may result.
•• Lead will be assessed using the EPA Lead Model 0.99d, Section 5.4.
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written permission or EPA.
H
n =
Human Health Risk Assessment
Davis Park Road Superfund Site
Section: 3 ·
Revision: O
Date: May 1997
s = \1--'-;-=.,1 ___ _
n-1
statistic determined by the standard deviation and sample size. (A method
to adjust for log-normal distributed data)
sample size for contaminant in the particular media set
3.5 EXPOSURE DOSE MODELS AND ASSUMPTIONS
This subsection presents .the mathematical models that are used to calculate the intakes (i.e.,
doses) of chemicals of potential concern by each receptor through the applicable exposure routes
(see Subsection 3.3, Conceptual Site Model). The exposure models and assumptions are
presented in the following tables. Each table defines the variables for the exposure route and
includes the assumptions (i.e., exposure parameters) used in the model for each scenario.
Additional information regarding the assumptions is presented in the text. EPA Region IV
Supplemental Guidance for Risk Assessment (EPA, 1992a, 1995) was used where appropriate.
Doses, expressed as chronic daily intakes in milligrams of contaminant per kilogram of body
weight (mg/kg-day), are calculated for each exposure route applicable to the current and future
residents. Doses are calculated based on two averaging times using the appropriate chemical
concentrations. Doses for the receptors are averaged over the number of days of exposure (years
of exposure x 365 days/year) to evaluate chronic noncarcinogenic health effects, and over a
lifetime (70 years x 365 days/year) to evaluate potential carcinogenic effects.
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This document was prepared by Roy F. Weston, Inc., expressly for EPA. It shall not be disclosed, in whole or in part, without the express
written permission of EPA.
Human Health Risk Assessment
Davis Park Road Superfund Site
Section: 3
Revision: 0
Dale: May 1997
The resident scenarios assume that individuals live on the site for 30 years. This value represents
the 90th percentile for time spent at one residence. In addition, it is assumed that the residents
take two weeks vacation per year, and, therefore spend 350 days per year at home (EPA, 1991a).
Two age groups are evaluated for the residential scenarios. These age groups include a child (age
1-6 years) and an adult. A body weight of 15 kg is used for the child (age 1-6 years) (EPA,
1991a). A body weight of70 kg is used for the adult future resident (EPA, 1991a).
3.5.1 Drinking Water Ingestion
Drinking water ingestion is considered to be a potential exposure route for the current and future
adult and child residents because residents in the proximity of the Davis Park Road site use wells
for potable water. The drinking water ingestion rates used for children and adults assume that all
daily water intake occurs at home. The equations and assumptions that are used to calculate.
drinking water ingestion doses are presented in Table 3-3. The drinking water ingestion rate for
the adult resident is 2 L/day (EPA, 1991 a). In the absence of data for children, it is assumed that
the children residents will ingest one-half(! L/day) of the adult amount.
3.5.2 Inhalation While Showering
Volatile organic compounds (VOCs) may be released to indoor air through a variety of home
activities, including showering, cooking, dish washing, and laundering clothes. Some scientific
investigators believe that inhalation doses of VOCs through typical home water uses may be as
great or greater than doses from the ingestion of water. Based on experimental results for the
transfer of TCE from water to air in the shower stall, McKone and Knezovich ( I 99 I) report that
inhalation exposures_ in showe_rs could be equivalent to an ingestion contact ranging from 1 to 4
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This document was prepared by Roy F. Weston, Inc., expressly ror EPA. It shall not be disclosed, in whole or in part, without the express
written permission of EPA.
Table 3-3
Model for Calculating Doses from
Ingestion of Groundwater
Human Health Risk Assessment
Davis Park Road Superfund Site
Section: 3
Revision: O
Date: May 1997
Groundwater Ingestion Dose CW x IR x EF x ED
(mg/kg-day) = BWxAT
Where:
CW = Chemical concentration in groundwater (mg/L)
IR = Ingestion rate (L/day)
EF = Exposure frequency (days/year)
ED = Exposure duration (years)
BW = Body weight (kg)
AT = Averaging time (days)
Assumptions:
cw = Chemical concentration in groundwater.
IR = I liter/day, for the child (age 1-6 years) resident (EPA, 1991a).
= 2 liters/day, for the adult resident (EPA, 1991a).
EF = 350 days/year for the child and adult residents (EPA, 1991a).
ED = 6 years for the child (age 1-6 years) resident (EPA, 1991a).
= 24 years for the adult resident (EPA, 1991 a).
BW = 15 kg for the child (1-6) resident (EPA, 1991a).
= 70 kg for the adult resident (EPA, 1991a).
AT = Exposure duration (years) x 365 days/year for evaluating noncancer risk.
= 70 years x 365 days/year for evaluating cancer risk.
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written permission of EPA. ·
Human Health Risk Assessment
Davis Park Road Superfund Site
Section: 3
Revision: o
Date: May 1997
liters. Inhalation while showering is evaluated to account for doses of voes received from
noningestion uses of water for the current and future adult and child residents. The dose from
inhalation of voes while showering is based on an ingestion equivalent of 2 liters per day as
described by McKone and Knezovich ( 199 I) and recommended by EPA Region IV (EPA,
1992b). For the purpose of evaluating inhalation exposures, a voe is defined as any organic
compound with a Henry's Law constant of IE-05 atm-m3/mole or greater and with a. molecular
weight of less than 200 g/mole (EPA, 1991b). The Henry's Law constants and molecular weights
of the groundwater contaminants of potential concern are presented in Table 3-4.
Dibromochloromethane has a molecular weight of208.29; therefore, it will not be evaluated in the
inhalation pathway.
3,5.3 Incidental Ingestion of Soil
Incidental soil ingestion can result from placing soil-covered hands or objects in the mouth. Soil
ingestion is a potential route of exposure for the current and future residents. The exposure dose
model and assumptions for the soil ingestion pathway are presented in Table 3-5.
It has been estimated that children ages 1-6 incidentally ingest 200 mg of soil on a daily basis and
that individuals over the age of 6 ingest I 00 mg of soil per day (EPA, I 99 I a). Therefore, an
incidental soil ingestion rate ,of 200 mg/day was used for the child age 1-6 and an ingestion rate of
I 00 mg/day was used for the adult resident. The soil ingestion rates for all age groups take into
account the ingestion of outdoor soil and indoor dust and represent reasonable upper-bound
residential exposure conditions.
NOR/K:IWP\04400\071\RPMJC002.DOC 3-13
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written permission or EPA. ·
Table 3-4
Human Health Risk Assessment
Davis Park Road Superfund Site
Section: 3
Revision: O
Date: May 1997
Physical/Chemical Parameters For Screening VOCs in Groundwater'
Chemical Chemical Henry's Law Molecular
Classificationh Constant Weight
(atm-m3/molc) (g/molc)
Bromodichloromethane voe 4.2E-1 163.8
Chlorofom1 voe 3.67E-3 119.39
I, 1-Dichloroethene ' voe 3.40E-02 97 .
Dibromochloromethane * voe 4.59E-3 208.29
Trichloroethene ' voe 2.30E-0I 131.4
Tetrachloroethene voe 2.69E-2 165.83
'EPA, 1986.
'
bVolatile organics determined by the following criteria: Henry's Law=> IE-05 atm-1113/1110I and MW<=
200 g/1110I (EPA, 1992b).
VOC = Volatile Organic Chemical
' • = The molicular weight for Dibromochloromethane exceeds 200 g/mol. Therfore, it will not be
evaluated as a VOC in the' groundwater inhalation pathway.
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written permission of EPA.
Table 3-5
Model for Calculating Doses from
Incidental Ingestion of Soil
Human Health Risk Assessment
Davis Park Road Superfund Site
Section: 3
Revision: 0
Date: May 1997
Soil Ingestion Dose CS x IR x CF x EF x ED
(mg/kg-day) = BWxAT
Where:
cs = Chemical concentration in soil (mg/kg)
IR = Soil ingestion rate (mg/day)
CF = Conversion factor (I E-6 kg/mg)
EF = Exposure frequency (days/year)
ED = Exposure duration (years)
BW = Body weight (kg)
AT = Averaging time (days)
Assumptions:
cs = Upper 95% confidence limit of the mean concentration in soil.
IR = 200 mg/day for the child (1-6) resident (EPA, 1991a).
= 100 mg/day for the adult resident (EPA, I99!a).
EF = 350 days/year for the children and adult residents (EPA, 199 la).
ED = 6 years for the child (1-6) resident (EPA, 1991a).
= 24 vears for the adult resident (EPA, 199 la).
BW = 15 kg for the child resident (EPA, 1991a).
= 70 kg for the adult resident (EPA, 199 I a).
AT = Exposure duration (years) x 365 days/year for evaluating noncancer risk.
= 70 years x 365 days/year for evaluating cancer risk.
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written permission or EPA.
3.5.4 Dermal Contact With Soil
Human Health Risk Assessment
Davis Park Road Superfund Site
Section: 3
Revision: 0
Date: May 1997
The dermal absorption of substances resulting from contact with surface soil is a potential route
of exposure for all the residential receptors. The equation and assumptions used to calculate
dermal absorption doses are presented in Table 3-6 (EPA, 1985, 1992b).
The exposed skin surface areas for both scenarios are based on the following body part and age
specific skin surface areas for males:
• Adult Resident (Current and Future):
Arms, hands, lower legs, feet (50% of exposure events)
One-half arms, hands (50% of exposure events)
• Child Resident Age 1-6 (Current and Future):
Arms, hands, one-half legs, feet (50% of exposure events)
One-half arms, hands (50% of exposure events)
Absorption of soil-bound substances through the skin involves three complex processes. First, the
substance must desorb from the soil to an extent that the compound is available for absorption.
Second, the substance must penetrate the first layer of skin and permeate through the remaining
layers. Third, the substance must be taken up by the microcirculation within the skin. Only when
. all of these processes occur can a substance be absorbed.
Information regarding the percentage of chemicals that can be absorbed from soil through the skin
was obtained from EPA Region IV. According to Regional guidance, a dermal absorption factor
of I percent should be used to evaluate organic chemicals and an absorption factor of 0. I pe,cent
should be used to evaluate inorganic chemicals (EPA, 1995).
NOR/K. IWP\04400\071 IRPMJC002. DOC 3-16
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This document was prepared by Roy F. Weston·, Inc., expressly for EPA. It shall not be disclosed, in whole or in part, without the express written permission of EPA.
Table 3-6
· Model for Calculating Doses from
Dermal Contact with Soil
Human Health Risk Assessment
Davis Park Road Superfund Site
Section: 5
Revision: 0
Date: May 1997
Soil Demial Absorption Dose CS x CF x SA x AF x ABS x EF x ED
(mg/kg-day) = BWxAT
Where:
cs = Chemical concentration in soil (mg/kg)
CF = Conversion factor (I E-6 kg/mg) '
SA = Skin surface area available for contact (cm2/day)
AF = Soil lo skin adherence factor (mg/cm2)
ABS = Dermal absorption factor (unilless)
EF = Exposure frequency (days/year)
ED = Exposure duration (years)
BW = Body weight (kg)
AT = Averaging time (days)
Assumptions:
cs = Upper 95% confidence limit of the mean concentration in soil.
SA = 2,125 cn1'/day for the child (1-6) resident. It represents the 50th percentile surface area of the
arms, hands, lower legs, and feel (50% of the exposure events) and forearms and hands (50%
of the exposure events) of a 1-6 year old (EPA, 1985).
= 4,145 cm2/day for the adult resident. It represents the 50l11 percentile surface area of the arms,
hands, lower legs, and feel (50% of the exposure events) and forearms and hands (50% of the
exposure events) ofan adult male (EPA, 1985).
AF = I mg/cm'; soil adherence factor (EPA, 1992b ).
ABS = 0.01 -organic compounds (EPA, 1992a).
= 0.00 I -inorganic compounds (EPA, 1992a).
EF = 350 days/year for the children and adult residents (EPA, 199 la).
ED = 6 years for the child (1-6) resident (EPA, 1991a).
= 24 vears for the adult resident (EPA, 199 la).
BW = 15 kg for the child resident (EPA, 199 la).
= 70 kg for the adult resident (EPA, 199 la).
AT = Exposure duration (years) x 365 days/year for evaluating noncancer risk.
= 70 years x 365 days/year for evaluating cancer risk.
NOR/K:\WP\04400\071 \TBMJCOO 1. DOC 3-17
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written permission of EPA.
Human Health Risk Assessment
Davis Park Road Superfund S.ite
Section: 3
Revision: O
Date: May 1997
3.6 CALCULATED DAILY INTAKES
Exposure doses evaluated for multi-media exposure point concentrations for the current and
future residents are presented in the following tables in Appendix B:
B-1
B-2
B-3
B-4
Current and Future Child (Age 1-6) Resident -Exposure Dose of a Duration of
Six Years
Current and Future Child (Age 1-6) Resident -Exposure Dose Averaged Over a
Lifetime
Current and Future Adult Resident -Exposure Dose ofa Duration of24 Years
Current and Future Adult Resident -Exposure Dose Averaged Over a Lifetime
3.7 REFERENCES
EPA (Environmental Protection Agency), 1985. Development of Statistical Distributions or
Ranges of Standard Fae/ors Used in Exposure Assessments. Office of Health and Environmental
Assessment. Washington, D.C. OHEA-E-161
EPA (Environmental Protection Agency), 1989. Risk Assessment Guidance for Superfund,
Volume 1, Human Health Evaluation Manual (Part A). Interim Final. Office of Solid Waste and
Emergency Response. Washington, D.C. EPN540/l-89/002.
EPA (Environmental Protection Agency), 199 I a. Human Health Evaluation Manual,
Supplemental Guidance: "Standard Default Lxposure Factors". Office of Solid Waste and
Emergency Response. Washington, D.C. OSWER Directive 9285.6-03.
EPA (Environmental Protection Agency), 1991b. Human Health Evaluation Manual, Part B:
"Development of Risk-Based Preliminwy Remediation Goals". Office of Emergency . and
Remedial Response. Washington, D.C. OSWER Directive 9285.7-01B. ·
EPA (Environmental Protection Agency), I 992a. Supplemental Region JV Risk Assessment
Guidance. Atlanta, GA (I 1 February 1992).
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written permission of EPA.
Human Health Risk Assessment
Davis Park Road Superfund Site
Section: 3
Revision: O
Date: May 1997
EPA (Environmental Protection Agency), 1992b. Dermal Exposure Assessment: Principles and
Applications. Interim Report. Office of Research and Development. Washington, D.C.
EPN600/8-91/0I IB.
EPA (U.S. Environmental Protection Agency), 1995. Supplemental Guidance to RAGS: Region
IV Bulletins, Nov. 1995.
Howard, Philip H. Handbook of Environmental Fate and Exposure Data, Volume I -.Large
Production and Priority Pollutants, Volume fl -Solvents. Lewis Publishers, Inc., 1990.
McKone, I.E., and J.P. Knezovich, 1991. The Transfer ofTrichloroethene (ICE) from a Shower
to Indoor Air: Experimental Measurements and Their Implications Journal of the Air and Waste
Management Association 41 :832-837.
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written permission of EPA.
4.1 INTRODUCTION
SECTION 4
TOXICITY ASSESSMENT
Human Health Risk Assessment
Davis Park Road Superfund Site
Section: 4
Revision: 0
Date; May 1 997
The purpose of the toxicity assessment is to select toxicity values ( criteria) for each chemical
evaluated in the risk assessment. The toxicity values are used in combination with the estimated
doses to which a human could be exposed (as discussed in the Exposure Assessment Section 3) to
evaluate the potential human health risks associated with each chemical. Human health criteria
(cancer slope factors and reference doses) developed by the EPA were obtained preferentially
from the Integrated Risk Information System (EPA, 1997) or the I 995 Health Effects Assessment
Summary Tables (HEAST; EPA, 1995). In some cases, the National Center for Environmental
Assessment (NCEA, 1997), was contacted to obtain criteria for chemicals which were not listed
in IRIS or HEAST.
4.2 TOXICITY SUMMARIES ON THE CHEMICALS OF POTENTIAL CONCERN
This section provides a brief description of each chemical of potential concern (Table 2-3) on the
effects associated with exposure to each chemical.
4.2.1 Organics
ALDRIN/DI.ELDRIN -Aldrin and dieldrin are two structurally similar compounds. These chemicals
are often discussed together because aldrin is readily metabolized into dieldrin in the body and
converted to dieldrin in the environment. In the past, aldrin and dieldrin entered the environment when
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Human Health Risk Assessment
Davis Park Road Superfund Site
Section: 4
Revision: O
Date: May 1997
they were used by fanners as insecticides on crops such as com and cotton and when extenninators
used them to kill tennites. These chemicals can still be found in soil, water, air, plants, and animals near
hazardous waste sites.
Deaths were reported in two incidences where humans had been exposed to aldrin or dieldrin by the
inhalation or dennal routes. These deaths were due to immunohemolytic anemia in one case and to
aplastic anemia in the other. Central nervous system excitation is the primary adverse effect observed in
humans chronically exposed to aldrin or dieldrin. In cases of long-tenn exposure to these chemicals,
workers have shown neurological effects including convulsions, headaches, dizziness, hyperirritability,
general malaise, nausea, vomiting, and muscle twitching. These effects occur because aldrin and
dieldrin bioaccumulate in the body, resulting in a gradual build-up of these agents in the blood to toxic
levels. Studies have found that some unusually sensitive individuals can develop a condition in which
aldrin or dieldrin causes the body to destroy its own blood cells. Respiratory effects are inconclusive
because only some workers that were studied showed an increased incidence of pneumonia and other
pulmonary diseases. No adverse liver lesions were found in workers exposed to these pesticides, but an
increase in liver enzymes associated with elevated serum levels of dieldrin was reported. There have
been no observed adverse kidney affects in workers exposed to aldrin or dieldrin. However, a man who
attempted suicide by consuming a large quantity of aldrin had a temporary increase in blood and
protein in the urine and a longer-lasting decrease in the ability of the kidney to concentrate urine.
Chronic studies in laboratory animals have also indicated that the nervous system is a major target
organ. In addition, these studies have demonstrated adverse effects of aldrin and dieldrin on the kidney
and liver. Animal studies also have shown that exposure to moderate levels of aldrin or dieldrin causes
a decreased ability to fight infections. There is conflicting infonnation concerning whether aldrin or
dieldrin cause birth defects or whether these chemicals affect the ability of male animals to reproduce.
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written permission of EPA.
Human Health Risk Assessment
Davis Park Road Superfund Site
Section: 4
Revision: 0
Date: May 1997
The EPA has classified these pesticides as probable human carcinogens (Group B2} Aldrin and/or
dieldrin have been shown to cause liver and thyroid tumors in laboratory animals. There are inadequate
human studies concerning the carcinogenic effects of aldrin or dieldrin (A TSDR, 1993a).
BROMODICHLOROMETHANE -Bromodichloromethane (BDCM) is used in the synthesis of fire
extinguishing agents and solvents. It is also produced and released naturally by several species of
' marine macroalgae. The primary source of environmental contamination results from its inadvertent
formation during chlorination processes of drinking, waste, and cooling waters. Aside from
occupational exposure, niost populations are exposed to BDCM through the consumption of
contaminated drinking water and food products. Exposure may also occur by inhaling vapors in the
ambient air or through dermal contact in chlorinated swimming pools. Human exposure to BDCM has
produced increased levels: of methemoglobin in the blood and disrupted central nervous system
function.
Acute oral ingestion by mice has resulted in sedation and anesthesia, fatty deposition in the liver, pale
kidneys, and hemorrhaging of the adrenal glands. Rats administered one acute oral dose experienced
sedation, flaccid muscle tone, ataxia, piloerection, prostration, elevated serum cholesterol levels, and
congestion of the kidneys and liver. Chronic oral ingestion by mice has resulted in reduced survival,
reduced body weight gain, ·non-neoplastic liver lesions, and an increased incidence of hepatocellular
adenomas and carcinomas.-Studies with laboratory animals have also confinned that BDCM has
mutagenic abilities and can alter sister chromatid exchange.
Based on inadequate human data and sufficient evidence of carcinogenicity in two animal species (mice
and rats), the EPA has classified BDCM as a Group B2, probable human carcinogen. BDCM has been
shown to increase the incidence of kidney tumors and tumors of the large intestine in male and female
rats, kidney tumors in male mice, and liver tumors in female mice (HSDB, 1994a).
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written permission of EPA.
Human Health Risk Assessment
Davis Park Road Superfund Site·
Section: 4
Revision: 0
Date: May 1997
CHLOROFORM -Humans are primarily exposed to chloroform through inhalation and ingestion.
People living near highly industrialized areas and those exposed in the workplace are susceptible to
health hazards associated with inhalation. As a result of chlorination, the general public can be exposed
to chloroform through drinking water. These exposures should not pose a high enough risk to cause
death. It is not known whether chronic exposures to low levels of chloroform shorten the life span of
·humans. Death in humans is more likely to be the result of the ingestion of large doses and is often
caused by respiratory failure or disturbances in cardi~c rhythm.
The primary target organs of chloroform toxicity in humans are the liver, kidneys, and central nervous
system. Information on the systemic effects of chloroform from inhalation has been obtained from
clinical reports of patients undergoing chloroform anesthesia. The data have shown that respiratory
failure is usually due to airway obstruction by the tongue due to jaw relaxation, central respiratory
paralysis, acute cardiac failure, or severe hepatic injury. Gastrointestinal side effects have been
observed in patients exposed through anesthesia as well as in individuals exposed to lower chloroform
concentrations in occupational settings. Impaired liver function has been reported at occupational
levels. The reports have shown that patients exposed through anesthesia most commonly had kidney
effects when associated with anoxia. Chlorofonn acts as a depressant to the central nervous system
when humans are exposed through ingestion and inhalation.
Epidemiological studies indicate that chronic exposure to chlorinated drinking water may be associated , .
with an increased risk of colon and bladder cancer in humans. It is not known whether the inhalation of
chloroform causes cancer in humans. Chloroform is carcinogenic in animals after oral exposure and is
classified as a Group B2, probable human, carcinogen by EPA (ATSDR, 1993b).
DIBENZOFURAN -Dibenzofuran is derived from coal tar. It is used to make other chemicals and as
an insecticide. Dibenzofuran can be released to the environment in atmospheric emissions emanating
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written permission of EPA.
Human Health Risk Assessment
Davis Park Road Superfund Site
Section: 4
Revision: O
Date: May 1997
from the combustion of coal, biomass, refuse, and diesel fuel. Wastewater emissions can occur from
coal tar, coal gasification, and shale oil operations. The general population is primarily exposed to
dibenzofuran through the inhalation of air which has been contaminated by a variety of combustion
sources including tobacco smoke . .Human exposure can also occur through the consumption of
contaminated food and drinking water. Occupational exposure can occur through inhalation and
dermal contact, particularly at sites engaged in combustion\carbonization processes such as coal tar and
coal gasification operation~.
There is little information known regarding the human health effects resulting from exposure to
dibenzofuran. Human studies have found that acute exposure to dibenzofuran through inhalation and
dermal contact causes irritation of the eyes, nose, and throat. Humans that are repeatedly exposed may
develop skin growths, rashes, and changes in skin color. Rash may be made worse by exposure to
sunlight. In one study it was found that rats acutely exposed by gavage had an increased incidence of
cleft palate and developed liydronephrosis.
There are no data on the possible carcinogenicity of dibenzofuran alone in humans. However, because
dibenzofuran is a derivative' of coal tar, a substance which is known to cause cancer in humans, there
may be a relevant concern for human exposure to dibenzofuran. Dibenzofiiran has not been tested for
its ability to cause cancer in' animals. The EPA has categorized dibenzofuran as a Group D agent, not
classifiable as to human carcinogenicity (HSDB, 1994b ).
DIBROMOCHLOROMETHANE -Dibromochloromethane (DBCM) is biosynthesized and emitted
to the environment by various species of marine macroalgae abundant in the world's oceans. DBCM's
predominant anthropogenic sources of release to the environment are its inadvertent formation during
I
water chlorination treatment processes and the subsequent use of chlorinated tap water to produce
food products. Environmental releases can also result from production and use processes, but because
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written permission of EPA.
Human Health Risk Assessment
Davis Park Road Superfund Site
Section: 4
Revision: a
Dale: May 1997
DBCM is not produced or used on a large commercial basis, significant releases do not occur from
these practices. The general population is exposed to DBCM through the ingestion of contaminated
drinking water, beverages, and food products, through the inhalation of contaminated ambient air, and
through dermal exposure to chlorinated swimming pool water.
Little information is available regarding the human health effects resulting from exposure to DBCM.
DBCM has been found to produce increased blood levels of methemoglobin and cause central nervous
system functional disturb'.111ces, including depression of rapid eye movement sleep. One study
concluded that human oral' carcinoma cells are sensitive to DBCM as indicated by a 50% inhibition of
cell growth.
Clinical signs that were observed following single oral doses of DBCM in rats and mice were elevated
serum cholesterol, flaccid muscle tone, ataxia, piloerection, and prostration. Liver and kidney
congestion, and hemorrhage of the adrenals were also found. No gross changes were observed in other
tissues. Lesions have manifested in the kidneys, liver, and salivary glands of rats and mice orally
exposed to DBCM for chronic durations. Other chronic exposure studies have reported that animals
exhibited higher occurrences of fatty metamorphosis, calcification, and necrosis of the liver and
kidneys. In addition, chronic exposure has been reported to increase the incidence of hepatocellar
adenomas and carcinomas, and reduce body weight gain and survival in laboratory animals.
The EPA_has classified DBCM as a Group C, possible human, carcinogen on the basis that there are no
epiderniologic studies ofDBCM alone. A concern for human exposure to DBCM is relevant, however,
because of positive carcinogenic evidence in animal studies, positive mutagenicity data, and DBCM's
structural similarity to other trihalomethanes, which are known animal carcinogens (HSDB, 1994c)
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written permission of EPA.
Human Health Risk Assessment
Davis Park Road Superfund Site
Section: 4
Revision: O
Date: May 1997
1,1-DICHLOROETHENE -The general public is most likely to be exposed to 1,1-dichloroethene
(1, 1-DCE) through the ingestion of contaminated food or water, and through the inhalation of
contaminated air near factories that produce or use it, hazardous waste sites, and areas near accidental
spills. Humans working with 1, 1-DCE in occupational settings are most likely to be exposed through
the inhalation and dermal routes.
The limited information on the human health effects occurring after exposure to l, 1-DCE primarily
comes from case reports and several insufficiently detailed fatality studies in which the concentration
and duration of exposure to 1, 1-DCE were not reported. Human evidence has indicated that the
central nervous system and the liver are susceptible to 1, 1-DCE toxicity. No deaths have been reported
in humans following I, 1-DCE exposure. There is no information available regarding cardiovascular,
hematological, renal, immunological, reproductive, or developmental effects of exposure to I, 1-DCE
in humans.
There is considerable information regarding the effects of 1, 1-DCE exposure in animals. The liver,
kidneys, and, possibly, the _lungs seem to be the major target organs in animals exposed to l, 1-DCE
through the inhalation and ingestion pathways. In addition, cardiovascular, neurological,
developmental, and genotoxic effects have been reported in animals following the inhalation of I, 1-
DCE, and gastrointestinal , effects have been reported after oral exposure. Death has occurred in
animals exposed to high levels of I, 1-DCE through the inhalation or oral routes.
There are no data indicating that exposure to I, 1-DCE causes cancer in humans. Animal studies have
found ca~cinogenic growths in rats and mice. Therefore, the EPA has classified I, 1-DCE has a Group
C, possible human, carcinogen (ATSDR, 1992a)
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written perriiission of EPA.
Human Health Risk Assessment
Davis Park Road Superfund Site
Section: 4
Revision: 0
Date: May 1997
POLYCYCLIC AROMATIC HYDROCARBONS (PAHs) -PAHs can be produced
anthropogenically from th_e burning of coal, oil, gas, garbage, or other organics, as well as naturally
from forest fires and volcanic eruptions. They are mainly used for research purposes, although a few of
the chemicals are used in dyes, plastics, and pesticides. P AHs are widespread in the environment and
are found in air (in vapor and particulate forms), soil, sediment, and water. Most PAHs do not exist
alone in the environment, but are found in mixtures of at least two P AH compounds. There are over
one hundred individual P AHs. The following chemicals are considered as one group in this profile:
Acenaphthene
Acenaphthylene
Anthracene
Benzo(a)anthracene
Benzo( a)pyrene
Benzo(b )fluoranthene
Benzo(g, h,i)perylene
Benzo(k)fluoranthene
Chrysene
Dibenzo( a,h )anthracene
Fluoranthene
Fluorene
Ideno( 1,2,3-cd)pyrene
Phenanthrene
Pyrene
These compounds usually occur together in the environment and may have similar toxicological effects.
People may be exposed to P AHs in the home, workplace, and environment. Nonoccupational P AH
exposure occurs through the inhalation of tobacco smoke and smoke from burning wood, and from the
ingestion of contaminated water, smoked meats, contaminated grains and vegetables, and processed
foods. The greatest potenti,al exposure for most people results from either working or living in areas
surrounding coal-tar production plants, coking plants, asphalt production facilities, smoke houses,
power and heat generating stations, coal-tarring activities, and municipal trash incinerators.
Studies regarding human exposure to P AHs are limited; most of the information is provided from
occupationally-exposed coal and coke workers. Coal tar and its byproducts have been associated with
bronchogenic cancer, buccal-pharyngeal cancer, cancer of the lip, gastrointestinal cancers, bladder
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Human Health Risk Assessment
Davis Park Road Superfund Site
Section: 4
Revision: O
Date: May 1997
cancer, scrotal cancer, and skin tumors. However, cancer induction by P AHs and other chemicals may
have a synergistic relationship, implying that the carcinogenic qualities of P AHs may be augmented
when present with other industrial byproducts. Other studies have revealed that chronic exposure may
also have noncancer effects including ocular photosensitivity and irritation, respiratory irritation, cough,
bronchitis, dermatitis and hyperkeratosis, and leukoplakia. One study reported an increased incidence
of melanosis of the colon and the rectum following chronic ingestion of anthracene-containing
la,atives. Tissues with rapid cellular regeneration such as bone man-ow, intestinal epithelium, lymphoid
tissues, and some reproductive tissues may be more susceptible to P AH toxicity.
Certain subsections of the population may be more susceptible to P AH toxicity than others. These
subsections include people_ with genetically inducible aryl hydrocarbon hydroxylase ( AHH) activity,
nutritional deficiencies, genetic disease that influence the efficiency of DNA repair, immunodeficiency
due to age or illness, and fetuses. Other susceptible populations to P AH toxicity include smokers,
people who have experienced excessive sun exposure, people with liver or skin diseases, and women,
especially of child-bearing age.
The acute ingestion of anthracene, benzo(a)anthracene, benzo(a)pyrene, and phenanthrene has
generated enzyme alterations in animal gastrointestinal mucosa. Lethal hematopoietic effects, including
aplastic anemia and pancytopenia, have been reported in mice following the acute ingestion of
benzo(a)pyrene. Hepatotoxicity studies in animals have shown that the acute ingestion of
benzo(a)pyrene induces preneoplastic hepatocytes, which have been con-elated with the development
of cancer. The acute ingestion of benzo(a)pyrene and benzo(a)anthracene has also increased liver
weight and altered liver enzyme production in rats. Liver regeneration, following acute oral exposure
to PAHs, increased in studies'performed with rats. The acute ingestion ofbenzo(a)pyrene by pregnant
rats and mice has been shown to decrease pup weight and increase the incidence of sterility in F 1
progeny. Adverse dermatological effects, including the destruction of sebaceous glands, skin
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Section: 4
Revision: 0
Date: May 1997
ulcerations, hyperplasia, and hyperkeratosis, have been documented in animals following acute and
subchronic dermal exposure.
Hematological effects ( e.g., aplastic anemia and pancytopenia) have been observed in mice following
subchronic oral exposure to benzo(a)pyrene. Similarly, rats chronically fed PAHs have developed
agranulocytosis, anemia, leukopenia, and pancytopenia. Decreased kidney size, congestion, and renal
cortical hemorrhages have been observed in rats exposed to various P AHs.
Skin, lung, liver, and gastric cancer have all been produced in laboratory animals chronically exposed to
various PAHs. Benzo(a)anthracene, benzo(a)pyrene, and dibenzo(a,h)anthracene have also been found
to be carcinogenic when ~dministered orally to animals. Benzo(a)pyrene also has been found to be
carcinogenic when applied dermally to animals. P AHs extracted from coal furnaces have caused skin
tumors in mice following chronic demial administration. Data have suggested that skin tumors are
primarily due to benzo(a)pyrene, alone or in combination with dibenzo(a,h)anthracene. However,
studies have also found benzo(a)anthracene, chrysene, benzo(b)fluoranthene, and benzo(k)fluoranthene
to induce skin tumors in mice and rats (ATSDR, 1990a).
The most significant P AH toxicity endpoint is carcinogenicity. Based on available human and animal
evidence, EPA has classified individual P AHs as follows:
• Group B2 (probable human carcinogen):
benzo(b )fluoranthene, benzo(k )fluoranthene,
ideno( 1,2,3-cd)pyrene.
benzo(a)anthracene, benzo(a)pyrene,
chrysene, dibenzo(a,h)anthracene, and
• Group D (not classifiable as to human carcinogenicity): acenaphthylene, anthracene,
benzo(g,h,i)perylene, fluoranthene, fluorene, phenanthrene, and pyrene.
The carcinogenic classification for acenaphthene is pending.
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Human Health Risk Assessment
Davis Park Road Superfund Site
Section: 4
Revision: 0
Date: May 1997
TETRACHLOROETHENE -Tetrachloroethene (PCE) is a synthetic chemical used in the dry
cleaning industry, consumer products, metal-degreasing, and the manufacture of other chemicals.
Humans can be exposed from occupational sources and consumer products through the inhalation
and ingestion pathways. Because PCE does not pass through the skin to any significant extent,
dermal exposure is not a pathway of great concern.
The acute inhalation of PCE has proven to be lethal to humans. Death resulting from inhalation is
presumed to be the result of excessive depression of the respiratory center or a fatal cardiac
arrhythmia. Acute ingestion and inhalation may also result in neurological disorders including
headache, dizziness, loss of motor coordination, ataxia, and coma.
Occupational inhalation has been reported to cause respiratory irritation, hepatocellular damage,
mild tubular damage to the kidneys, neurological and behavioral changes, menstrual disorders,
and spontaneous abortions. An epidemiological study suggested that chronic exposure of children
to PCE via drinking water increased the incidence of leukemia, urinary tract infections, and
respiratory infections. In one instance, an infant developed obstructive jaundice and hepatomegaly
after exposure to PCE through the ingestion of breast milk.
Based on available animal cancer studies and new ancillary data, PCE is ranked by EPA between
Group B2 (probable human carcinogen) and Group C (possible human carcinogen) (ATSDR,
1993c).
TRJCHLOROETHENE -Trichloroethene (TCE) is a synthetic chemical mainly used as a metal
degreaser and in the manufacture of other chemicals. It is found in such household products as
typewriter correction fluid, paint remover, and adhesives. People living near hazardous waste sites,
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Human Health Risk Assessment
Davis Park Road Superfund Site
Section: 4
Revision: 0
Date: May 1997
using TCE-containing products, or working in factories using the chemical may be exposed by the
inhalation of vapors or ingestion of contaminated food and drinking water.
Human deaths have occurred following the inhalation of high concentrations of TCE vapors in the
workplace or by intentional inhalation or ingestion. Skin irritation and rashes have developed as a result
of occupational exposure ,to TCE. Workers chronically exposed to high vapor concentrations have
developed neurological symptoms such as di~iness, headache, drowsiness, confusion, nausea, blurred
vision, facial numbness, fa6gue, vertigo, and short-term memory loss. A few reports of occupational
inhalation exposure suggested minor effects on serum or urinary measures of liver function. Studies of
workers exposed to TCE vapors are not conclusive, but demonstrate a marked increase in the
incidence of chromosomal aberrations. One study suggested an increase in respiratory disorders,
gastrointestinal ailments, urinary tract infections, and skin lesions in children chronically exposed to a
contaminated water supply. However, accurate exposure levels were confounded because the wells
involved were also contaminated with several solvents other than TCE.
Associations drawn from cancer studies in humans and animals are suggestive, yet inconclusive.
Therefore, EPA has not yet determined a carcinogenic classification for TCE (ATSDR, 1993d).
4.2.2 lnorganics
ALUMINUM (Al) -Aluminum, which makes up approximately 8% of the earth's crust, is ingested
daily through the diet, primarily from food grown in aluminum-contaminated soil. Exposure to
aluminum has no known benefits. Health risks that have been associated with exposure to aluminum
include respiratory problems from breathing the dust. There is also a possibility of neurological,
teratogenic, and skeletal effects from drinking water containing high levels of aluminum.
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written permission of EPA. '
Human Health Risk Assessment
Davis Park Road Superfund Site1
Section: 4
Revision: 0
Date: May 1997
There have been no reported lethal cases in humans following exposure to aluminum. Asthma and
cough have often been reported in workers exposed to aluminum dust. The symptoms, however, may
be due to concurrent exp~sure to other inhalation toxicants. People treated with aluminum for silicosis
showed no adverse effects. Aluminum is often found at higher than normal concentration in the brains
of people with Alzheimer's disease. It is not known whether aluminum accumulation is a result of the
disease or its cause.
Bone "diseases have been found in persons undergoing renal dialysis. The bone abnormalities may not
have been caused by the· direct effects of aluminum that was present during the treatment, but to
phosphate retention or to renal failure. Encephalopathy has occurred in premature infants who were
put on renal dialysis where the intravenous fluid was contaminated with aluminum. Infants with kidney
problems who were given oral aluminum hydroxide developed bone disease.
Aluminum may cause some nerve effects by affecting the DNA in neurons and other cells. It is not
known to cause cancer in humans. Although workers in aluminum industries have shown a higher than
expected incidence of cancer, this was attributed to the fact that these workers were exposed to other
carcinogens, such as polycyclic aromatic hydrocarbons and tobacco smoke.
Laboratory animals have been found to die from aluminum exposure only afler large doses; infant
animals were more susceptible to the high doses. Animals do not develop Alzheimer's disease when
exposed to aluminum. However, their learning-memory performance was affected when it was
administered directly into the brain or under the skin. In rabbits, injection of aluminum into the heart
caused degeneration of neuron fibers and brain effects. Rats, mice, and rabbits subjected to the injection
of aluminum into the abdomen, the blood, or under the skin showed delayed skeletal and
neurobehavioral development in pups. Genotoxic effects have been found in mice injected with
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Human Health Risk Assessment
Davis Park Road Superfund Site
Section: 4
Revision: o
Date: May 1997
aluminum chloride in the abdomen. Animal studies did not indicate that aluminum is carcinogenic. The
EPA has not categorized aluminum as to its carcinogenic potential (ATSDR, 1992b).
ARSENIC-Inorganic arsenic is toxic by the inhalation and oral routes. Humans exposed to arsenic
near hazardous waste sites could inhale arsenic dust in the air, ingest it in water, food, or soil, or
contact it dermally in soil or water. The greatest effect via inhalation is the increased risk of lung
cancer. Orally, the effects most likely to be seen are gastrointestinal irritation, nerve and blood
problems, and a group of skin diseases, including cancer. The main effect of direct dermal contact with
inorganic arsenic is local irritation and dermatitis.
Acute exposure to arsenic has caused death due to heart and lung failure, while death caused by
repeated exposure has resulted from the failure of more than one tissue injured by arsenic. Inhalation of
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inorganic arsenic dusts (mainly arsenic trioxide) irritates the nasal passages. However, workers exposed
to high levels of arsenic trioxide in air have usually shown no signs of chronic respiratory fun°ctional
impairment. Injuries to the lung have been more pronounced following high (near lethal) oral doses.
Orally, long-term exposure to low levels of inorganic arsenic has resulted in "Blackfoot disease" and
gangrene. Bot_h acute high dose and repeated low dose exposures can cause irritation of the
gastrointestinal tract. Similar effects have been observed with subchronic or chronic inhalation
exposure. Anemia and leukopenia are common observations in humans exposed to inorganic ars~nic by
the oral and inhalation routes. Kidney effects, largely vascular in origin, were found in humans, orally
exposed to inorganic arsenic. Skin lesions are an early sign of chronic oral exposure to inorganic
arsenic. Certain lesions (i.e., hyperkeratinized corns) may develop into skin cancer.
Neurological effects are common in humans exposed orally to arsenic and have been reported in' some
workers exposed by inhalation. Acute high doses lead to brain dysfunction which can end in seizures
and coma in more severe cases. Peripheral nerve damage has occured with lower-level exposure.
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Human Health Risk Assessment
Davis Park Road Superfund Site
Section: 4
Revision: O
Date: May 1997
Human data indicate that ·exposure to inorganic arsenic increases the chances of developing cancer.
Lung cancer is the predominant effect by the inhalation route; some tumors have been observed at
other sites. Increased skin cancer incidence has been observed in several populations consuming
drinking water with high arsenic concentrations. Based on these findings the EPA has categorized
arsenic in Group A. human carcinogen (ATSDR, 1993e).
BERYLLIUM -Beryllium does not occur naturally in the earth's· crust as a pure element, although it
can be found as a chemical component of certain rocks, coal, oil, soil, and volcanic dust. Berylliuri1 also
occurs in some foods. People can be exposed to beryllium through air, food, water, and soil. The intake
of beryllium for the general population is very low. Occupational exposure to beryllium is the primary
route of human exposure to this chemical. Workers engaged in machining metals containing beryllium,
in recycling beryllium from scrap alloys, or in using beryllium products can be exposed to higher levels
of beryllium The respiratory system and heart are the primaty targets of toxicity in individuals exposed
through the inhalation of beryllium
In humans, death has resulted from respiratory distress caused by occupational exposure to beryllium.
Human exposure to elevated concentrations of beryllium has resulted in beryllium pneumonitis with
symptoms including cough, substemal burning, shortness of breath, anorexia, and increasing fatigue.
Lower concentrations of the less soluble fonns of beryllium have caused chronic beryllium lung disease
characterized by granulomas, fibrosis, and emphysema. Beryllium exposure in the workplace has
caused enlargement of the heart muscles. Some case reports showed hepatic and renal effects in
workers, whereas a study of 25 people exposed to beryllium dust showed no liver effects during
autopsies. A wide range of skin lesions and eye effects have resulted in humans exposed to beryllium in
the workplace.
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Human Health Risk Assessment
Davis Park Road Superfund Site
Section: 4
Revision: O
Date: May 1997
Epidemiology studies regarding beryllium's carcinogenic potential are considered to be inadequate.
Beryllium has been shown to cause lung cancer through inhalation in rats and monkeys and to cause
osteosarcomas in rabbits through intravenous or intramedullary injection. EPA has classified beryllium
as a Group B2, probable human, carcinogen (ATSDR, 19931).
LEAD (Pb) -Children are more susceptible to lead toxicity than adults because they engage in
physical activities associated with significant hand-to-mouth ingestion of nonfood items containing
lead, and are physiologically more prone than adults to develop high circulating blood levels following
exposure. Bone acts as a repository for ingested and inhaled lead, and may be a source of blood lead
' during growth, pregnancy, disease, or stress. No systemic toxicity from chronic lead exposure is
estimated to occur if the lifetime daily intake is less than 0.3 mg.
Genotoxic and cancer-causing effects of lead in human and animal studies are the subject of current
debate. The only consistent reports oflead genotoxicity comes from plant studies. Reports of kidney
tumors have been reported in animals and humans; however, human tumor incidence is not statistically
significant. Environmental lead exposures and potentially cancer-causing doses of lead have been
difficult to measure in human epidemiological studies. Based on sufficient animal evidence, EPA has
categorized lead as a Group B2, probable human, carcinogen.
The most sensitive target in children for the adverse noncancer effects of lead is the nervous system. '
For adults, it is the blood and heart. EPA and the Centers for Disease Control (CDC) have developed a
range of blood lead levels that may be associated with specific toxic effects. Toxicity can range from
subtle neurobehavioral effects in children ( e.g., decreased learning performance, small deficits in
intelligence scores; I 0-15 µg/dL) to severe brain damage in adults or children (80-100 ,tg/dL). Both
prenatal and postnatal lead exposure are influential on postnatal neurobehavioral perfom1ance. The
critical toxic effect in middle-aged adult males is high blood pressure (5 to 30 ,tg/dL) Lead may also
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Human Health Risk Assessment
Davis Park Road Superfund Site
Section: 4
Revision: O
Date: May 1997
affect a variety of other organs at intermediate blood levels. Kidney damage, anemia ( similar to that
caused by iron deficiency), muscle paralysis, and severe vomiting and stomach pain may occur. Effects
on the human immune system are inconsistent; positive results tend to be at high blood lead levels.
Encephalopathy (brain swelling) is the most life-threatening effect of lead toxicity, and typically occurs
at blood levels of 80 µg/dL or higher. Severe lead toxiciiy may cause sterility, abortion, and infant
mortality (ATSDR, 1993g).
MANGANESE (Mn) -Most data in humans and animals show that exposure to manganese does not
cause serious effects to the systemic organs. However, when ingested or in contact with the skin it may
cause harsh corrosion at the point of contact if it is in its + 7 valence state.
Manganese has a low acute toxicity. There have been no reported lethal cases in humans following
inhalation exposure to manganese Although, two individuals died following the ingestion of
manganese-contaminated well water, there is significant doubt that manganese was the cause of the
deaths.
Workers exposed by inhalaiion to moderately high concentrations of manganese dusts in the workplace
have developed respiratory inflammation. Manganism, a critical and disabling neurological disease, has
occured in humans exposed to manganese through the chronic inhalation of dusts in mines and
factories. Studies from humans and animals suggest that the intake of high levels of manganese might
lead to developmental effects, but there were no firm conclusions drawn. Reproductive effects such as
decreased libido and impotence were found in workers occupationally exposed to high levels of
manganese dusts by the inhalation route, and data suggest that the number of infants born to these
workers might be less than average. Fewer data are available for the reproductive effects in females,
but the results of animal studies suggest that females may be less sensitive than males.
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Human Health Risk Assessment
Davis Park Road Superfund Site
Section: 4
Revision: 0
Date: May 1997 ·
There is a limited amount of information regarding the potential carcinogenic effects of manganese, and
the interpretation of the available data has been difficult. Inhalation of manganese dusts in humans has
not been associated with causing lung cancer (ATSDR, 1992c).
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VANADIUM (V) -Variadium occurs naturally in the earth's crust, fuel oils, and coal. Vanadium
oxides are the most common man-made form and are used in the manufacture of steel, plastic, rubber,
ceramics, and certain other synthetic chemicals. Vanadium is found in many foods and in drinking
' water at low concentrations. Thus, humans are exposed to vanadium through drinking water and food
ingestion, and breathing dusts containing vanadium .
The respiratory system is the primary target organ for vanadium toxicity and workers are the most
likely population to be exposed. No other organ systems in humans appear to be sensitive to the toxic
effects of vanadium. For respiratory symptoms to occur in humans near a hazardous waste site, large
amounts of dust would have to generated. Inhalation of vanadium by workers can cause mild
respiratory distress ( coughing, wheezing), lung irritation, chest pain, runny nose, sore throat, and red
irritated eyes. Coughing frqm vanadium inhalation in controlled human tests disappeared within several
days of cessation of exposure. Severe vanadium exposure can cause tongue discoloration (greenish-
black) and pneumonitis, characterized by nosebleeds, lobar pneumonia, bronchopneumonia, and acute
bronchitis. Chronic ingestion of vanadium compounds by humans for 3 months resulted in intestinal ' ' cramping and diarrhea. 1
A number of in vitro mutagenic studies with vanadium showed positive results, and human white blood
cells from exposed worker,s have shown evidence of mutagenicity. These reports indicate there is a
potential for human genoto;<icity. However, there is no human or animal evidence of cancer formation
by any route of vanadium exposure. Some in vitro human evidence suggests that vanadium might have I
antitumor properties. Two animal studies were inadequate to assess the carcinogenic potential of
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Section: 4
Revision: O
Date: May 1997
vanadium by oral ingestion. Tumors were found at the injection site in rats treated by the injection of
' vanadium for 43 weeks (ATSDR, 1992d).
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4.3 CARCINOGENidAND NONCARCINOGENIC TOXICITY VALUES
In evaluating potential health risks, both carcinogenic and noncarcinogenic health effects must be i .
considered. The potential for producing carcinogenic effects is limited to substances that have
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been shown to be carcinogenic in animals and/or humans. Excessive exposure to all substances,
carcinogens and noncarcinogens, can produce adverse noncarcinogenic effects. Therefore,
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reference doses are ideritified for every chemical selected regardless of its classification, and
cancer slope factors are identified for those that are classified as carcinogenic.
4.3.1 Estimates of Carcinogenic Potency
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Cancer slope factors (CSFs) are developed by the EPA under the assumption that the risk of '
cancer from a given chelilical is linearly related to dose. EPA may develop cancer slope factors I
from laboratory animal or epidemiological studies in which relatively high doses of the chemical I
were administered. It is; conservatively assumed that these high doses can be extrapolated
downward to extremely small doses, with some incremental risk of cancer always remaining until
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the dose is zero. This rionthreshold theory assumes that even a small number of molecules I
(possibly even one molecule) of a carcinogen may cause changes in a single cell that could result
in uncontrolled cell division, eventually leading to cancer. There is some dispute as to whether the
extrapolation from high to low doses is a realistic approach. It has been argued that at low doses, ' .
cells may have the abilit} to detoxify carcinogens or repair chemical-induced cellular damage. I
Although it is important to recognize the possibility that some carcinogens may have a threshold,
it was assumed in the estimates of cancer risk that no threshold exists.
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written permission of EPA.
I
Human Health Risk Assessment
Davis Park Road Superfund Site
Section: 4
Revision: O
Date: May 1997
The slope factor for a chemical is usually derived by EPA using a linearized multistage model and
reflects the upper-boundl limit of the cancer potency of the chemical. As a result, the estimated
carcinogenic risk is likely to represent a plausible upper limit to the risk. The actual risk is
I unknown, but is likely to be considerably lower than the predicted risk (EPA, 1989), and may
even be as low as zero.
The categorization of caicinogens according to the EPA (EPA, 1997) are included in Table 4-1.
I
Risk assessments follo\V the rationale used by EPA in developing these categories of I
classification. Only those'chemicals classified by the EPA as "A" have sufficient human evidence
of carcinogenicity. Carcinogens classified as "B" and "C" have insufficient human data to support I ,
their cancer-causing potential, but have varying degrees of supportive animal data. It should be I
noted that both known , and potential A, B, and C carcinogens are evaluated through the
carcinogenic exposures iri risk assessments or as carcinogens according to EPA guidance (EPA,
1989). Finally, it is important to note that slope factors are periodically under review by the EPA.
In some cases, the EPA may withdraw the criteria until the review is completed
I
4.3.2 Estimates of Carcinogenicity
The carcinogenic potency of a substance depends on its route of entry into the body (e.g., oral,
inhalation or dermal). Therefore, slope factors are developed and classified according to the route
of administration. In somk cases, a carcinogen may produce tumors only at or near a specific '
route of entry (e.g., nasal passages) and may not be carcinogenic through other exposure r?utes.
Table 4-l presents the cancer slope factors by route of exposure. In some cases, unit risk factors I
[mg!m'r1
) or ([mg/Lr1 are used by the EPA to express cancer risk as the inhalation or oral unit
risk per cubic meter or per liter, respectively. To convert the unit risk factors to units of
(mg/kg-day)"' which are cbmplementary to exposure doses calculated as mg/kg-day, the unit risk
NOR/K:IWP\04400\0711RPMJC002.DOC 4-20
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Table -t-1
Carcinogenic Toxicity Data
Weight Oral Inhalation
of Slope Factor Tumor Animal Slope Factor Tumor Animal
Chemical Evidence (ml!/k!!ldayr1 TYIJC Snecies Reference• (mulSu1davr' Tvne Snecies Reference•
Volatiles
Bromodichloromcthane B2 6.2E-02 Kidney tumors Mouse IRIS NTV ----Chloroform !32 6.1 E-03 Kidncv tumors Rat IlUS 8.1 E-02 Liver carcinomas Mouse IRIS
Liver adenoma or
Dibromochloromcthane C 8.4E-02 carcinoma Mouse IRIS NTV ----Adrenal Kidney
I, 1-Dichlorocthenc C 6.0E-01 pheochromoc)1omas Rat_ IRis--I.SE-01---adenocarcinoma--Mouse IRIS ----Tetrachloro"etlienC C-82 5.2E-02 NA NA NCEA 2.0E-03 NA NA NCEA Trichlorocthene 82 l. lE-02 NA NA NCEA 6.0E-03 NA NA NCEA LS'emi-Vo/atiles
IAcenaphthcne NC -----------Dibenzofuran NC ------------2-Methylnaphthalene NC ---------------Naohthaknc NC -----------Phenanthrcne NC ----------IPyrene NC -----------Pesticides
Oicldrin 132 l.6E+OI Liver carcinomas Mouse IRIS 1.6E+OI Liver carcinomas Mouse IRIS ltwrganics
Aluminum NC ---
IArsenic A 1.5E+OO Skin cancer Human IRIS l.5E+OI Lung cancer Human IRIS
Gross tumors, all site
Bervllium 82 4.3E+OO combined Rat IRIS 8.4E+OO --Human IRIS Lead B2 NTV --IRIS NTV --IRIS Manganese NC ----------Vanadium NC -------------
Notes:
a = IRIS = Integrated Risk Information System (m...Is, 1997).
NCEA = National Center for Environmental Assessment (EPA, 1997).
NA= Not available.
NC= Not classified as a carcinogen.
NTV ~ No toxicitv value available (EPA, 1997; HEAST, 1995; NCEA, 1997).
t-lOR/X."\INP\0.«00\07\IOAVISP.XtS hblt (..1 4-21
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written permission of EPA. ·
Human Health Risk Assessment
Davis Park Road Superfund Site
Section: 4
Revision: 0
Date: May 1997
factor is adjusted by ass~ming 2 liters of water are consumed per day or 20 m3 of air are inhaled !
per day and that the human body weight is 70 kg.
4.3.2.1 Oral
Oral slope factors are used to evaluate the risk from exposure to potential carcinogens through '
oral exposure pathways $uch as incidental sediment ingestion and groundwater ingestion. Oral
slope factors were available for all of the carcinogens listed in Table 4-1 except for lead. Lead is
I
considered to be a potential carcinogen through the oral route, however, an oral slope factor is
not available as it is currently under review by EPA (EPA, 1997; ATSDR, 1993g). I .
4.3.2.2 Inhalation
' Inhalation slope factors are used to evaluate the risk from inhalation exposure to potential
carcinogens through path~ays such as the inhalation of volatile chemicals from groundwater
while showering. These slope factors are listed in Table 4-1. For several of the chemicals of
potential concern through ,the inhalation route of exposure, EPA has not derived inhalation slope
I
factors: bromodichloromethane, dibromochloromethane, and lead.
4.3.2.3 Dermal
Dermal slope factors are not available from the EPA, but it is assumed that chemicals which are '
carcinogenic orally could potentially produce cancer by dermal exposure. In the absence of dermal
slope factors, the oral slope factor is divided by an appropriate gastrointestinal (GI) absorption
factor (EPA, 1989). The GI factor adjusts the orally administered dose for the amount absorbed
since dermal exposure doses are expressed as "absorbed" doses (note that oral and inhalation
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written permission of EPA.
Human Health Risk Assessment
Davis Park Road Superfund Sile
Section: 4
Revision: O
Date: May 1997
doses are usually expresJed as "administered" doses). Oral slope factors are normally developed
I
from long-term studies w_here a substance is administered orally to laboratory animals. Depending
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on the form in which the 'chemical is administered, the relative absorption of the chemical through
the gastrointestinal tract I (and therefore the relative absorption factor) may vary considerably.
Based on U.S. EPA guidance (EPA, 1995b), oral absorption factors are 0.8 for VOCs, 0.5 for I
SVOCs, pesticides and dioxin, and 0.2 for inorganic chemicals. For dermal carcinogenic slope
I
factors (CSF), the al CSF was divided by the oral absorption factor. This approach has a high
I level of associated uncertainty, as does any route-to-route extrapolation.
4.3.2.4 Other Issues Pe~taining to Cancer Slope Factors
Although lead is classified by the EPA (EPA, 1997) as a Group B2 (probable human) carcinogen, I . .
Federal EPA and EPA 'rv recommend that its carcinogenicity not be quantitated in risk ' I
assessments because of the uncertainty of its carcinogenic potency (EPA, I 997, ATSDR, 1993g).
Note that EPA has statedi that lead does not appear to be a potent carcinogen and that at low
doses "the noncancer effects of lead are of greatest concern for regulatory purposes" (EPA, '
1995a). As with carcinog~nicity, lead was not evaluated quantitatively for noncarcinogenic risk.
I
See Subsection 5.4 in the Risk Characterization Section for the lead evaluation results. As I
required by EPA IV (EPA, 1995b), lead was evaluated in this risk assessment by predicting blood
levels in children using t~e Lead Uptake/Biokinetic Model (Version 0.99d). The blood level
predicted by the model was then compared to the level (10 µg/dL) in children which is considered
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to be associated with several potential noncarcinogenic effects, such as neurotoxicity and altered '
hemoglobin synthesis.
NOR/K:\WP\04400\071\RPMJC002.DOC 4-23
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This document was prepared by Rby F. Weston, Inc., expressly for EPA. ti shall not be disclosed, in whole or in part, without the express
written permission of EPA.
4.3.3 Estimates of Noncarcinogenic Toxicity
Human Health Risk Assessment
Davis Park Road Superfund Site
Section: 4
Revision: O
Date: May 1997
The toxicity criteria used to evaluate potential noncarcinogenic health effects are termed reference
I
doses (Rills). Unlike t11e approach used in evaluating carcinogenic risk, it is assumed in
developing Rills that a t~reshold dose exists below which there is no potential for human toxicity.
'
The term RID was developed by the EPA to refer to the daily intake of a chemical to which an
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individual can be exposed without any expectation of noncarcinogenic effects occurring during a
given exposure period (fg., organ damage, biochemical alterations, birth defects). The RID is
derived from a no-obseived-adverse-effect level (NOAEL) or lowest-observed-adverse-effect
I
level (LOAEL) obtained :from human or animal studies by the application of standard uncertainty
factors, and in certain ca~es, an additional modifying factor to account for professional assessment
of scientific uncertainties 'in the available data (EPA, I 989).
A NOAEL is the highest dose of chemical at which no toxic effects are observed in any of the test
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' subjects or animals. The lstudy chosen to establish the NOAEL is based on the criterion that the
measured toxic endpoint! represents the most sensitive ("critical") target organ or tissue to that
chemical (i.e., that target organ or tissue that shows evidence of damage at the lowest dose).
Since many chemicals cah produce toxic effects on several organ systems, the distinction of the
critical toxic effect provides added confidence that the NOAEL is protective of health. In contrast
to a NOAEL, a LOAEL ,is the lowest dose at which the most sensitive toxic effect is observed in
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any of the test subjects or animals. If a LOAEL is used in place of a NOAEL to derive a RID, an
I
additional level of uncertainty is involved and, therefore, an additional uncertainty factor is I
applied.
A variety of regulatory agencies have used the threshold approach for noncarcinogenic substances
in the development ofhe~lth effects criteria, such as worker-related threshold limit values (TL Vs),
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Human Health Risk Assessment
Davis Park Road Superfund Site
Section: 4
Revision: O
Date: May 1997
air quality standards, and food additive and drinking water regulations. Chronic Rills have been
developed for the oral and inhalation routes, but not for the dermal route. As with carcinogenicity
classification, human data are used preferentially if they are deemed adequate through scientific
evaluation. However, in many cases, adequate human toxicity data are not available, and
therefore, animal studies have to be used.
4.3.4 Reference Doses
Table 4-2 presents the route-specific Rills for the chemicals of potential concern (Section 2.3).
Specific consideration was given to oral, inhalation, and dermal noncarcinogenic health criteria.
4.3.4.1 Oral
Chronic Rills were available for most chemicals of potential concern at the Davis Park Road site.
Chemicals for which no Rills were available are: lead. Rills was not derived for this chemical in
accordance with guidance from EPA IV (Personal Communication, 1993). The Rills for
naphthalene, 2-methylnaphthalene, and phenanthrene were sithdrawn in the database; however,
these chemicals are considered P AHs like pyrene. Therefore, the RID for pyrene was used based
on similar structural activity.
4.3.4.2 Inhalation
As directed by EPA IV for organic compounds, oral RfDs were not used as inhalation Rills if
none was available from IRIS (EPA, 1997), HEAST (EPA, 1995a) or NECA ( 1997).
NOR/K: \WP\04400\071 IRPMJC002. DOC 4-25
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Table -1-2
Non-Carcinogenic Toxicity Data
Or.11 RID Confidence Tox.kit)'
Chemical (mg/kg/day) Level Endpoint
r1oh1tiles
Bromodichloromethane 2.0E-02 !-.tedium Kidnev cy1omega!v
Chloroform J.0E-02 l\1edium Fatty cvst fomiation in liver
Dibromochloromethane 2.0E-02 l\ledium Liver lesions
I, 1-Dichloroethene 9.0E-03 1'.ledium Liver lesions
Tetrachloroethene J.0E-02 Low Liver toxicity; weight gain
T richloroetho;;ne 6.0E-03 NA NA
Semi-Volnliles
Acenaohthenc 6.0E-02 Low Liver toxicity
Dibenzofuran 4.0E-03 NA NA
2-1'--.h!thvlnaphthalene 3.0E-02 • ..
Naphthalene 3.0E-02 • ..
Phenanthrene 3.0E-02 • ..
Kidney tubular pathology,
P:,.Tene 3.0E-02 Low decreased kidney weights
Pesticides
Dieldrin I 5.0E-05 l\ledium Liver lesions
lnorga11ics
Aluminum l.0E+00 NA NA
Hyperpigmentation, keratosis
., and possible vascular
Arsenic 3.0E-04 i\ledium complications
Beryllium 5.0E-03 Low No adverse effocts observed
Lead NTV -..
i\lagnesium NTV .. ..
i\langanese (food) 1.4E-01 i\ledium CNS effects
i\!anganese (nondietar>) 4.7E-02 i\!edium CNS effects
Vanadium 7.0E-03 NA No infonnation
Nore~:
a= IRIS= !nkgrated Risk lnfonnation System {IRIS, 1997).
NCEA = National Center for Environmental Assessment (EPA, 1997).
• = 1l1e toxicity values arc the same as P}Tene~ based on siffiifar structural activity.
NA = Not available.
NC = Not classified as a carcinogen.
NTV = No toxicity value available.
NOl't!K_Wll~00".:171\D,'.I/ISPJILS Tot>le4-2
Inhalation RID
UF/~IF Reference" (mg/kg/day)
!000/1 IRIS NTV
!000/1 IRIS NTV
1000/1 IRIS ·NTV
1000/1 IRIS NTV
!000/1 IRIS NTV
NA NCEA NTV
3000/1 IRIS NTV
NA NCEA NTV
.. .. NTV
.. .. NTV
.. NTV
3000/1 IRIS NTV
I00/1 IRIS NTV
NA NCEA NTV
3/1 IRIS NTV·
100/1 IRIS NTV
.. .. NTV .. .. NTV
Iii IRIS
Iii IRIS !.4E-05
I.0E+02 BEAST NTV
4-26
iiiil ---
Confidence Toxicity
Len! Endpoint UF/MF Reference"
.. .. .. . .
.. ..
.. .. .. ..
.. .. -..
-..
.. .. .. ..
.. -.. ..
.. .. .. ..
.. . . . .
.. .. . .
.. .. . .
.. .. .. . .
I ..
.. -.. . .
.. .. -..
.. .. .. . .
.. .. .. . .
.. . . .. -
Impaim1ent of
i\ledium neurobeha\foral function !000/1 IRIS
.. -.. ..
,,,,,,
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This document was prepared by Roy F. Weston, Inc., expressly for EPA. It shall not be disclosed, in whole or in part, without the express
written permission of EPA.
4.3.4.3 Dermal
Human Health Risk Assessment
Davis Park Road Superfund Site
Section: 4
Revision: 0
Date: May 1997
As in the case of cancer slope factors, no Rills have been developed by EPA for the dermal route.
Therefore, dermal Rills were derived for the chemicals of potential concern in accordance with
EPA guidelines (EPA, 1995b). A chronic dermal RID was derived for each chemical by
multiplying the value used as the chronic oral RID by an appropriate oral absorption factor. The
approa_ch used to select the oral absorption factor is the same as that previously described for
cancer slope factors. The absorption factors were 0.8 (volatile organic), 0.5 (semivolatile
organics), and 0.2 (inorganics).
4.3.4.4 Other Issues Pertaining to Reference Doses
Only chronic Rills, which are developed to evaluate potential toxicity at greater than seven years
of exposure were used in estimating both childhood and adult noncarcinogenic risk (Table 4-2).
Subchronic Rills are sometimes used to evaluate subchronic exposures of a duration ranging from
2 weeks to 7 years, which may be more appropriate to address childhood exposure (1-6 years).
However, chronic Rills, which are lower than subchronic Rills, are used in this risk assessment
to ensure a conservative estimate of risk.
As with carcinogenicity, lead was not evaluated quantitatively for noncarcinogenic risk. See
Subsection 5 .4 in the Risk Characterization Section for the lead evaluation results. As required by
EPA IV (Personal Communication, 1993), lead was evaluated in this risk assessment by
predicting blood levels in children using the Lead Uptake/Biokinetic Model (Version 0.99d). The
blood level predicted by the model was then compared to the level ( 10 µg/dL) in children which is
considered to be associated with several potential noncarcinogenic effects, such as neurotoxicity
and altered hemoglobin synthesis.
NOR/K:IWP\04400\0711RPMJC002.DOC 4-27
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This document was prepared by Roy F. Weston, Inc., expressly for EPA. It shall not be disclosed, in whole or in part, without the express
written permission of EPA.
4.4 REFERENCES
Human Health Risk Assessment
Davis Park Road Superfund Site '
Section: 4
Revision: 0
Date: May 1997
ATSDR (Agency for Toxic Substances and Disease Registry), I 989b. Toxicological Profile for
Cadmium. Agency for Toxic Substances and Disease Registry, Atlanta, GA. PB89-l 94476.
ATSDR (Agency for Toxic Substances and Disease Registry). I 990a. Toxicological Profile for
Benzo(b)jluoranthene. U.S. Department ofHealth and Human Services. Atlanta, GA PB90-24765 l.
ATSDR (Agency for Toxic Substances and Disease Registry). 1990a. Toxicological Profile for
Benzo(a)pyrene. U.S. Department of Health and Human Services. Atlanta, GA PB90-258245.
ATSDR (Agency for Toxic Substances and Disease Registry). 1990a. Toxicological Profile for
Chrysene. U.S. Department ofHealth and Human Services. Atlanta, GA PB90-247644.
ATSDR (Agency for Toxic Substances and Disease Registry). 1990a. Toxicological Profile for
Polycyclic Aromatic Hydrocarbons. U.S. Department of Health and Human Services. Atlanta, GA
PB91-181537.
ATSDR (Agency for Toxic Substances and Disease Registry). I 992a. Toxicological Profile for 1,1-
Dichloroethene. Draft. U.S. Department of Health and Human Services. Atlanta, GA
ATSDR (Agency for Toxic Substances and Disease Registry). 1992b. Toxicological Profile for
Aluminum and Compounds·. U.S. Department of Health and Human Services. Atlanta, GA PB93-
l 10633.
ATSDR (Agency for Toxic Substances and Disease Registry). 1992c. Toxicological Profile for
Manganese and Compo1111d5. U.S. Department of Health and Human Services. Atlanta, GA PB93-
l l 078 l.
ATS DR (Agency for Toxic Substances and Disease Registry). I 992d. Toxicological Profile for
Vanadium and Compounds. Atlanta, GA PB93-l l 0880.
ATSDR (Agency for Toxic Substances and Disease Registry). 1993a. Toxicological Profile for
Aldrin/Dieldrin. U.S Department of Health and Human Services. Atlanta, GA PB93-l 82368.
NOR/K:IWP\04400\0711RPMJC002.00C 4-28
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This document was prepared by Roy F. Weston, Inc., expressly for EPA. It shall not be disclosed, in whole or in part, without the express
written permission of EPA.
Human Health Risk Assessment
Davis Park Road Superfund Site
Section: 4
Revision: 0
Date: May 1997
ATSDR (Agency for Toxic Substances and Disease Registry). 1993b. Toxicological Profile for
Chloroform. U.S. Department of Health and Human Services. Atlanta, GA. PB93-l 82426.
ATSDR (Agency for Toxic Substances and Disease Registry), 1993c. Toxicological Profile for
Tetrachloroethene. U.S. Department of health and Human Services. Atlanta, GA. PB93-l82525.
ATSDR (Agency for Toxic Substances and Disease Registry). l 993e. Toxicological Profile for
Arsenic. U.S. Department ofHealth and Human Services. Atlanta, GA. PB93-l82376.
ATSDR (Agency for Toxic Substances and Disease Registry). l 993f Toxicological Profile for
Beryllium. U.S. Department of Health and Human Services. Atlanta, GA. PB93-l 82392.
ATSDR (Agency for Toxic Substances and Disease Registry). 1993g. Toxicological Profile for Lead
U.S. Department ofHealth and Human Services. Atlanta, GA. PB93-l82475.
EPA (U.S. Environmental Protection Agency), 1989. Risk Assessment Guidance for Superfund,
Volume I: Human Health Evaluation Manual (Part A); Interim Final EPN540/l-89/002.
EPA (U.S. Environmental Protection Agency), 1995a. Health Effects Assessment Summary
Tables, Annual FY-1995. OERR 9200.6-303 (95-1). NTIS No. PB 95-92119. March, 1995.
EPA (U.S. Environmental Protection Agency), 1995b. Supplemental Guidance to RAGS: Region
IV Bulletins, Nov. 1995.
HSDB (Hazardous Substance Data Bank). 1994a. National Library of Medicine. Bethesda, MD (CD-
ROM Version). Micromedex, Inc. Englewood, CO (Edition expires 7/31/95).
HSDB (Hazardous Substance Data Bank). 1994b. National Library of Medicine. Bethesda, MD (CD-
ROM Version). Micromedix, Inc. Denver, CO (Edition expires 7/31/94).
HSDB (Hazardous Substance Data Bank). 1994c. National Library of Medicine. Bethesda, MD (CD-
ROM Version). Micromedix, Inc. Denver, CO. (Edition expires 7/31/94) .
NCEA (National Center for Environmental Assessment), 1997. Superfund Health Risk Technical
Support Center.
NOR/K:\WP\04400\071\RPMJC002.DOC 4-29
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This document was prepared by Roy F. Weston, Inc., expressly for EPA. II shall not be disclosed, in whole or in part, without the express
written permission of EPA.
Human Health Risk Assessment
Davis Park Road Superfund Site
Section: 4
Revision: O
Date: May 1997
Personal Communication, 1993. Phone conversation with Julie Keller, EPA Region IV Health
Risk Assessment Group, Atlanta, GA, January 8, 1993, by Dr. Robert Warwick, WESTON Risk
Assessment Group. WESTON, West Chester, PA 19380.
NOR/K:IWP\04400\0711RPMJC002.DOC 4-30
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This document was prepared by Roy F. Weston, Inc., expressly for EPA. It shall not be disclosed, in whole or ln part. without the express
written permission of EPA.
SECTION 5
RISK CHARACTERIZATION
5.1 INTRODUCTION
Human Health Risk Assessment
Davis Park Road Superfund Site
Section: 5
Revision: O
Dale: May 1997
The risk characterization is an evaluation of the nature and degree of potential carcinogenic and
noncarcinogenic health risks posed to hypothetical current and-future residential receptors at the
Davis Park Road site. The pathways of exposure are described in Section 3 _ Human health risks
for carcinogenic and noncarcinogenic effects are discussed independently because of the different
toxicological endpoints, relevant exposure durations, and methods employed in characterizing
risk. The potential for carcinogenic effects is limited to exposure to only those chemicals classified
as carcinogens, while both carcinogenic and noncarcinogenic chemicals are evaluated for potential
noncarcinogenic effects.
Carcinogenic and noncarcinogenic risks were evaluated for each exposure pathway and scenario
by integrating the exposure doses calculated in Section 3 (Exposure Assessment) with the toxicity
criteria for the chemicals of potential concern determined in Section 4 (Toxicity Assessment). The
general approaches to evaluating risk are summarized in Subsection 5.2, and the results of the risk
characterization are summarized in Subsection 5.3.
NORJK:\WP\04400\071 IRPMJC002. DOC 5-1
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This document was prepared by Roy F. Weston, Inc., expressly for EPA. II shall not be disclosed, in whole or in part, without the express written permission of EPA.
5.2 APPROACHES TO EVALUATING RISK
5.2.1 Carcinogenic Risk
Human Health Risk Assessment
Davis Park Road Superfund Site
Section: 5
Revision: O
Date: May 1997
Carcinogenic risk is calculated by multiplying the estimated daily dose that is averaged. over a
lifetime (lifetime-averaged doses) by a compound and exposure route-specific (oral, inhalation,
dermal) carcinogenic slope factor (CSF). The calculation of carcinogenic risk, assuming a low-
dose, linear relationship, is illustrated by the following equation:
Where:
RISK= CDI x CSF
CDI = Chronic daily intake (intake averaged over a 70-year lifetime) (mg/kg-day)
CSF = Compound and route-specific carcinogenic slope factor (mg/kg-day)"1
The linear equation is valid only at low risk levels (i.e., below estimated risks of IE-02 or 0.01).
For sites where doses and risks 111ay be high, the alternative one-hit equation should be used. This
exponential equation takes into account doses that exceed the linear portion of the dose-response
curve. The calculation of carcinogenic risk assuming a high-dose, non-linear relationship is
illustrated by the following equation:
R. k I (·CD!' CSF) 1s = -exp
Where:
NOR/K:\WP\04400\071\RPMJC002.DOC 5-2
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written permission of EPA.
Human Health.Risk Assessment
Davis Park R0ad Superfund Site
Section: 5
Revision: 0
Date: May 1997
CDI = Chronic daily intake (intake averaged over a 70-year lifetime) (mg/kg-day)
CSF = Compound and route specific slope factor (mg/kg-day/
The combined potential_ upper bound cancer risk for a particular exposure route is then estimated
by summing the risk estimates for all chemicals of potential concern for that route. This approach
is in accordance with the U.S. EPA guidelines on chemical mixtures, in which risks associated
with carcinogens are considered additive (EPA, 1986). This approach assumes independence of
action by the chemicals (i.e., that there are no synergistic or antagonistic interactions) and that the
chemicals have the same toxicological endpoint (i.e., cancer). The total potential upper bound
cancer risk to an individual member of a receptor population is estimated by summing the
combined cancer risks from all relevant exposure routes. For the current and future resident,
child, and adult, risks are summed to provide total lifetime cancer risk estimate.
In assessing the carcinogenic risks posed by a site, the NCP establishes an excess cancer risk of
I E-06 as a "point of departure" for establishing remediation goals. Excess cancer risks lower that
I E-06 are not addressed by the NCP. Excess cancer risks in the range of I E-06 to I E-04 may or
may not be considered acceptable, depending on site-specific factors such as the potential for
exposure, technical limitations to remediation, and data uncertainties.
In April 199 l, OSWER Directive 9355.0-30 from the U.S EPA Assistant Administrator to
Regional Directors (EPA, 1991), the U.S. EPA further clarified the acceptable carcinogenic risk
range by stating that when reasonable maximum exposures for. both current and future land use
are less than I E-04, action is generally not warranted, unless there are adverse environmental
impacts. However, it should be noted that the same directive indicates that the risk manager may
decide that risk less than I E-04 is unacceptable due to site-specific issues.
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5.2.2 Noncarcinogenic Risk
Human Health Risk Assessment
Davis Park Road Superfund Site
Section: 5
Revision: 0
Date: May 1997
Noncarcinogenic health effects are evaluated by comparmg the estimated daily intake ,of the
chemical of potential concern, which is averaged over the period of exposure, to its respective
reference dose (RID). This is accomplished by the calculation of hazard quotients and hazard
indices. The hazard quotient (HQ) for a particular chemical of potential concern is the ratio, of the
estimated daily intake through a given exposure route and the applicable RID. Estimated daily
intakes for individual chemicals and routes of exposure are compared to RIDs The RID
represents the daily intake of a chemical to which a receptor can be exposed over a given ,length
of time without any reasonable expectation of adverse noncarcinogenic health effects. The HQ-
RID relationship is illustrated by the following equation:
Where:
HQ= CDI/RID
HQ = Hazard quotient
CDI = Chronic daily intake (averaged over the exposure period) (mg/kg-day)
RID= Reference dose (mg/kg-day)
The hazard quotients determined for each chemical of potential concern by exposure pathway and
age group are summed within an exposure scenario to obtain a hazard index (HJ). The H1 is an
expression of the additivity of noncarcinogenic health effects. The principle of additivity assumes
that similar organ systems and health endpoints will be affected by the chemicals of potential
concern. Since the RIDs determined for the multiple chemicals in a given exposure scenano
usually represent a range of target organs or systems, the calculated HI is conservative.
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written permission or EPA.
Human Health Risk Assessment
Davis Park Road Superfund Site
Section: 5
Revision: O
Date: May 1997
The methodology used to evaluate noncarcinogenic risk, unlike the methodology used to evaluate
carcinogenic risk, is not a measure of quantitative risk. The HQ or HI is not a mathematical
J
prediction of the incidence or severity of those effects (EPA, 1989). !fan HQ or HI exceeds unity
(one), there might be a potential for noncarcinogenic health effects occurring under the defined
exposure conditions. Note, however, that the calculation of an individual RID assumes a margin
of safety (refer to "Toxicity Assessment"), and the range of Rills for a series of chemicals in an
exposure scenario can potentially represent a number of individual toxic endpoints (as discussed
above). Therefore, an HQ or HI of greater than one does not necessarily indicate that a
noncarcinogenic adverse effect is likely to occur. Furthermore, a HI of less than or equal to one
indicates that it is unlikely for even sensitive populations to experience adverse noncarcinogenic
health effects.
5.3 RISK RES UL TS
Carcinogenic risks for the current and future resident are summarized by medium in Table 5-1, by
chemical exceeding 1 E-06 risk (Table 5-2), and by pathway of exposure (Table 5-3).
Noncarcinogenic risks are respectively presented in Tables 5-4 through 5-6. Detailed risk tables
are presented in Appendix C.
5.3.1 Potential Risks Associated With Current Resident
The current resident at the Davis Park Road site was assumed to be potentially exposed to
chemicals in the groundwater and soil contiguous to the site.
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Exposure Medium
Groundwater
Soil
Total
NOR/K:\WP\04-400\071 \TBMJCOOl . DOC
Table 5-1
Human Health Risk Assessment
Davis Park Road Superfund Site
Section: 5
Revision: 0
Date: May 1997
Lifetime Cancer Risk-Current and Future Scenarios
Reasonable Maximum Exposure Concentrations
Current Resident Future Resident
l.2E-5 1.2E-5
6.SE-4 6.SE-4
6.6E-4 6.6E-4
5-6
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written permission or EPA.
Table 5-2
Chemicals of Concern
Human Health Risk Assessment
Davis Park Road Superfund Site
Section: 5
Revision: a
Date: May 1997
That Pose a Carcinogenic Risk Exceeding One in One Million (11J"6)
ExJJosurc Medium Current Resident Future Resident
Groundwater Chloroform (l.3E-6) Chloroform (l.3E-6)
I, 1-Dichloroethene (8.1 E-6) I, 1-Dichloroethenc (8. IE-6)
Soil Dieldrin (3.SE-4) Dieldrin (3.SE-4)
Arsenic (2.5E-6) Arsenic (2.5E-6)
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Table 5-3
Human Health Risk Assessment
Davis Park Road Superfund Site
Section: 5
Revision: O
Date: May 1997
Total Carcinogenic Risk by Exposure Pathway
at Reasonable Maximum Exposure Concentrations
Exposure Medium Current Resident Future Resident'
Groundwater Ingestion 9.0E-6 9.0E-6
Non-Ingestion Uses of Qroundwater 3.5E-6 3.5E-6
Incidental Ingestion of Soil 4.7E-4 4.?E-4
Dermal Contact with Soil l.8E-4 I.SE-4
Total 6.6E-4 6.6E-4
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written permission of EPA.
Exposure Medium
Groundwater
Soil
Total
Table 5-4
Human Health Risk Assessment
Davis Park Road Superfund Site
Section: 5
Revision: 0
Date: May 1997
Total Hazard Index -Current and Future Resident Scenarios
Reasonable Maximum Ex11osure Concentrations
Current Resident Future Resident
'
1-6 yr. old Adult 1-6 yr. old Adult
0.06 0.03 0.06 0.03
68.0 11.21 68.0 11.21
68 11.24 68.0 11.24
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This document Vias prepared by Roy F. Weston, Inc., expressly for EPA. It shall not be disclosed, in whole or: in part, without the express written permission of EPA.
Table 5-5
Chemicals of Concern
Human Health Risk Assessment
Davis Park Road Superfund Site
Section: 5
Revision: O
Date: May 1997
Exceeding a Hazard Index of 0.1 when Hazard Index for Exposure Scenario Exceeded 1.0
Exposure Current Resident Future Resident
M·edium 1-6 yr. old Adult 1-6 yr. old Adult
Groundwater None None None None
Soil Aluminum 0.7 Dibenzofuran ( 1.27 Aluminum 0. 7 Dibenzofuran (1.27 Acenaphthene (0.3) Dicldrin (0.91) Acenaphthene (0.3) Dieldrin (0.91) Dibcnzofuran (7.7) 2-mcthylnaphthalcnc (7.95) Dibenzofuran (7. 7) 2-methylnaphthalene (7. 95) Dicldrin (5.6) Naphthalene (0.85 Dieldrin (5.6) Naphthalene (0.85 2-methylnaphthalene ( 48.3) 2-methylnaphthalene (48.3) Naphthalene (5.1) Naphthalene (5.1)
Phenanthre_nc (0.3) Phcnanthrene (0.3)
Pyrene (0 .2) Pyrene (0.2)
Vanadium (0.1) Vanadium (0.1)
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Exposure Pathway
Groundwater Ingestion
Table 5-6
Human Health Risk Assessment
Davis Park Road Superfund Site
Section: 5 '
Revision: 0
Date: May 1997
Total Hazard Index by Exposure Pathway at
Reasonable Maximum Exposure Concentrations
Current Resident Future Resident
1-6 yr. old Adult 1-6 yr. old Adult
0.06 0.03 0.06 0.03
Non-Ingestion Uses of Groundwater 0.00 0.00 0.00 0.00
Incidental Ingestion of Soil 56.4 6.22 56.4 6.22
Denna! Contact with Soil 11.95 4.99 11.95 4.99
Total 68.0 11.24 68.0 11.24
NE -Not evaluated.
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5.3.1.1 Potential Carcinogenic Risk
Human Health Risk Assessment
Davis Park Road Superfund Site
Section: 5
Revision: O
Date: May 1997
The total incremental lifetime cancer risk for the current resident through exposure to 95 percent
upperbound concentrations of chemicals was 6.6E-4 (Table 5-1 ). Dieldrin contributed the highest
' individual risk (3.SE-4), while arsenic (2.5E-6), I, 1-dichloroethene (8. IE-6), and chloroform
( 1.3E-6) contributed the remaining risk. Table 5-3 summarizes the carcinogenic risks by individual
pathway.
5.3.1.2 Potential Noncarcinogenic Risks
The total hazard index for the current residents age I to 6 years old and the adult were 68.0 and
11.2, respectively (Table 5-4). The majority of this risk was due to 2-methylnaphthale.ne,
dibenzofuran, and naphthalene through the soil ingestion pathway in both groups (Table 5-5).
Table 5-6 summarizes the noncancer risks by individual pathway.
5.3.2 Potential Risks Associated With Hypothetical Future Resident Exposures
The future resident at the Davis Park Road site was assumed to be potentially exposed to
chemicals in the groundwater and soil contiguous to the site. As stated in Section 3.2.4, current
chemical concentrations detected in groundwater and soil were not assumed to change in the
future scenario. Therefore, the carcinogenic and noncarcinogenic risks for the future scenarios are
identical to the current risks.
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written permission of EPA. ·
5.4 LEAD TOXICITY
5.4.1 Backgrouud
Human Health Risk Assessment
Davis Park Road Superfund Site
Section: 5
Revision: O
Date: May 1997
Currently there is not an EPA slope factor or reference dose for lead. EPA believes that the
available studies in animals or humans do not provide sufficient quantitative information for their
calculation (ATSDR, 1993). Although lead is currently classified as a B2 carcinogen (EPA.
1997), the EPA considers the noncarcinogenic neurotoxic effects in children to be the critical
toxic effect in terms of health based environmental cleanup. The neurotoxic effects of chronic
low-level lead exposure in children may occur at blood levels as low as 10 µg/dL.
In the absence of lead health criteria, EPA recommended predicting mean lead blood levels in
children using the Lead Uptake/Biokinetic Model (Version 0.99d) (EPA, 1995). The results from
the Lead Uptake/Biokinetic Model provided in Appendix E are presented in the following
subsection.
5.4.2 Lead Uptakeilliokinetic Model
Blood levels oflead in the age group ranging from O to 6 years of age can be predicted with the
Lead Uptake/Biokinetic Model. The use of the model in Superfund risk assessments to
characterize potential risk is currently not required by the Federal EPA. However, some EPA
regions (including Region IV) recommend its use to provide an estimation of chronic blood lead
concentrations in children based on site-specific data as much as possible. Such data can assist in
the risk management decision regarding cleanup of lead at hazardous waste sites. The biokinetics
of lead are very complex, and the assumptions·used in this model are continually being modified.
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written permission of EPA.
Human Health Risk Assessment
Davis Park Road Superfund Site
Section: 5
Revision; O
Date: May 1997
Therefore, the results presented are hypothetical since many of the assumptions used in the model
are subjects of scientific debate.
The model allows the input of specific lead exposure parameters associated with the site, where
available. Lead was only detected in soil samples ranging from 20 to 630 mg/kg with an average
concentration of 156 mg/kg. Where site-specific information was not available, standard default
factors were substituted. Asterisked parameters (listed below) represent conservative default
values that were used in the model. A predicted blood level less than the current benchmark of
concern of 10 µg/dL indicates that exposure to lead at the site is not of concern in view of current
knowledge of lead toxicity in children. Scientific but controversial evidence suggests that subtle
neurobehavioral effects in children such as lowered IQ scores, learning disabilities, and attention
deficits may occur at chronic blood lead levels of between 10 and 15 µg/dL. These blood levels
may also be associated with decreased hemoglobin production in the red blood cells with resultant
anemia.
The following parameters were evaluated to represent a current/future child resident:
• The air default concentration of lead 0.100 µg/m3 (*) was used to represent potential
exposure to airborne background levels of lead.
• A daily dietary intake of 2-3. 5 µg (*) of lead was assumed as a default in the model.
• Lead was ingested in the drinking water by children using drinking water ingestion rates
ranging from 0.5 to 0.6 L/day (l-6 of age) and 0.2 L/day for infants (0-l year). The
default lead concentration detected in groundwater was 4.0 µg/L.
• An average surface soil concentration of 156 µgig(*) was used.
• A soil and dust ingestion rate of 156 µg Pb/g per day was assumed for the 0-6 year old
child.
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written permission of EPA.
• No lead intake from paint chip ingestion was assumed.
Human Health Risk Assessment
Davis Park Road Superfund Site
Section: 5
Revision: 0
Date: May 1997
• A maternal blood lead level at birth of2.5 µg/dL (*) was assumed.
Using these parameters in the model, the results indicated that 99.23 percent of the 1-6 year old
child hypothetically exposed at the Davis Park Road site would have blood lead levels less than
the 10 µg/dL benchmark (Figure 5-1). The predicted mean blood lead concentration was 3.2
µg/dL. This value is very conservative relative to the site-specific and default assumptions used in
the model. The actual blood lead level of the future child resident (if exposed at the Davis Park
Road site) would likely be the same as currently predicted, assuming that the parameters used in
the model do not change.
5.4.3 Conclusions
Since the predicted blood level of lead was less than the 10 µg/dL under very conservative
assumptions, it is reasonable to assume lead will not pose a health problem.
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written permission of EPA.
Figure 5-1
Human Health Risk Assessment
Davis Park Road Superfund Site
Section: 5
Revision: 0
Date: May 1997
Bell Curve Distribution of Blood Levels
I I ' . ' . ' I ' ' ' .
(\ Cutort: 10.0 ug/dL
% Above 0,77
% Delo1-1 99.23
/ \ G. Hean 3,2
r .
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\ I +' "' \ , 'O C 0 \ • 0 " I .c , V -\ -+' '-
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~-' / ' ' ' '
..____,
' ' ; ' ·r·
0 2 4 6 B 10 12 14 16 1B
LEAD 0.99d BLOOD LEAD CONCENTRATION ( ug/dL >
0 to 84 Months
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written permission of EPA. '
5.5 REFERENCES
Human Health Risk Assessment
Davis Park Road Superfund Site
Section: 5
Revision: O
Date: May 1997
ATSDR (Agency for Toxic Substances and Disease Registry). 1993. Toxicological Profile for Lead
U.S. Department ofHealth and Human Services. Atlanta, GA. PB93-182475.
EPA (U.S. Environmental Protection Agency), 1986. Superjund Public Health Evdiuation
Manual. Office of Emergency and Remedial Response. OSWER Directive 9285.4-1.
EPA (U.S. Environmental Protection Agency), 1989. Risk Assessment Guidance for Superfund,
Volume 1, Human Health Evaluation Manual (Part A). Interim Final. Office of Solid Waste and
Emergency Response. Washington, D.C. EPA1540/l-89/002.
EPA (U.S. Environmental Protection Agency), 1991. Role of the Baseline Risk Assessmerit in
Superfund Remedy Selection Decisions. OSWER Dir. 9355.0-30.
EPA (U.S. Environmental Protection Agency), 1995. Supplemental Guidance to RAGS: Region
IV Bulletins, Nov. 1995.
EPA (U.S. Environmental Protection Agency), 1997. Integrated Risk Information System, l 997.
U.S. EPA Toxicological Database, Washington, D.C.
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6.1 INTRODUCTION
SECTION 6
UNCERTAINTY ANALYSIS
Human Health Risk Assessment
Davis Park Road Superfund Site
Section: 6
Revision; O
Date: May 1997
The principal goals of the uncertainty analysis are to provide to the appropriate decision makers a
discussion of the key assumptions made in the risk assessment that significantly influence the risk
results and to assess the contribution of these factors to the under-or overestimation of risk The
uncertainty analysis should show that the calculated risks are relative in nature and do not
represent an absolute quantification.
In recent months, the U. S EPA has placed even more emphasis on the uncertainty analysis. In a
26 February 1992 memorandum from the Deputy Administrator to all assistant and regional
administrators (EPA, 1992), U.S. EPA provides additional guidance on explaining risks and all
their underlying data so that the strengths and weaknesses of the assessment become clear. This
section of the risk assessment attempts to explain the key assumptions used in this report and
present a range of the variability inherent in these assumptions.
In the absence of empirical or site specific data, assumptions are developed based on best
estimates of data quality, exposure parameters and dose-response relationships. To assist in the
development of these estimates, the EPA recommends the use of guidelines and standard factors
in risk assessments conducted under CERCLA (EPA, 1989; 1991 ). The use of these standard
factors is intended to promote consistency among risk assessments where assumptions must be
made. Although the use of standard factors no doubt promotes comparability, their usefulness in
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Human Health Risk Assessment
Davis Park Road Superfund Site
Section: 6
Revision: O
Date: May 1997
accurately predicting risk 1s directly proportional to their applicability to the site-specific
conditions.
The carcinogenic and noncarcinogenic risk estimates for the Davis Park Road site were based on
a number of assumptions that incorporated varying degrees of uncertainty resulting from several
sources, including:
• Selection of exposure pathways, input parameters, algorithms and scenarios;
• Confidence in toxicological data used to estimate cancer potency factors and reference
doses.
6.2 EXPOSURE PATHWAYS AND CHEMICALS ASSOCIATED WITH SIGNIFICANT
CANCER AND NONCANCER RISK
Tables in Section 5 summarize the exposure pathways and chemicals that contributed substantially
to carcinogenic and noncarcinogenic risk.
The total carcinogenic risk for the current and future resident is 6.6E-4 with 6.4E-4 generated by
soil exposure. In soil, dieldrin was a chemical of concern (COC) posing the highest risk at 3.8E-4.
In groundwater, chloroform and I, 1-dichloroethene were the COCs with risks 1.3E-6 and 8.1 E-6,
respectively.
The noncarcinogenic risk is divided into the child and adult. The child hazard index was 68.0 and
the adult was 11.2. Several chemicals generated a hazard quotient greater than 0.1, the largest
being 2-methylnaphthalene at 48.3 for the child and 7.95 for the adult. No VOCs were considered
COCs in soil.
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Human Health Risk Assessment
Davis Park Road Superfund Site
Section: 6
Revision: O
Date: May 1997
These chemicals and their associated uncertainties are the main focus of the following discussion.
General uncertainties are presented where they are relevant to the Davis Park Road site.
6.3 UNCERTAINTIES ASSOCIATED WITH EXPOSURE ASSESSMENT
The exposure assumptions directly influence the calculated doses (daily intakes), and ultimately
the calculation of risk. In general, conservative exposure assumptions were made in calculating
exposure doses such as the selection of exposure routes and scenarios, and the exposure factors
(e.g., contact rate, exposure frequency, exposure duration, body weight and surface area) used to
estimate exposure doses. In most cases, this uncertainty overestimates the realistic exposures, and
therefore, overestimates risk. This is appropriate when performing risk assessments of this type so
that risk managers can be reasonably assured that the risks to the public are not underestimated,
and so that risk assessments for different locations and scenarios can be compared.
The Reasonable Maximum Exposure (RME) concept was used to develop exposure doses in the
current and future residents, and is defined as the "maximum exposure that is reasonably expected
to oc~ur at the site (EPA, 1989)." Several variables that determine the exposure dose for the
RME are based on upper-bound (typically 90th percentile or greater) estimates. These are:
• The 95 percent upper confidence limit of the medium concentration for the chemical used
to calculate the exposure dose.
• Intake/contact rate (IR) (upper-bound value).
• Exposure frequency (EF) (upper-bound value).
• Exposure duration (ED) (upper-bound value).
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Human Health Risk Assessment
Davis Park Road Superfund Site
Section: 6
Revision: O
Date: May 1997
Therefore, the calculated exposure dose for any given chemical, which results from integration of
all of these variables, represents an upper-bound estimate of the probable exposure dose. The use
of these upperbound exposure parameters, coupled with conservative estimates of toxicity, in turn
will yield risk results that represent an upper-bound estimate of the occurrence of carcinogenic
and noncarcinogenic health effects. Below are discussed several site specific uncertainties which
relate to calculation of exposure concentration.
6.3.1 Estimation of Exposure Point Concentrations for the Groundwater and Soil
Pathways
6.3.1.1 Degradation of Volatiles
In the exposure assessment, it was assumed that the concentration of volatile substances in the
groundwater would remain unchanged for a lifetime of exposure. As a result, the carcinogenic and
noncarcinogenic risks by this pathway could be overestimated.
6.3.1.2 Well Location and Contamination
The exposure point concentrations for the groundwater pathway were based on an evaluation of
the contaminated wells as discussed in Section 3.2. The 95 percent upper confidence limit (UCL)
of the groundwater concentration for the contaminated wells was used. In the case of the Davis
Park Road site, the exposure point concentration defaulted to the UCL value for almost every
chemical evaluated due to the relatively low frequency of detection. Therefore, the actual
exposure point concentration could be higher or lower, although the range of variability cannot be
directly quantified.
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6.3. 1.3 Soil Depth
Human Health Risk Assessment
Davis Park Road Superfund Site
Section: 6
Revision: O
Date: May 1997
The soil samples included in the surface soil exposure pathway were collected from O to 5 feet in
depth. Typically, sutface and exposure is limited to 0-12 inch~s; however, this interval was not
analyzed separately. Hence, the exposure depth is greater and may either under or overestimate
the risks to soil by ingestion and dermal contact.
6.4 UNCERTAINTIES ASSOCIATED WITH TOXICITY ASSESSMENT
For a risk to exist, both significant exposure to the contaminants of potential concern and toxicity
at these predicted exposure levels must exist. The toxicological uncertainties primarily relate to
the methodology by which carcinogenic and noncarcinogenic criteria (i.e., cancer slope factors
and reference doses) are developed. In general, the methodology currently used to develop cancer
slope factors and reference doses is very conservative, and likely results in overestimation of
human toxicity (EPA, 1989). These and other factors are discussed in the subsections below.
6.4.1 Cancer Slope Factors
Although there is evidence to suggest some carcmogens may exhibit thresholds, cancer slope
factors are developed assuming there is no safe level of exposure to any contaminant proven or
suspected ·to cause cancer. This uncertainty implies that exposure to even a single molecule of a
chemical may be associated with a finite risk, however small. The assumption is that even if
relatively large doses of a pollutant were required to cause cancer in laboratory animals (i.e.,
much higher than a person would ever likely be exposed to over a lifetime), these exposure doses
can be linearly extrapolated downward many orders of magnitude to estimate slope factors for
NOM<:IWP\04400\071 IAPMJC002.DOC 6-5
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This document was prepared by Roy F. Weston, Inc., expressly for EPA. It shall not be disclosed, in whole or in part, without the express
written permission of EPA.
Human Health Risk Assessment
Davis Park Road Superfund Site
Section: 6
Revision: O
Date: May 1997
humans. A significant uncertainty for the carcinogens ts whether the cancer slope factors
accurately reflect the carcinogenic potency of these chemicals at low exposure concentrations.
The calculated slope factor is used to estimate an upperbound lifetime probability of an individual
developing cancer as a result of exposure to a particular level of a carcinogen. Therefore, the
cancer slope factors developed by EPA are generally conservative and represent the upperbound
limit of the carcinogenic potency of each chemical. The actual risk posed by each chemical is
unknown, but is likely to be lower than the calculated risk, and may even as low as zero (EPA
1989). The conclusion is that these toxicity assumptions will typically result in an overestimation
of carcinogenic risk.
The assumption that all carcinogens (whether A, BI, B2, .or C) can cause cancer in humans is also
conservative. Only those chemicals classified as "A" carcinogens by the EPA are unequivocally
considered human carcinogens. The other three classes are probable (BI, B2) or possible (C)
human carcinogens. In this risk assessment, all "probable" and "possible" carcinogens are given
the same weight in the toxicity assessment (and consequently in the estimation of risk) as·true
human carcinogens. This assumption most likely overestimates actual carcinogenic risk to human
receptors.
6.4.1.1 Tetrachloroethene
The oral and inhalation slope factors for tetrachloroethene (PCE) are currently under review by
EPA (IRIS, 1997) PCE is currently classified as a B2 carcinogen (See Table 4-1 ). Until questions
regarding the adequacy of the critical studies and the toxicity criteria are resolved, there is some
uncertainty in the cancer risk associated with PCE. The criteria used in this report (NCEA, 1997)
may either under-or overestimate the carcinogenic risks from groundwater ingestion from TCE.
NORiX :\WP\04400\071 \RPM JC 00 2 .DOC 6-6
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This document was prepared by Roy F. Weston, Inc., expressly for EPA It shall not be disclosed, in whole or in part, without the express
written permission of EPA.
6.4.1.2 1,1-Dichloroethene (l,1-DCE)
Human Health Risk Assessment
Davis Park Road Superfund Site
Section: 6
Revision; O
Date: May 1997
Although 18 studies have been evaluated by EPA for potential cancer risk, only a single inhalation
animal toxicity study showed I, 1-DCE to exhibit carcinogenicity, which was considered by EPA
to be sufficient evidence that I, 1-DCE is a complete carcinogen. Thus, there is question as to
whether I, 1-DCE is truly a carcinogen in humans. It is currently classified as "C" carcinogen (see
Table 4-1 ). The conclusion is that the potential risk from exposure by both inhalation and
ingestion/noningestion of groundwater is probably an overestimate.
6.4.2 Reference Doses
In the development of reference doses (Rills) for each chemical by exposure route, it is assumed
that a threshold dose exists below which there is no potential for adverse health effects to the
most sensitive individuals in the population. The RID is typically derived from dose-response
studies in animals in which a NOAEL (no-observed-adverse-effect level) or a LOAEL (lowest-
observed-adverse-effect level) is determined by applying several uncertainty factors of l O each.
An additional modifying factor of up to IO can be applied which accounts for a qualitative
professional assessment of additional uncertainties in the available toxicity data (EPA, I 989). The
final degree of extrapolation for a given chemical can range anywhere between IO and I 00,000
and therefore result in a human subthreshold dose of one tenth to one-hundred thousandth of the
study dose. In general, the calculated RID is likely overly protective, and its use probably results
in an overestimation of noncarcinogenic risk.
NO RIK ;\WP\0440010 71 \RPMJCOO 2. DOC 6-7
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This document was prepared by Roy F. Weston, Inc., expressly for EPA. It shall not be disclosed, in whole or in part, without the express
wrttten permission of EPA.
6.4.2. l Use of Chronic RIDs in Children
Human Health Risk Assessment
Davis Park Road Superfund Site
Section: 6
Revision: O
Date: May 1997
Oral chronic RIDs were used in calculating hazard quotients for the I to 6 year old child. The use
of chronic RIDs in this age group is conservative and will result in an overestimation of risk.
Chronic RIDs are developed assuming a lifetime daily exposure.
6.4.2.2 2-Methylnaphthalene
The oral RID for 2-methylnaphthalene likely represents an overestimate of toxicity in humans.
There is no toxicity values specifically calculated for this chemical. The toxicity value for pyrene,
a structurally similar P AH chemical was used. 2-methylnaphthalene contributed greatly _to the
noncancer risk for both the adult and child resident, therefore, potentially resulting in an
overestimation of risk.
6.4.2.3 Naphthalene
The oral RID for naphthalene likely represents an overestimation of toxicity in humans. The
toxicity value for naphthalene was withdrawn from the IRIS database. Therefore, by using the
RID for pyrene, a structurally similar chemical, the health risk could be potentially overestimated.
6.4.2.4 Phenanthrenc
The oral RID for phenanthrene likely represents an overestimation of toxicity in humans. The
toxicity value for phenanthrene was withdrawn from the IRIS database. Therefore; by using the
RID for pyrene, a structurally similar chemical, the health risk could be potentially overestimated.
NO R/K:\WP\04400\0 71 \RPMJC002 .DOC 6-8
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This document was prepared by Roy F. Weston, Inc., expressly for EPA. It shall not be disclosed, in whole or in part, without the express
written permission of EPA.
Human Health Risk Assessment
Davis Park Road Superfund Site
Section: 6
Revision: 0
Date: May 1997
6.5 UNCERTAINTIES ASSOCIATED WITH RISK CHARACTERIZATION
Table 6-1 summarizes the primary uncertainties and their relative impact on risk.
6.6 REFERENCES
EPA (U.S. Environmental Protection Agency), 1989. Risk Assessment Guidance for Superfund,
Volume 1, Human Health Evaluatio,1 Manual (Part A). Interim Final. Office of Solid Waste and
Emergency Response, Washington, D.C. EPN540/l-89/002.
EPA (U.S. Environmental Protection Agency), 1991. Human Health Evaluation Jvfanual,
Supplemental Guidance: "Standard Default Exposure Factors". Office of Solid Waste and
Emergency Response, Washington, D.C. OSWER Directive 9285.6-03.
EPA (U.S. Environmental Protection Agency), 1992. Guidance 011 Risk Characterization for Risk
Managers and Risk Assessors. Memorandum from F. Henry Habicht, II to Assistant and Regional
Administrators. Feb. 26, 1992.
EPA (U.S Environmental Protection Agency), 1995b. Health Effects Assessment Summa,y
Tables, Annual FY-1995. OERR 9200.6-303 (95-1). NTIS No. PB 95-92119. March, 1995.
Howard, P M., 1991. Fate and Exposure Data. Volume !. Large Production and Priority
Pollutants. Lewis Publishers, Chelsea, Michigan.
IRIS (Integrated Risk Information System), 1997 On-Line Toxicological Database Maintained by
the U.S. EPA. Washington, D.C.
NOR/K:\WP\044001071 IRPMJC002.00C 6-9
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This document was prepared by Roy F. Weston, Inc., expressly for EPA. It shall not be disclosed, in whole or in part, without the express
written permission of EPA.
Uncertainty Element
Ex:2osure Parameter Estimation
• Media intake rates
• Groundwater characterization
• Exposure frequencies
• Exposure to soil
• Exposure durations
• Exposure point concentration for
volatiles in groundwater
Toxicitv Data
• Use of chronic Rills for
estimating noncancer risk in
children
• Cancer slope factors
-I, 1-Dichloroethene
-Tctrachlorocthcne
• Reference doses
-2 methyl naphthalene
-Naphthalene
-Phenanthrene
NOR/K:\WP\04400\071 I TBMJCOO 1. DOC
Table 6-1
Human Health Risk Assessment
Davis Park Road Superfund Site
Section: 6
Revision: O
Date: April 1997
Summary of Uncertainty Analysis
North Belmont PCE Site
Effects on Risk Estimate
Potential for Potential for Potential for Over or
Overestimation Underestimation Underestimation
Moderate
Moderate
Moderate
High
Moderate
Moderate
High
High
High
High
High
High
High
High
6-10
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This document was prepared by Roy F. Weston, Inc., expressly for EPA It shall not be disclosed, in whole or in part, without the express
written permission of EPA.
APPENDIX A
RAW DATA
NOR/K:\WP\0440010711RPMJC002.00C
Human Health Risk Assessment
Davis Park Road Superfund Site
Section: Appendix A
Revision: 0
Date: May 1997
-- -A1 .. AH43
DAVIS PARK ROAD
SOIL
NOV-96
MG/KG
DPRSS.WK1
Metals
Aluminum
Arsenic
Barium
Beryllium
Cadmium
Chromium
Cobalt
Copper
Lead
Manganese
Mercury
Nickel
Strontium
Titanium
Vanadium
Yttrium
Zinc
Calcium
Magnesium
Iron
Potassium
Sodium
Dieldrin
Toluene
Ethyl Benzene
M-and/or P-Xylene
0-Xylene
2-Methylnaphthalene
Acenaphthene
Dibenzofuran
Naphthalene
Phenanthrene
Pyrene
Toxaphene
- - --
1-SLA
DP1 -W001
2900
15
72
2 U
2 U
18
8.5
26
22
140
0.05 U
11
15
890
56
17
110
5900
3000
22000
1900
400 U
50 U
l!!!!!!I !!!!!I
1-SLB
DP2-W001
47000
4.7
70
I!!!!!
2.5 U
2.5 U
16
5.1
25
20
130
0.05 U
10 U
10
880
90
6.7
57
250 U
2100
39000
1600
500 U
50 U
420 J
94000
1200 J
2000 J
10000
600 J
==
1-SLC
DP3-W001
51000
8.1
110
2.5 U
2.5 U
23
5.4
33
26
200
0.05 U
10 U
10
1300
120
17
87
660
3600
51000
3200
500 U
50 U
2400 J
liiiil
950
liiil
2-SLA
DP4-W001
28000
5.8
91
liiil
2U
2U
13
6.5
21
29
160
0.05 U
9.9
19
5
45
16
50
2100
2600
19000
2400
400 U
50 U
-
2-SLB
DP5-W001
52000
5.1
75
3U
3U
12
6U
29
26
120
0.05 U
12 U
16
1300
59
7.9
64
300 U
3100
24000
2600
600 U
50 U
1111
-- -A1 .. AH43
DAVIS PARK ROAD
SOIL
NOV-96
MG/KG
DPRSS.WK1
Metals
Aluminum
Arsenic
Barium
Beryllium
Cadmium
Chromium
Cobalt
Copper
Lead
Manganese
Mercury
Nickel
Strontium
Titanium
Vanadium
Yttrium
Zinc
Calcium
Magnesium
Iron
Potassium
Sodium
Oieldrin
Toluene
Ethyl Benzene
M-and/orP-Xylene
O-Xylene
2-Methylnaphthalene
Acenaphthene
Dibenzofuran
Naphthalene
Phenanthrene
Pyrene
Toxaphene
-- -
2-SLC
DP6-W001
35000
SU
88
2U
2U
7.1
5.7
26
26
170
0.05 U
BU
9.1
1600
42
9.3
74
200 U
4200
18000
4500
400 U
50 U
--I!!!!!!
3-SLA
DP7-W001
21000
13
100
1 .1
1 .4
23
6.8
45
630
220
0.08
12
18
820
46
16
230
3000
3100
22000
2100
200 U
50 U
!!!Ill
3-SLB
DP8-W001
40000
10 U
87
2 U
2 U
8.6
4.8
11
240
130
0.05 U
BU
19
930
46
6.9
65
420
2600
19000
2800
400 U
50 U
11 J
35 J
31 J
1900
660 J
600 J
380 J
liiii
3-SLC
DP9-W001
37000
10 U
100
2 U
2U
6.4
5.9
5.7
25
160
0.05 U
BU
31
1400
42
11
65
370
3400
17000
3500
400 U
50 U
iiiil ..
4-SLA
DP10-woo1
28000
7.2
81
1.5 U
1.5 U
17
4.8
22
450
160
0.06
9.3
21
630
38
6.4
190
7200
2800
16000
1600
300 U
50 U
4-SLB
DP11-woo
36000
5
52
2
2
8.6
4
18
21
94
0.05
8
5.4
610
52
6.3
37
550
1800
21000
2000
400
50
-- -A 1..AH43
DAVIS PARK ROAD
SOIL
NOV-96
MG/KG
DPRSS.WK1
Metals
Aluminum
Arsenic
Barium
Beryllium
Cadmium
Chromium
Cobalt
Copper
Lead
Manganese
Mercury
Nickel
Strontium
Titanium
Vanadium
Yttrium
Zinc
Calcium
Magnesium
Iron
Potassium
Sodium
Dieldrin
Toluene
Ethyl Benzene
M-and/or P-Xylene
O-Xylene
2-Methylnaphthalene
Acenaphthene
Dibenzofuran
Naphthalene
Phenanthrene
Pyrene
Toxaphene
--
u
u
u
u
u u
u
u
- -
4-SLC
DP12-W001
34000
12
81
2U
2U
7.4
4U
29
27
87
0.05 U
BU
4
600
50
9.5
40
480
1800
20000
1800
400 U
50 U
--!!!!I
5-SLA
DP13-W001
20000
9.6
73
1.5 U
2.6
30
11
56
450
310
0.06
27
37
1000
49
13
300
28000
9200
26000
3200
300 U
18 J
91 R
==
5-SLB
DP14-W001
41000
7.1
89
2.5 U
2.5 U
9.2
5.9
24
30
100
0.05 U
10 U
38
770
57
SU
52
570
2000
23000
2000
500 U
50 U
liiil
5-SLD
DP15-W001
20000
12
74
1.5 U
3.2
32
11
54
460
360
0.03
25
28
820
46
10
290
23000
10000
38000
3400
300 U
12 J
6-SLA
DP16-W001
40000
4.8
99
2U
2U
9.5
5
18
20
150
0.05 U
BU
15
820
47
5.5
64
370
1900
18000
1900
400 U
50 U
1111
-- -
A1 .. BN46
DAVIS PARK ROAD
GROUNDWATER
NOV-96
UG/L
DPRGW.WK1
-
Volatile Organic Chemicals
Bromodichloromethane
Carbon Disulfide
Chloroform
Dibromoch!oromethane
1, 1 -Dichloroethene
1 , 1 -Dichloroethane
Cis -1 ,2-Dichloroethene
Tetrachloroethene
1, 1, 1 -Trichloroethane
Trich!oroethene
Methoxymethylpropane
-
Semi-Volatile Organic Chemicals
Brornocyc1ohexanol
Chlorocyclohexanol
Chloromethylbenzofuran
Dichlorohexane
Pesticide/PCBs
Alpha -Chlordane
Gamma-Chlordane
Trans-Nonachlor
Metals
Aluminum
Barium
Copper
Manganese
Strontium
Titanium
Vanadium
Zinc
Calcium
Magnesium
Iron
Sodium
Potassium
-- --
54-PW 96-PW
DP1 -W001 DP2-W001
5.8 J 1 U
2.5 U 2.5 U
40 J 1 U
0.58 J ,u
1 U 1U
1 U 1U
1 U 1 U
1 U 1 U
1 U 1 U
1U 1 U
NA NA
l!!!!I!!! i:::;;;a liiiii'I iiiiil -
100-PW 108-PW 121-PW 122-PW
DP3-W001 DP4-W001 DP5-W001 DP6-W001
,u ,u ,u 1 U
2.5 U 1.8 J 2.5 U 2.5 U
1 U 1 U 1U 1 U
1 U 1 U 1 U 1 U
1 U 1 U 1 U 1 U
1U 1 U 1 U 1 U
1 U 1 U 1.6 J 1 U
0.66 J 1 U 1 U 1 U
1U 1 U 1U 1 U
1U 1 U 15 J 0.92 J
NA NA NA NA
-- ----Al .. 8N46
DAVIS PARK ROAD
GROUNDWATER
NOV-96
UG/L
DPRGW.WK1
Volatile Organic Chemicals
Bromodichforomethane
Carbon Disulfide
Chloroform
Dibromochloromethane
1, 1 -Dichloroethene
1, I -Dichloroethane
Cis - 1 .2 -Dichloroethene
Tetrachloroethene
1 , 1 , 1 -Trichloroethane
Trichloroethene
Methoxymethylpropane
Semi-Volatile Organic Chemicals
Bromocyclohexanol
Chlorocyclohexanol
Chloromethy!benzofuran
Dichlorohexane
Pesticide/PCBs
Alpha-Chlordane
Gamma-Chlordane
Trans-Nonachlor
Metals
Aluminum
Barium
Copper
Manganese
Strontium
Titanium
Vanadium
Zinc
Calcium
Magnesium
Iron
Sodium
Potassium
131-PW
DP7-W001
NA
1U
2.5 U
1 U
1U
1 U
1U
1 U
1 U
1 U
3 J
--
131-PWD
DP8-W001
1U
2.5 U
1 U
1 U
1 U
1 U
1 U
1 U
1U
3 J
NA
-
150-PW
DP9-W001
NA
1U
2.4 J
1U
1U
.6
u
u
u
1 u
1 U
20 R
1000 R
20R
1000 A
0.25 U
0.25 U
20
12
2.5 U
190
2.5 U
2.5 U
4.4
8000
1200
14
10000
1500
l!!m
170-PW
DP10-W001
1 U
2.5 U
1 U
1 U
1 U
0.57 J
1 U
1 U
1 U
1U
NA
lllliia iiilil -
172-PW
DP11-W001
1 U
2.5 U
1 U
1 U
1 U
1 U
1 U
1 U
1 U
1 U
NA
177-PW
DP12-W001
1 U
1.3
u
1U
1U
1U
1 U
1 U
1 U
1 U
NA
-- -
A 1 .. BN46
DAVIS PARK ROAD
GROUNDWATER
NOV-96
UG/L
DPRGW.WKI
-
Volatile Organic Chemicals
Bromodichloromethane
Carbon Disulfide
Chloroform
Dibromoch!oromethane
1, 1 -Oichloroethene
1, 1 -Dichloroethane
Cis - 1 .2-Dichloroethene
T etrachloroelhene
1, 1, 1 -Trichloroethane
Trichloroethene
Methoxymethylpropane
Semi-Volatile Organic Chemicals
Bromocyclohexanol
Ch!orocyclohexanol
Chloromethylbenzofuran
Dichlorohexane
Pesticide/PCBs
Alpha-Chlordane
Gamma-Chlordane
Trans -Nonach1or
Metals
Aluminum
Barium
Copper
Manganese
Strontium
Titanium
Vanadium
Zinc
Calcium
Magnesium
Iron
Sodium
Potassium
- -
181-PW
DP13-W001
NA
1U
2.5 U
1 U
1 U
1U
1U
.7 J
1U
1U
18 J
- -
187-PW
DP14-W001
,u
2.5 U
1U
1 U
1 U u u u
1U
2.6 J
NA
- -
195-PW
DP15-W001
,u
2.5 U
u
1U
1 U u
u u
1 U
1 U
NA
l!!!!!!I 1!11!1
211-PW
DP16-W001
1U
2.5 U
1U
1 U
1U
1U
1 U
1 U
1 U
1U
NA
liiiil liiii
217-PW
DP17-W001
1U
2.5 U
1 U
1 U
1 U
1 U
1 U
1U
1U
1U
NA
-
221-PW
DP18-W001
,u
2.5 U
1 U
1 U
1 U
1 U
1 U
1 U
1 U
1 U
NA
-- -
Al .. BN46
DAVIS PARK ROAD
GROUNDWATER
NOV-96
UG/L
DPRGW.WK1
-
Volatile Organic Chemicals
Bromodichloromethane
Carbon Disulfide
Chloroform
Dibromochloromethane
1. 1 -Dichloroethene
1, 1 -Dichloroethane
Cis-1 ,2 -Dichloroethene
Tetrachloroethene
1, 1, 1 -Trichloroethane
Trichloroethene
Methoxymethy!propane
Semi-Volatile Organic Chemicals
Bromocyclohexanol
Chlorocyclohexanol
Chloromethylbenzofuran
Dich!orohexane
Pesticide/PCBs
Alpha-Chlordane
Gamma-Chlordane
Trans-Nonachlor
Metals
Aluminum
Barium
Copper
Manganese
Strontium
Titanium
Vanadium
Zinc
Calcium
Magnesium
Iron
Sodium
Potassium
- -
230-PW
DP19-W001
NA
JU
2.5 U
1 U
JU
JU
0.52 J
JU
0.62 J
1 U
1 U
-I!!!!!!
232-PW
DP20-W001
1U
2.5 U
JU ,u
1U
1U
JU
0.76 J
1 U ,u
NA
I!!!!!
236-PW
DP21-W001
JU
2.5 U
1 U
1 U
1 U
1 U
1 U
JU
JU ,u
NA
==
239-PW
DP22-W001
1 U
2.5 U
JU
1 U
3.6
1 U
1 U
10
7.6
32
NA
liiiiii iiiil iliil
252-PW
DP23-W001
1 U
2.5 U
1 U
JU
JU
1U
1 U
0.52 J
1 U
1 U
40 R
iiil
267-PW
DP24-W001
NA
1U
2.5 U
1U
1 U
1 U
1 U
1 U
JU
1U
JU
0.25 U
0.25 U
0.25U
50 U
21
3.4
2.5 U
130
2.5 U
4.2
5
6200
1100
12U
8300
2200
-- -- --A 1 .. 8N46
DAVIS PARK ROAD
GROUNDWATER
NOV-96
UG/l
DPRGW.WK1
Volatile Organic Chemicals
Bromodichloromethane
• Carbon Disulfide
Chloroform
Dibromochloromethane
1. 1 -Dichloroethene
1, 1 -Dichloroethane
Cis-1 ,2 -Dichloroethene
Tetrachloroethene
1, 1, 1 -Trichloroethane
Trichloroethene
Methoxymethy!propane
Semi-Volatile Organic Chemicals
Bromocyclohexanol
Chlorocyclohexanol
Chloromethylbenzofuran
Dich!orohexane
Pesticide/PCBs
Alpha-Chlordane
Gamma-Chlordane
Trans-Nonach!or
Metals
Aluminum
Barium
Copper
Manganese
Strontium
Titanium
Vanadium
Zinc
Calcium
Magnesium
Iron
Sodium
Potassium
275-PW
DP25-W001
NA
1U
2.5 U
1U
1U
1U
1U
1 U
1 U
1 U
1U
-I!!!!!
285-PW
DP26-W001
1U
2.5 U
1U
1U
0.66 J
1U
1U
6.4 J
1.2 J
14 J
NA
0.0097 R
0.0073 J
0.004 R
50 U
14
2.5 U
2.5 U
200
2.5 U
2.5 U
7.3
11000
2400
26
8800
1400
300-PW
DP27-W001
1U
2.5 U
1U
u
u
1 u
1U
u
u
u
NA
0.25 U
0.25 U
0.25 U
50 U
14
2.5 U
2.5 U
140
2.5 U
5.9
4.6
9600
3700
12 U
9100
2500
==
332-PW
DP28-W001
1 U
2.2 J
1 U
1U
1U
1 U
1 U
1 U
1U
1U
NA
liiiiJ liiilii
334-PW
DP29-W001
1U
2.5 U
1 u
1U
1U
1 U
1 U
1 U
1 U
1 U
NA
liiiil
348-PW
DP30-W001
1 U
2.5 U
1U
1 U
1U
1U
1U
1U
u
1 U
NA
MW-1
DP31 -WOO
1
2.5
NA
460
81
2.5
24
200
8.8
2.5
16
8100
3200
170
16000
2700
-- - --A1 .. BN46
DAVIS PARK ROAD
GROUNDWATER
NOV-96
UG/L
DPRGW.WK1
Volatile Organic Chemicals
Bromodichlorornethane
Carbon Disulfide
Chloroform
Oibromochloromethane
1, 1 -Dichloroethene
1 , 1 -Dichloroethane
Cis-1,2-Dichloroethene
Tetrachloroelhene
1, 1, 1 -Trichloroethane
Trichloroethene
Methoxyrnethy!propane
Semi-Volatile Organic Chern icals
Brornocyclohexanol
Ch!orocyc!ohexanol
Chloromethylbenzoluran
Dichlorohexane
Pesticide/PCBs
Alpha -Chlordane
Gamma -Chlordane
Trans-Nonachtor
Metals
Aluminum
Barium
Copper
Manganese
Strontium
Titanium
Vanadium
Zinc
Calcium
Magnesium
Iron
Sodium
Potassium
u
u u
u
u
u
u
u
u
u
u
u
-
MW-2
DP32-W001
NA
1 U
2.5 U
1 u
1 U
1 U
1 U
u
u
u
u
56
72
2.5 U
22
180
2.5 U
2.5 U
70
7300
2900
49
16000
2500
I!!!! !!l!!l 1111111 == liiiil -lliiiiil liilil
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This document was prepared by Roy F. Weston, Inc., expressly for EPA. Jt shall not be disclosed, in whole or in part, without the express
written permission of EPA.
APPENDIX B
EXPOSURE DOSES
NOR/K:\WP\04400\071\RPMJC002.DOC
Human Health Risk Assessment
Davis Park Road Superfund Site
Section: Appendix B
Revision: O
Date: May 1997
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TABLE B-1
Current and Future Resident (1-6 yr old)
Estimated Daily Intakes Through All Exposures Routes
Over a 6-Year Exposure Duration
Based on the Exposure Point Concentrations
----Ingestion Noningestion Ingestion
Chemical of Uses of of
Groundwater Groundwater Soil
('!'_g/kg-day_)_
Organics
J'!'_g/kg-day)_ jmg/kg-day)_
Bromodichloromethane 4.4E-05 4.4E-05 NA
Chloroform 6.7E-05 6.7E-05 INA
Dibromochloromethane 3.3E-05 3.3E-05 INA
1, 1 -Dichloroethene 4.4E-05 4.4E-05 NA
Trich!oroethene 2.SE-04 2.SE-04 INA
Tetrachloroethene 6.4E-05 6.4E-05 NA
Acenaphthene NA NA 1.SE-02
Dibenzofuran 1NA 1NA 2.SE-02 ' INA 2-Methylnaphthalene INA 1.2E+00
Naphthalene
'
NA INA 1.3E-01
Phenanthrene 1NA 1NA 7.6E-03 I Pyrene NA NA 4.BE-03
Dieldrin 1NA ' NA 2.3E-04
lnorganics
Aluminum ,NA INA 6.6E-01
Arsenic NA 1NA 1.3E-04
Beryllium 'NA
1NA 1.4E-05
-
I Dermal
Contact with
Soil
('!'_g/kg-day)_
"'A
1-JA
NA
INA
INA
NA
1.6E-03
2.7E-03
1.3E-01
1.4E-02
8.2E-04
5.2E-04
2.4E-05
7.1 E-03
1.4E-06
1.SE-07
Lead 'NA ;NA INA NA
Manganese (SOIL) 1NA INA 2.6E-03 I' 2.BE-05
Vanadium ' NA NA B.1E 04 B.6E 06
NA = Not Applicable
iilil liiiii iiiil liiil iiiii1 lillil
----
TABLE B-2
Current and Future Resident (1-6 yr old)
Estimated Daily Intakes Through All Exposures Routes
Over a 70-Year Lifetime
Based on the Exposure Point Concentrations
Ingestion NoningE!slf()ji"". Ingestion Dermal
Chemical of Uses of of ontact with
Groundwater Groundwater Soil i Soil
l-;c;--~-------t(rr,_g/kg-day)_ (mg/kg-day)_ (rr,_g/kg-day) (rr,_g/kg-day)_
Organics
Bromodichloromethane 3.8E-06 3.BE-06 :NA NA
Chloroform 5.BE-06 5.BE-06 NA !NA
Dibromochloromethane 2.BE-06 2.BE-06 ~A ('JA
1, 1 -Dichloroethene 3.BE-06 3.SE-06 jNA f'JA
Trichloroethene 2.1 E-05 2. 1 E-05 jNA l~A
Tetrachloroethene 5.SE-06 5.SE-06 NA NA
Acenaphthene jNA NA 1.3E-03
Dibenzofuran INA f'JA 2.2E-03
2-Methylnaphthalene iNA ~A 1.0E-01
Naphthalene 1NNAA INA 1.1E-02
Phenanthrene NA 6.SE-04
Pyrene 1NA ~A 4.1E-04
Dieldrin rA NA 2.0E-05
lnorganics I ..
Aluminum NA
Arsenic f\JA
Beryllium NA
Lead :N~:A Manganese (SOIL) ,
Vanadium
NA 5.?E-02
~A 1.lE-05
NA 1.2E-06 1NA NA A I _I NA 2.2E-04 1NA 6.9E-05
NA = Not Applicable
1.4E-04
2.3E-04
1.1E-02
1.2E-03
7.0E-05
4.4E-05
2.lE-06
6.0E-04
1.2E-07
1.3E-08
2.4E-06
7.4E-07
liiil liiiJ iiiil -liiiill _,
iiii liiii liii1 iiil iiiiil liiil ..
TABLE B-3
Current and Future Adult Resident
Estimated Daily Intakes Through All Exposures Routes
Over a 24-Year Exposure Duration
Based on the Exposure Point Concentrations
Ingestion Noningestion Ingestion
Chemical of Uses of of
Groundwater Groundwater Soil
("!_g/kg-dayL (mg/kg-day) _(mg/kg-day)_
Organics
Bromodichloromethane 1.9E-05 1.9E-05 NA
Chloroform 2.8E-05 2.BE-05 NA
Dibromochloromethane 1.4E-05 1.4E-05 NA
1, 1 -Oichloroethene 1.9E-05 1.9E-05 NA
Trichloroethene 1.1 E-04 1.1E-04 NA
Tetrachloroethene 2.7E-05 2.7E-05 NA
Acenaphthene 1NA NA 1.7E-03
Oibenzofuran NA INA 2.8E-03
2-Methylnaphthalene !NA NA 1.3E-01
Naphthalene INA NA 1 .4E-02
Phenanthrene ;NA ~A 8.4E-04
Pyrene
1: i 5.3E-04
Dieldrin 2.SE-05
1norganics
Aluminum ,NA INA 7.3E-02
Arsenic NA INA 1.4E-05
Beryllium 1NA 1NA 1.5E-06
iiiil
I Dermal
Contact with
Soil
("!_g/kg-da\')_
rA
NA 1NA
INA
INA
NA
6.8E-04
1.1E-03
5.3E-02
5.7E-03
3.4E-04
2.2E-04
1.0E-05
3.0E-03
5.7E-07
6.2E-08
Lead 1NA jNA NA NA I Manganese (SOIL) NA 1NA 2.9E-04 I' 1.2E-05
Vanadium ' NA NA 8.9E 05 3.6E 06
NA = Not Applicable
liiiii] iiiil liiii liiii'I
- ---.. liiiiil iiiil iili1
TABLE B-4
Current and Future Adult Resident
Estimated Daily Intakes Through All Exposures Routes
Over a 70-Year Lifetime
Based on the Exposure Point Concentrations
Ingestion Noningestion Ingestion
Chemical of Uses of of
Groundwater Groundwater Soil
(rllg/1<g-dax)_ Jr11_g/1<g-dax)_ (rTlg/1<g-dax)_
Organics
Bromodichloromethane 6.5E-06 6.5E-06 INA
Chloroform 9.9E-06 9.9E-06 NA
Dibromochloromethane 4.BE-06 4.BE-06 INA
1, 1 -Dichloroethene 6.5E-06 6.5E-06 INA
T richloroethene 3.?E-05 3.?E-05 f'JA
Tetrachloroethene 9.4E-06 9.4E-06 NA
Acenaphthene NA ~: 5.6E-04
Dibenzofuran ~A 9.4E-04
2-Methylnaphthalene NA INA 4.4E-02
Naphthalene 1NA 1NA 4.?E-03 1NA ' Phenanthrene jNA 2.BE-04 ' Pyrene
1NA NA 1.BE-04 ' Dieldrin NA
[:
B.5E-06
lnorganics
Aluminum NA 2.4E-02 ' 1NA Arsenic NA 4.BE-06
Beryllium :NA 1NA 5.2E-07
Dermal
Contact with
Soil
(rTlg/1<g-dax)_
NA
1NA
INA
~A ~:
2.3E-04
3.BE-04
1.BE-02
1.9E-03
1.1E-04
7.2E-05
3.4E-06
9.9E-04
1.9E-07
2.1 E-08
Lead NA ~A INA NA
Manganese (SOIL) ' NA , f'JA 9.6E-051· 3.9E-06
Vanadium NA NA 3.0E-05 1.2E 06
NA = Not Applicable
iii) -iiill iiiil -
---liill iiiiil liiill liiiil iiiil iiiil iiii1 -liiiiil lilil liiiiil -
Health Criteria for Davis Park Road Absorption Factors Used
Oral Oral Inhalation Inhalation Dermal Dermal Relative Dermal
Slope Factor Reference Dose Slope Factor Reference Dose Slope Factor Reference Dose Absorption Chemical (mg,kg/day) ~ -(mg,kg/day) (mg,kg/day) ~ -(mg,kg/day) (mg,kg/day) ~ -(mg,kg/day) Factor Organics
Bromodichloromethane 6.20E-02 2.00E-02 NA NA 7.75E-02 1.60E-02 0.80 Chloroform 6.10E-03 1.00E-02 8.10E-02 NA 7.63E-03 8.00E-03 0.80 Dibrcmochloromethane 8.40E-02 2.00E-02 NA NA 1.05E-01 1.60E-02 0.80 1, 1 -Dichloroethene 6.00E-01 9.00E-03 1.80E-01 NA 7.50E-01 7.20E-03 0.80 Trichloroethene 1.10E-02 6.00E-03 6.00E-03 NA 1.38E-02 4.80E-03 0.80 Tetrach!oroethene 5.20E-02 1.00E-02 2.03E-03 NA 6.50E-02 8.00E-03 0.80 Acenaphthene NA 6.00E-02 NA NA NA 3.00E-02 0.5 Dibenzofuran NA 4.00E-03 NA NA NA 2.00E-03 0.5 2-Methylnaphthalene NA 3.00E-02 NA NA NA 1.50E-02 0.5 Naphthalene NA 3.00E-02 NA NA NA 1.50E-02 0.5 Phenanthrene NA 3.00E-02 NA NA NA 1.50E-02 0.5 Pyrene NA 3.00E-02 NA NA NA 1.50E-02 0.5 Dieldrin 1.60E+01 5.00E-05 NC NA 3.20E+01 2.50E-05 0.5
lnorganics
Aluminum NA 1.00E+OO NA NA NA 2.00E-01 0.2 Arsenic 1.50E+OO NC NA 7.50E+OO NA 0.2 Beryllium NA NC NA NA NA 0.2 Lead NA NTV NA NA NA NA 0.2 Manganese (SOIL) NA 1.40E-01 NA NA NA 2.80E-02 0.2 Vanadium NA 7.00E-03 NA NA NA 1.40E-03 0.2
liiil
Chemical
Organics
Bromodichloromethane
Chloroform
Dibromochlorornethane
1.1 -Dichloroethene
Trichloroethene
Tetrachloroethene
Acenaphthene
Dibenzofuran
2-Methylnaphthalene
Naphthalene
Phenanthrene
Pyrene
Dieldrin
lnorganics
Aluminum
Arsenic
Beryllium
Lead
Manganese (SOIL)
Vanadium
iiiiil liiil liiii1
GWCURRENT
Expo Pt Cone
ABS MG/L
0.01 0.00069
0.01 0.00105
0.01 0.00051
0.01 0.00069
0.01 0.0039
0.01 0.001
0.01 NA
0.01 NA
0.01 NA
0.01 NA
0.01 NA
0.01 NA
0.01 NA
0.001 NA
0.001 NA
0.001 NA
0.001 NA
0.001 NA
0.001 NA
liiiiiil -
SOIL
Expo Pt Cone
MG/KG
NA
NA
NA
NA
NA
NA
1200
2000
94000
10000
600
380
18
52000
10.12
1.1
NA
205
63.5
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This document was prepared by Roy F. Weston, Inc., expressly for EPA. It shall not be disclosed, in whole or in part, without the express
written permission of EPA.
APPENDIX C
RISK TABLES
NOR/K:\WP\04400\071\RPMJC002.DOC
Human Health Risk Assessment
Davis Park Road Superfund Site
Section: Appendix C
Revision: O
Date: May 1997
Ill] --
TABLE C-1
Current and Future Child Resident
Hazard Quotients and Indices Through alt Exposure Routes
Over a 6 Year Exposure Duration
Ingestion
Chemical of
Groundwater
(n,_g/kg_:-day)_
Organics
Bromodichloromethane 0.002
Chloroform 0.007
Dibrornochloromethane 0.002
1, 1-Dichloroethene 0.005
Trichloroethene 0.04
Tetrachloroethene 0.006
Acenaphthene 1NA
Dibenzofuran 1NA
2-Methylnaphtha!ene NA
Naphthalene 1NA
Phenanthrene 1NA ' Pyrene iNA
Dieldrin NA
lnorganics
Aluminum NA
Arsenic 1NA 1NA Beryllium ' Lead NA
Manganese (SOIL) 1NA ' Vanadium NA
..!_ota_!_~y Pathway I 0.06
NA = Not Applicable
NC = Not of Concern in this Pathway
NTV = No Toxicity Value
Noningestion Ingestion J. Dermal
Uses of of Contact with
Groundwater Soil Soil
(n,_g/kg-day)_ (n,_g/kg -day)_ (n,_g/kg-day)
NTV ~: ~: NTV
NTV INA ]NA
NTV NA NA
NTV INA ;NA
NTV NA NA
1NA 0.25 0.05 NA 6.35 1.36
f'JA 39.79 8.52
NA 4.23 0.91
INA 0.25 0.05 1NA 0.16 0.03 1NA 4.57 0.98
1NA 0.66 0.04
NA NTV NTV
' 1NA NTV NTV
1NA NA NA
NA 0.02 0.001 1NA 0.12 0.01
0.00 56.41 11.95 --
-liiil -..,
Total
Hazard Quotien
by
Chemical
0.002
0.007
0.002
0.005
0.04
0.006
0.3
7.7
48.3
5.1
0.3
0.2
5.6
0.70
0.00
0.00
0.00
0.02
0.12
68
liiiliJ lliiil -1111 1111· -
TABLE C-2
Current and Future Child Resident
Cancer Risks Through All exposure Routes
Over a 70-Year Lifetime
Ingestion Noningestion Ingestion
-
Dermal
Chemical of Uses of of Contact with
Groundwater
(f!l_g/kg-day)_
Organics
Bromodichloromethane 2.4E-07
Chloroform 3.5E-08
Dibromochloromethane 2.4E-07
1, 1 -Dichloroethene 2.3E-06
Trichloroethene 2.4E-07
Tetrachloroethene 2.9E-07
Acenaphthene 1NA
Dibenzofuran NA
2-Methylnaphthalene :NA
Naphthalene NA
Phenanthrene INA
Pyrene !NA I Oieldrin NA
lnorganics
Aluminum 1NA
Arsenic 1NA
Beryllium NA
Lead 1NA
'.NA Manganese (SOIL)
Vanadium 1NA
Total by Pathway 3.31 E-06
NA "" Not Applicable
NC = Not of Concern in this Pathway
NTV = No Toxicity Value
Groundwater Soil Soil
(mg/kg-dayL (f!l_g/kg-day)_ _(rr,g/kg-day)
NTV ~A
~A 4.?E-07 NA A
NTV !NA A
6.8E-07 '"A ~: 1.3E-07 NA
1.1E-oa lNA NA
1NA NTV NTV
1NA NTV NTV
1NA NTV NTV
NA NTV NTV :NA NTV NTV
f NTV NTV
3.1E-04 6.?E-05
NA NTV NTV
' NA 1.?E-05 8.8E-07 ' 1NA NTV NTV
NA NA NA ' iNA NTV NTV
NA NTV NTV
1.29E-06 3.30E-04 6.77E-05
.. lillil
Total
Cancer Risk
by
Chemical
2.4E-07
5.0E-07
2.4E-07
3.0E-06
3.6E-07
3.0E-07
NC
NC
NC
NC
NC
NC
3.8E-04
NC
1.?E-05
NC
NC
NC
NC
4.0E-04
liiiQ liiill iillil iiiiiJ fiiii1, liiii1
TABLE C-3
Current and Future Adult Resident
Hazard Quotients and Indices Through all Exposure Routes
Over a 24 Year Exposure Duration
Ingestion Noningestion Ingestion
Chemical of Uses of of
Groundwater Groundwater Soil
J,:n_gJ\<g-day)_ (mg/\<g-day) _ j,:n_g/\<g-dayl_ ----~ Organics
Bromodichloromethane 0.001 NTV INA
Chloroform 0.003 NTV INA
Dlbromochloromethane 0.001 NTV 1NA
1, 1 -Dichloroethene 0.002 NTV NA ' Trichloroethene 0.02 NTV iNA
Tetrachloroethene 0.003 NTV NA
Acenaphthene NA ,NA 0.03
Dibenzofuran 1NA 1NA 0.70
2-Methylnaphthalene !NA NA 4.39
Naphthalene 1NA 1NA 0.47
Phenanthrene ~A :NA 0.03
Pyrene f'JA r: 0.02
Dieldrin
rA
0.50
lnorganics
Aluminum NA NA 0.07
Arsenic 1NA INA NTV 1NA ' Beryllium
1NA NTV
Lead :NA 1NA NA
Manganese {SOIL) NA NA 0.002 , ,
Vanadium ,NA , NA 0.01 --
!._otal by Pathway 0.031 0.00 6.22
NA = Not Applicable
NC = Not ol Concern in this Pathway
NTV : No Toxicity Value
I, Dermal
Contact with
Soil
j,:n_g/\<g-day)
NA
NA
1NA
tJA NA 1NA
0.02
0.57
3.56
0.38
0.02
0.01
0.41
0.01
NTV
NTV
NA
0.0004
0.003
4.99
,l'iiiil liiiiiiil liiilll
Total
Hazard Quotien
by
Chemical
0.001
0.003
0.001
0.002
0.02
0.003
0.05
1.27
7.95
0.85
0.05
0.03
0.91
0.09
0.00
0.00
0.00
0.002
0.02
11.24
-.. -1111111 l!!!l!!I
TABLE C-4
Current and Future Adult Resident
Cancer Risks Through All exposure Routes
Over a 70-Year Lifetime
Ingestion Noningestion Ingestion Dermal
Chemical of Uses of of Contact with
Groundwater Groundwater Soil
(~g/kg-day)_
Organics
J~g/kg-day)_ J_rri_g/kg-day)_
Bromodichloromethane 4.0E-07
Chloroform 6.0E-08
Oibromochloromethane 4.0E-07
1.1 -Dichloroethene 3.9E-06
Trichloroethene 4.0E-07
Tetrachloroethene 4.9E-07
Acenaphthene NA l'IA INA Oibenzofuran
INA
jNA
2-Methylnaphthalene NA
Naphthalene INA NA
Phenanthrene INA ~A
Pyrene !NA NA
Dieldrin !NA INA
!norganics
Alum.inum iNA f'JA
Arsenic ,NA ,NA
Beryllium NA NA
Lead 1NA ' NA
Manganese (SOIL) INA 1NA
Vanadium ' NA ' ,NA
Total_by Pathway __ ] 5.65E-06_j_
NA = Not Applicable
NC = Not of Concern in this Pathway
NTV = No Toxicity Value
NTV INA
B.OE-071NA
NTV tJA
1.2E-06 jNA
2.2E-07 INA
1.9E-08 NA
NTV
NTV
NTV
NTV
NTV
NTV
1.4E-04
NTV
7.1 E-06
NTV
NA
NTV
NTV
2.21 E-06 1.42E-04
Soil
(mg/kg-day)
NA
:NA
INA
INA
NA
NA
NTV
NTV
NTV
NTV
NTV
NTV
1.1E-04
NTV
1.4E-06
NTV
NA
NTV
NTV
1.1 lE-04
== == llllil
Total
Cancer Risk
by
Chemical
4.0E-07
8.6E-07
4.0E-07
5.lE-06
6.2E-07
5.1 E-07
NC
NC
NC
NC
NC
NC
2.4E-04
NC
8.6E-06
NC
NC
NC
NC
2.6E-04
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This document was prepared by Roy F. Weston, Inc., expressly for EPA. It shall not be disclosed, in whole or in part, without the express
written permission of EPA.
NOR/K:IWP\04400\071 \APPEN _ D. DOC
APPENDIX D
Human Health Risk Assessment
Davis Park Road Superfund Site
Section: Appendix D
Revision: O
Date: May 1997
REMEDIATION GOAL OPTIONS
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This document was prepared by Roy F. Weston, Inc., expressly for EPA. It shall not be disclosed, in whole or in part, without the express
written permission of EPA.
Human Health Risk Assessment
Davis Park Road Superfund Site
Section: Appendix D
Revision: o
Date: May 1997
REMEDIATION GOAL OPTIONS
This section provides the site-specific Remediation Goal Options (RGOs) and the methodology
used to calculate these goals for the Davis Park Road site. RGOs were developed for all the
chemicals and the exposure media which have risk levels greater than or equal to I E-6 for
carcinogens or a hazard quotient (HQ) greater than or equal to 0.1 for those pathways that have a
hazard index that exceeds I. 0 for noncarcinogens.
Tables C-1 through C-4 were used to select the exposure media and the chemicals for those
exposure media for which RGOs need to be calculated using the above mentioned criteria. The
RGOs calculated for selective chemicals in groundwater reflect exposure through the ingestion
route and the inhalation route ( only for volatile organic chemicals (VOCs)). The RGOs calculated
for selective chemicals in soil reflect exposure through ingestion of soil and dermal contact with
soil for current and future use scenarios.
The exposure assumptions and the models used in the risk assessment were used to develop the
RGOs. This leads to the risk level being directly proportional to the exposure concentration for a
chemical. The following equation was used to calculate the RGOs.
Where:
Remediation Goals = TR x EC
TR
RG CR
= Target Risk Level (HQ = 0.1, I, and 3 noncarcinogenic effects and risk
level= I E-6, IE-5, and IE-4 for carcinogenic effects)
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EC =
CR =
Human Health Risk Assessment
Davis Park Road Superfund Site
Section: Appendix 0
Revision: O
Date: May 1997
Exposure Concentration in Soil and Groundwater (Table 3-2)
Calculated Risk Level (Tables C-1 through C-4 for future noncarcinogenic
and carcinogenic effects)
Table D-1 presents RGOs for groundwater and surface soil based on carcinogenic effects for a
current resident and future resident, respectively. The Maximum Contaminant Levels (MCLs) and
North Carolina Drinking Water Standards are presented in a separate column for comparison with
the calculated RGOs. Table D-2 presents the RGOs for groundwater and soil based on
noncarcinogenic effects for a child (age 1-6 years) for the current and future scenarios. Table D-3
presents RGOs for groundwater and soil based on noncarcinogenic effects for an adult for the
current and future scenarios
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This document was prepared by Roy F. Weston, Inc., expressly for EPA. It shall not be disclosed, in whole or in part, without the express
written permission of EPA.
Chemicals
I, 1-Dichloroethene
DieldrinBenzo(a)pyrene
Arsenic
Table D-1
Human Health Risk Assessment
Davis Park Road Superfund Site
Section: Appendix D
Revision: 0
Date: May 1997
Risk Based RGOs -Based on Lifetime Cancer Risk
Current and Future Resident (Combined Child 1-6, and Adult Exposures)
Based on Cancer
Risk= IE-6
0.05
4.0
Based on Cancer
Risk= IE-5
0.5
40.0
Based on Cancer
Risk= IE-~
5.0
400
Federal MCL
Standards
NA
NA
MCL = Maximum Contaminant Level, State of Nonh Carolina Drinking Water Standards.
NA = Not Applicable.
NOR/K:IWP\04400\071\APPEN_D.DOC D-3
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Groundwater
Standards
NA
NA
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This document was prepared by Roy F. Weston, Inc., expressly for EPA. It shall not be disclosed, in whole or in part, without the express
written permission of EPA.
Table D-2
Human Health Risk Assessment
Davis Park Road Superfund Site
Section: Appendix D
Revision: 0
Date: May 1997
Risk Based RGOs -Based on Noncancer Risk
Current and Future Child Resident (Age 1-6 years)
Chemicals
Acenaphthene
Aluminum
Dibenzofuran
Dieldrin
2-Mcthylnaphthalene
Naphthalene
Phenanthrenc
Pyrcne
Vanadium
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Based on
HI= 0.1
400
7,428
26.0
0.32
194.6
196.0
3.333
190
52.9
D-4
Based on
HI= 1.0
4.000
74,285
260
3.2
1,946
1,960
33,333
1,900
529
Based on
HI= 3.0
12.000
222,857
780
9.6
5,838
5,882
99,999
19,000
1,587
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This document was prepared by Roy F. Weston, Inc., expressly for EPA. It shall not be disclosed, in whole or in part, without the express
written permission or EPA.
Table D-3
Human Health Risk Assessment
Davis Park Road Superfund Site
Section: Appendix D
Revision: O
Date; May 1997
Risk Based RGOs -Based on Noncancer Chemicals of Concern
Current and Future Adult Resident (age 1-6 years)
Chemicals
Dibenzofuran
2-Methylnaphthalene
Naphthalene
Dieldrin
NOR/K:\WP\04400\071\APPEN_D.DOC
Based on
HI= 0.1
157.5
I, 182
1,176
1.97
D-5
Based on
HI= 1.0
1,575
11,823
11,764
19.7
Based on
HI= 3.0
4,724
35,472
35.294
59.3
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written permission of EPA.
APPENDfX E
LEAD MODEL RESULTS
NOR/K:\WP\04400\071\RPMJC002.DOC
Human Health Risk Assessment
Davis Park Road Superfund Site
Section: Appendix D
Revision: 0
Date: May 1997
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This document was prepared by Roy F. Weston, Inc., expressly for EPA. It shall not be disclosed, in whole or in part, without the express
written permission of EPA.
APPENDIX E
LEAD MODEL RESULTS
Human Health Risk Assessment
Davis Park Road Superfund Site
Section: Appendix E
Revision: 0
Date: May 1997
The Lead Model Version 0.99d is a computer software application designed to determine the
uptake of lead and predict blood-lead levels in children ages 1-6 exposed to lead in air, diet,
drinking water, indoor dust, soil, and paint.
The Model is designed to accept site specific variables where applicable and provides default
values where data is not available. Lead was only detected in the soil samples. The average site-
specific value was entered for lead in surface soil (156 mg/kg). Table E-1 presents the model
parameters. Figure 5-1 presents the bell-curve distribution which shows that 0. 77 percent of the
population would have blood lead levels exceeding IO µg/1. The geometric mean is a blood lead
level of3.2 µg/1.
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This document was prepared by Roy F. Weston, Inc., expressly for EPA. It shall not be disclosed, in whole or in part, without the express
written permission of EPA.
Table E-1
ABSORPTION METHODOLOGY: Non-Linear Active-Passive
AIR CONCENTRATION: 0.100 µg Pb/m3 DEFAULT
Indoor AIR Pb Cone: 30.0 percent of outdoor.
Other AIR Parameters:
Age Time Outdoors (hr)
0-1 1.0
1-2 2.0
2-3 3.0
3-4 4.0
4-5 4.0
5-6 4.0
6-7 4.0
DIET: DEFAULT
DRJNKING WATER Cone: 4.0 µg Pb/L
Water Consumption: DEFAULT
SOIL & DUST:
Soil: constant cone.
Dust: constant cone.
Vent.
Human Health Risk Assessment
Davis Park Road Superfund Site
Section: Appendix E
Revision: 0
Date: May 1997
Rate (1113/day) Lung Abs. (%)
2.0 32.0
3.0 32.0
5.0 32.0
5.0 32.0
5.0 32.0
7.0 32.0
7.0 32.0
Age Soil (µg Pb/g) House Dust (µg Pb/g)
0-1 156 156
1-2 156 156
2-3 156 156
3-4 156 156
4-5 156 156
5-6 156 156
6-7 156 156
Additional Dust Sources: None DEFAULT
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This document was prepared by Roy F. Weston, Inc., expressly for EPA. It shalt not be disclosed, in whole or in part, without the express
written permission of EPA.
PAINT Intake: 0.00 µg Pb/day DEFAULT
MATERNAL CONTRIBUTION: Infant Model
Maternal Blood Cone. 2.50 µg Pb/dL DEFAULT
CALCULATED BLOOD Pb and Pb UPTAKES:
Human Health Risk Assessment
Davis Park Road Superfund Site
Section: Appendix E
Revision: O
Date: May 1997
Soil+Dust Uptake
Year Blood Level (µg/dL) Total Uptake (µg/day) (µg/day)
0.5-1 3.6 6.64 3.69
1-2 3.9 9.43 5.82
2-3 3.7 9.91 5.87
3-4 3.5 9.93 5.93
4-5 3.0 8.46 4.47
5-6 2.6 8.30 4.05
6-7 2.-l 8.44 3.83
Diet Uptake Water Uptake Paint Uptake Air Uptake
Year (µg/day) (µg/day) (µg/day) (µg/day)
0.5-1 2.55 0.37 000 0.02
1-2 2.66 0.92 0 00 0.03
2-3 3.01 0.97 0.00 0.06
3-4 2.93 1.00 0.00 0.07
4-5 2.87 1.05 0.00 0.07
5-6 3.05 I.I 1 0.00 0.09
6-7 3.37 1.14 0 00 0.09
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