NCD991278540_20000516_Weyerhaeuser Company_FRBCERCLA SAP QAPP_Draft Final Problem Formulation (Folder)-OCR

CJ
CDM ~. . -·: '
Federal Progrz.h}s Corporatton
,.,.
A subsidiary of Camp Dresser & McKee Inc.
consulting 1526 Cole Boulevard
engineering Building 3, Suite 150
construction Golden, CO 80401
op,w:n'ons Tel: 303 232·0131 Fax: [phone]
May 16, 2000
Ms. Beth Brown Walden
EPA RAC Region IV Remedial Project Manager
U.S. Environmental Protection Agency
61 Forsyth Street, S.W.
Atlanta, Georgia 30303-3104
Subject: Transmittal of Draft Final Problem Formulation for the Lower Roanoke River
Document No: 3280-030-RT-RISK-07784
Dear Ms. Brown Walden:
Attached to this letter are two copies of the Draft Final Problem Formulation document
for the Lower Roanoke River. Individual copies have been sent to other members of
the ETAG.
CDM Federal Programs Corporation is pleased to assist EPA with this work
assignment, and we look forward to providing further technical assistance. If you have
any questions concerning the attached, please call me at 303-232-0557 ext. 343.
Sincerely yours,
CDM FEDERAL PROGRAMS CORPORATION
EZ ... ~~ ~(',~
(~~eatty \Oc-
Ecologist
Attachment
cc: Lynn France, CDM Federal, Atlanta
Sharon Thoms, El' A, Region IV
Ken Mallary, EPA, Region IV
Lynn Wellman, EPA, Region IV
Bobby Lewis, El' A, Athens, Georgia
CDM Fcdcrnl Progrnrns Cc1r!1rion
Ken Seeley, US FWS, Edison, NJ
Tom Augspurger, US FWS, Raleigh, NC
Nile Testerman, DENR, Raleigh, NC
Linda George, EPA Region IV
Tom Dillon, NOAA
Del Baird, COM Federal, Oak Ridge
Project File
Document Control
•
• •
RECORD OF ET AG MEETING PROCEEDINGS
LOWER ROANOKE RIVER SITE
MARTIN, WASHINGTON, AND BERTIE COUNTIES, NORTH CAROLINA
TO:
FROM:
Beth Brown
Lynne France
DOCUMENT CONTROL NUMBER: 3280-030-CO-EPOU-07188
DATE:
LOCATION:
PURPOSE:
ATTENDEES:
MARCH 17, 2000; 1000 -1500
EPA REGION IV HEADQUARTERS, ATLANTA, GEORGIA
ETAG MEETING
REPRESENTATIVE AFFILIATION PHONE E-MAIL
Beth Walden EPA [phone] [e-mail]
Sharon Thoms EPA [phone] [e-mail]
Jennifer Wendel EPA [phone] [e-mail]
Kevin Koporec EPA [phone] [e-mail]
I
Lynn H. Wellman EPA-OTS [phone] wellman.l~[e-mail]
Bobby Lewis EPASESD [phone] lewis.bobbycaleQa.gov
Scott Fredericks EPA/ERT [phone] [e-mail]
Ken Seeley USFWS [phone] kenneth seele~@fws.gov
Tom Augspurger USFWS [phone] tom [e-mail]
Nile Testerman NC Superfund [phone] [e-mail]
Wayne Hall ATSDR ( 404) 639-0622 [e-mail]
Linda S. George ILS-ESAT ( 404) 562-8643 [e-mail]
Tom Dillon NOAA [phone] [e-mail]
Del R. Baird COM Federal [phone] [e-mail]
Shayne Wood COM Federal [phone] [e-mail]
Lynne France COM Federal [phone] [e-mail]
Brenda Beatty COM Federal [phone] beatn,:[e-mail]
• •
ETAG MEETING MINUTES
1000 Beth Walden began the meeting with introductions and stated that the overall goals of
meeting were to determine if we have adequate information:
1) to support source control for Weyerhaeuser OU1 and Georgia Pacific ROOs; and
2) to determination of extent of contamination
1015 Lynne France, COM Federal, presented the preliminary data characterization report for
river sediment and wetland soil data. This data was associated with the site recon and
the RI sampling conducted in 1999 by COM Federal, SESO and ERT.
An issue arose during the river sediment data presentation concerning the river
sediment samples taken for toxicity testing versus the river sediment samples collected
for the remedial investigation. The analytical results for the samples used for the
toxicity testing are generally elevated, sometimes by a factor of 4 or more, as compared
to corresponding normal river sediment samples. Tom Augspurger suggested that
normalizing the data using the TOC data may be of assistance. Some of the possible
explanations for the elevated results included:
1)
2)
sampling techniques used for the toxicity testing were not exactly the
same as compared to the RI river sediment sampling techniques, and
the toxicity samples may have contained more organic matter such as
leaves and sticks.
1045 Jennifer Wendel raised the question of whether or not methyl mercury should be listed
as a COPC. The Weyerhaeuser RI data could be used to assist in this decision because
• •
the river sediment samples that RMT took were tested for methyl mercury.
1050 Tom Dillon raised the issue of whether or not the high detection limits for SVOCs
creates a problem for properly evaluating the nature and extent of PCP. The meeting
participants reached a consensus that the risk could be evaluated using the full
detection limit and that the lab should be contacted to see if there is anyway to "clean
up" the sample to obtain a better detection limit. Tom Dillon also suggested that
ETAG may have to develop a screening value for PCP since Region IV does not have a
screening value. It was suggested that the Dutch or Region V screening values for PCP
could be used but the group was not in agreement about using these values. Some
members of the group felt that these values were not conservative enough. It was
mentioned that PCP is important because it is the only COPC that is unique to Georgia
Pacific.
1055 Tom Dillon also raised the high detection limit issue with respect to PAHs
1100 Presentation of River Sediment Data concluded.
1110 Tom Augspurger suggested that the background levels established for river sediment
and wetland soil be referred to as reference values instead of background. Also, to
keep in mind that the river does at times flow "backward" and that the background
locations might be close enough to the source areas that minimal impact is possible.
1115 Ken Seeley presented the results of the toxicity testing. During the field investigation,
ERT collected frogs and were responsible for processing the sediment samples for
toxicity testing. The Hyalella toxicity test showed toxicity at every station, Including
100% toxicity at station 419. The earthworm and Lumbriculus tests were not run
correctly.
1130 A discussion arose concerning the toxicity tests that failed due to problems with the
laboratory. Beth Walden wanted to know if the lab still had soil remaining to re-run
• •
the toxicity tests and did ETAG want that lab to re-run the tests or would it be better to
have SESD run the tests. Ken Seeley said that he would see if the lab had enough soil
to re-run the tests and Bobby Lewis said he would check with the SESD lab to see if
they had the capability and capacity to run the toxicity tests.
1135 Bobby Lewis (SESD) Begins Tissue Sampling/Data discussion. During sampling,
salinity of the water created difficulties in using the elctroshocking technique and clams
were not available.
1150 Tom Augspurger raised the question of whether or not there should be a concern because
the clams where not collected due to the die off that resulted from the saltwater wedge.
The overall consensus was that this is a concern because the worm toxicity test data is
suspect. The suggestion was made that if the worm toxicity tests could not be re-run, the
possibility of collecting different types of clams should be considered. There is a concern
that after last years clam die-off, only young clams would be available. Tom Augspurger
stated that clams collected from the Sound would be more useful.
There was a discussion of the fish fillet data available from Weyerhaeuser. Only two
dioxin congeners are analyzed for. Lynn Wellman wanted to know if there was a
downstream trend in the data. Jennifer Wendel said that she has the data and that she
would check for trends.
Tom Augspurger wanted to know if the data from the EPA study had been validated and
was assured that it had been.
There was a question about whether a benthic community analysis had been conducted
during the 1999 reconnaissance. One was done, but was not comprehensive. Lynn
Wellman stated that that study was not really sensitive to what we were looking at.
1200 to 1300 Lunch
• •
1315 Resumed meeting with a Working Session of Problem Formulation led by Brenda
Beatty. The group discussed the list of COPCs. Several additions to the COPC list were
suggested, including PCP and methyl mercury. Sharon Thoms suggested that
aluminum be screened out but that all other COPCs be retained. Tom Dillon suggested
adding a "Frequency of Detection" column to the screening table in the Problem
Formulation. Tom will send Brenda the Navy screening levels. In evaluating the data,
total PAHs will be used.
1320 Lynn Wellman suggested that a refined list of COPCs be circulated among the ETAG
members for comment.
The group discussed updating the toxicity profiles. Tom Augspurger wants to update
the toxicity profiles from the Oak Ridge Toxline Plus. It was pointed out that
Weyerhaeuser used the Oak Ridge numbers. Jennifer Wendel was concerned that we
stay consistent with what EPA has asked Weyerhaeuser to do. It was decided that we'll
use the numbers that Weyerhaeuser used, but also update the toxicity profiles and
compare the numbers to those used by Weyerhaeuser.
1330 The ETAG agreed that only the Recon Data and the RI data would be used in the Risk
Assessment. ETAG requested that Brenda update the Problem Formulation with the RI
data.
The group discussed an assessment endpoint table provided by Brenda.
Lynn Wellman noted that measurement endpoints should not be in the Problem
Formulation.
1350 The question of why surface water was not sampled was raised. It was pointed out that
there are permitted discharges in the area. Also, most of the COPCare those that will be
entrained in the sediments. Tom Dillon pointed out that early life stage toxicity could
be screened with surface water data. Lynn Wellman pointed out that with the outfalls,
• •
suspended sediment could be a problem in sampling. A consensus was reached that
lack of surface water data may be a data gap.
1400 Scott Fredericks presented some ideas on Innovative Technologies that may be
pertinent to the site. He noted that PRPs will often apply pressure to have the
contaminants remain in place. He mentioned that Mr. Ernie Watkins has been working
on a model for decision-making for sites dealing with contaminated sediments.
Tom Dillon noted that there are three good websites that provide remedial technologies.
He'll provide the group with those website addresses.
1420 Other Data gaps were discussed. It was pointed out that we don't know what else is
upstream that may be eroding into the river. Tom Augspurger said that there are other
known sources upstream.
Sharon Thoms stated that attribution is still a data gap.
Jennifer Wendel brought in Weyerhaeuser fish fillet data and noted that there is only
one sample from the river. Dioxin levels in fish from the Sound were higher.
1430 Beth.Walden leads a wrap up session and action items are reviewed. In response to the
question "Does the Risk Assessment support source control for the Weyerhaeuser and
Georgia Pacific sites?" the consensus was that it does. Jennifer Wendel pointed out that
Weyerhaeuser knows that there will be source control at the chlorine plant and Welch
Creek.
The group reach a consensus that additional sampling for nature and extent, at least to
finish sampling that was originally planned, should be done.
The action items were reviewed and assigned to individuals for completion. (See
Attached List)
• •
1500 Meeting is Adjourned
ACTION ITEMS
1. COM Federal will distribute a draft of the refined COPCs for comment by the group.
2. COM Federal will update toxicity profiles and compare to Oak Ridge numbers. Oak
Ridge numbers will be used unless there is a significant difference.
3. COM Federal will contact Ernie Watkins in reference to the model for river sediment
removal.
4. Tom Dillon will distribute the addresses of the web sites of sediment work groups.
5. COM will explore other possible dioxin inputs that could be up river of
Weyerhaeuser. Jennifer Wendel will look for a report that may contain this
information. Tom Augspurger will distribute a reference list of point sources on the
Roanoke River.
6. Ken Seeley will contact the toxicity lab to determine if there is sufficient sediment to
re-run some of the toxicity tests.
7. Bobby Lewis will explore SESD' s capability and capacity to re-run toxicity tests.
8. Lynn Wellman will develop a screening number for PCP
9. COM Federal will evaluate PAHs as total PAHs I when preparing the RI Report and
Risk Assessment.
10. COM Federal will evaluate background data to see how many reference samples
would be required to meet 90 or 95 percent upper confidence level.
11. COM Federal will update the reference list for the RI Report. Tom Augspurger will
provide COM with a list of the missing references.
"!
.-.. .. OPPENHEIMER. -----OPPENHEIMER WOLFF & DONNELLY LLP
1350 Eye Street N.W., Suite 200
Washington, D.C. 20005-3324
202.312.8000
Fcu 202.312.8100
Direct Dial:
E-Mail:
February 22, 2000
Carol M. Browner, Administrator
United States Environmental
Protection Agency
401 M Street S.W.
Washington, D.C. 20460
Timothy Fields, Jr., Assistant Administrator
Office of Solid Waste and
Emergency Response
United States Environmental
Protection Agency
Mail Code 5101
401 M Street S.W.
Washington, D.C. 20460
Gary S. Guzy, General Counsel
United States Environmental
Protection Agency
1200 Pennsylvania Avenue N.W.
Mail Code 2310-A
Washington, D.C. 20460
Re: Georgia-Pacific Corporation v.
Environmental Protection Aucncv
Our File No. I 1533/25
Dear Sirs/Madams:
Bill Holman, Secretary
North Carolina Department
of Natural Resources
I 60 I Mail Service Center
[ ~ -, .. , ··-
1-. •· ::· -.,-,· .... •··
L · i4.m.~'~rU~-m: ·.· ;~ _: ~ Kc~:·y9fk_:
-0range County
Paris
Saint Paul
Silicol1 Vall.:y
Raleigh, North Carolina 27699-1601
Janet Reno
Attorney General of the United States
United States Department of Justice
Tenth Street and Constitution Avenue N.W.
Washington, D.C. 20530
RECEIVED,
CFFiCE OF GENERAL COUNSEL
Enclosed and served upon you by hand-delivery, please find enclosed the following
documents filed on February 22, 2000 in the above-captioned action:
(I) Docketing Statement;
(2) Statement of Issues To Be Raised;
OPPENHEIMER
OPPENHEIMER WOLFF & DONNELLY LL~
February 22, 2000
Page 2
•
(3) Certificate of Counsel
•
( 4) Statement Concerning Deferred Appendix.
MS:sf
Enclosures
cc: Ronald T. Allen
Gary P. Genge!
Sincerely,
) ~liJ~ ~ l;J:iouvA
Margar&: Strand
' · ..
I "!
• •
UNITED STATES COURT OF APPEALS
FOR THE DISTRICT OF COLUMBIA CIRCUIT
GEORGIA-PACIFIC CORPORATION,
Petitioner
V.
ENVIRONMENT AL PROTECTION
AGENCY,
Respondent
)
)
)
)
)
)
)
)
The issues to be raised in this matter are as follows:
No. 00-1014
STATEMENT OF ISSUES
TOBE RAISED
I. Whether the United States Environmental Protection Agency ("EPA") failed to
establish a valid Hazard Ranking System ("HRS") score of at least 2,8.5 for the Georgia-Pacific
Hardwood Sawmill site in Plymouth, North Carolina ("Sawmill Site" or "Site") such that EPA
has no authority to list the Sawmill Site on the National Priorities List for Uncontrolled
Hazardous Waste Sites ("NPL") pursuant to the Comprehensive Environmental Response,
Compensation and Liability Act ("CERCLA") Section 105(a)(8)(b) and the regulations
promulgated thereunder.
2. Whether EPA's unsupported assumptions regarding the overland flow at the
Sawmill Site, EPA's errors in evaluating the sample results for the Sawmill Site and in
calculating the factors required for the Site's HRS score, and EPA's failure to show that the
Sawmill Site was the source of an observed release to the Roanoke River invalidate EPA's HRS
score for the Sawmill Site such that EPA has no authority to list the Site on the NPL pursuant to
CERCLA Section 105(a)(8)(b) and the regulations promulgated thereunder.
3. Whether EPA failed to properly consider certain material in the record before the
agency when it made its decision, which invalidates the HRS score for the Site such that EPA
• •
has no authority to list the Site on the NPL pursuant to CERCLA Section 105(a)(8)(b) and the
regulations promulgated thereunder.
Date: February 22, 2000 Respectfully submitted,
Gary P. Genge!
Minnesota Attorney License No. 158598
and
1stnct o olumbia Circuit Bar No. 25262
Vanessa L. P. Johnson
Minnesota Attorney License No. 0269906 ·
OPPENHEIMER WOLFF & DONNELLY LLP
3400 Plaza VII Building
45 South Seventh Street
Minneapolis, MN· 55402
Telephone: [phone]
Facsimile: [phone]
ATTORNEYS FOR PETITIONER
2
• •
UNITED STATES COURT OF APPEALS
FOR THE DISTRICT OF COLUMBIA CIRCUIT
GEORGIA-PACIFIC CORPORATION,
Petitioner
V.
ENVIRONMENT AL PROTECTION
AGENCY,
Respondent
)
)
)
)
)
)
)
)
No. 00-1014
Pursuant to the January 20, 2000 Order of this Court, Petitioner Georgia-Pacific
Corporation hereby submits an original and one copy of the following documents:
(1) Docketing Statement;
(2) Statement ofissues To Be Raised;
(3) Certificate of Counsel
(4) Statement Concerning Deferred Appendix.
Date: February 22, 2000 Respectfully submitted,
Gary P. Genge!
Minnesota Attorney License No. 158598
Columbia Circuit Bar No. 25262
Vanessa L. P. Johnson
Minnesota Attorney License No. 0269906
OPPENHEIMER WOLFF & DONNELLY LLP
3400 Plaza VII Building
45 South Seventh Street
Minneapolis, MN 55402
Telephone: [phone]
Facsimile: [phone]
ATTORNEYS FOR PETITIONER
I. CASENO.
3. CASENAME
(lead parties only)
4. TYPE OF CASE:
UlllH:U "[ates LOUr[ 01 Appea1s
• District of Columbia Circuit •
DOCKETING STATEMENT
Administrative Agency Review Proceedings
(To be completed by appellant/petitioner)
00-1014 2. DA TE DOCKETED January 18, 2000 ------~-~~~~---
Georgia-Pacific Corporation v. Environmental Protection Agency
(Jg Review [ ] Appeal [ ] Enforcement [ ] Complaint [ ] Tax Court
5. JS TI!IS CASE REQUIRED BY STATUTE TO BE EXPEDITED? YES ____ NO X
IfYES, cite statute: -------------------------------------
6. CASE INFORMATION:
a. Identify agency whose order is to be reviewed: _____ E=n=v-=i-=r-=o-=nm=e""n'-'t'-'a'-'l'-'P'-'r'-'o'-'t'-'e:..:c:..:tec1:c· o:cn:.:...:Aeog.,_e=n=c.,_y ____ _
b. Give agency docket or order number(s): ~F~R2=2~0~C~9~9~-~l=l ______________________ _
c. Give date(s) oforder(s):· _ ---=O-=c'-'t'-"o-=b-=ec:er---=Zc:eZc.1.....olc,:9-"9-"9 ______________________ _
d. Has a request for rehearing or reconsideration been filed at the agency? YES ____ NO -~X~_
Jfso, when was it filed? _____ By whom? _______________________ _
Has the agency acted? YES____ NO___ If so, when? ________________ _
e. Are any other cases involving the same underlying agency order pending in this Court or in any other Court?
YES · NO X* IfYES, identify case name(s), docket num.ber(s), and court(s): To the best of Georgia-
Pacific's knowledge and belief, there are no other cases involv1ng.ttie listing of the Georgia-Pacific Hardwood Sawmill site on the National Priorities List pending in this Court or in any other court.
f. Are any other cases, to counsel's knowledge, pending before the agency, this Court, another Circuit Court, or the
Supreme Court which involve substantially the same issues as the instant case presents?
YES____ NO X IfYES, give case name(s) and number(s) of these cases and identify court/agency:
g. Have the parties attempted to resolve the issues in this case through arbitration, mediation, or any other alternative for
dispute resolution? YES ____ NO X If so, provide the name of the program and the dates of
participation. --------------------------------------
Signature /0l~aµil ~ a(
Name of Party (Print) orgi a-Pacific Corpora ti on
Date February 22, 2000
Name of Counsel for Appellant/Petitioner (Print)'.,ary P. Gen gel /Margaret N. St.rand Firm OPPENHEIMER WOLFF & DONNELLY LLP
Address Plaza VII, 45 South Seventh Street, Suite 3400, Minneapolis, MN 55402-1609
Phone_--'('-"6"'1"-2'--) -=6.e.07c..-..:.7.e.00e.:D:.._ _______________ _ Fax No. [phone]
ATTACH A CERTIFICATE OF SER VICE
Note: If counsel for any other party believes that the information submitted is inaccurate or incomplete, counsel may so
advise the Clerk within IO days by letter, with copies to all other parties, specifically referring to the challenged
statement. An original and three copies of such letter should be submitted.
USCA FORM 7
(Rev. 1/99)
"!
• •
UNITED STATES COURT OF APPEALS
FOR THE DISTRICT OF COLUMBIA CIRCUIT
GEORGIA-PACIFIC CORPORATION,
Petitioner
V.
ENVIRONMENT AL PROTECTION
AGENCY,
Respondent
)
)
)
)
)
)
)
)
No. 00-1014
PROVISIONAL CERTIFICATE OF
PETITIONER GEORGIA-PACIFIC
CORPORATION AS TO PARTIES,
RULINGS, AND RELATED CASES
Pursuant to Circuit Rule 28(a)(l) of the United States Court of Appeals for the District of
Columbia Circuit and the January 20, 2000 Order of the Court, Petitioner Georgia-Pacific
Corporation ("Georgia-Pacific") submits this Certificate as to Parties, Rulings, and Related
Cases.
A. Parties and Amici
This case involves review of the United States Environmental Protection Agency's
("EPA's") decision to list the Georgia-Pacific Corporation Hardwood Sawmill site ("Sawmill
Site"), located in Plymouth, North Carolina, on the National Priorities List ("NPL") for
Uncontrolled Hazardous Waste Sites pursuant to the Comprehensive Environmental Response,
Compensation and Liability Act ("CERCLA") Section !05(a)(8)(b) and the regulations
promulgated thereunder. The undersigned counsel of record for Petitioner certify that the parties
appearing in this action are Georgia-Pacific and "EPA.
Georgia-Pacific is a company incorporated in the state of Georgia for the purpose of
doing business as a manufacturer and distributor of building products, pulp, paper and related
chemicals used in papermaking and the production of building products. Georgia-Pacific is one
"!
• •
of the former owners of the Sawmill Site, which Georgia-Pacific operated as a sawmill from
approximately 1959 until 1980. Georgia-Pacific has no parent company or any publicly-held
company that has a 10% or greater ownership interest.
B. Ruling Under Review
Petitioner Georgia-Pacific seeks review of EPA's order listing the Georgia-Pacific site
located in Plymouth, North Carolina on the NPL. This listing is set forth at 64 Fed. Reg. 56966
(Oct. 22, 1999).
C. Related Cases .
To the best of Georgia-Pacific's knowledge and belief, this case was not previously
before this Court or any other court, and no other related cases involving the listing of the
Georgia-Pacific site located in Plymouth, North Carolina on the NPL currently are pending
·'·
before this Court or any Court.
2
• Date: February 22, 2000
.,_
•
Respectfully submitted,
Gary P. Genge!
Minnesota Attorney License No. I 58598
olumbia Circuit Bar No. 25262
Vanessa L. P. Johnson
Minnesota Attorney License No. 0269906
OPPENHEIMER WOLFF & DONNELLY LLP
3400 Plaza VII Building
45 South Seventh Street
Minneapolis, MN· 55402
Telephone: [phone]
Facsimile: [phone]
,·.
ATTORNEYS FOR PETITIONER
3
"!
• •
UNITED STATES COURT OF APPEALS
FOR THE DISTRICT OF COLUMBIA CIRCUIT
GEORGIA-PACIFIC CORPORATION,
Petitioner
V.
ENVIRONMENT AL PROTECTION
AGENCY,
Respondent
)
)
)
)
)
)
)
)
No. 00-1014
STATEMENT CONCERNING
DEFERRED APPENDIX
Petitioner Georgia-Pacific Corporation intends to utilize a deferred appendix pursuant to
Fed. R. App. P. 30(C).
Date: February 22, 2000 Respectfully submitted,
Gary P. Genge!
Minnesota Attorney License No. 158598 ·
.4(/1 . ~
Margar.
District of Columbia Circuit Bar No. 25262
Vanessa L. P. Johnson
Minnesota Attorney License No. 0269906
OPPENHEIMER WOLFF & DONNELLY LLP
3400 Plaza VII Building
45 South Seventh Street
Minneapolis, MN 55402
Telephone: [phone]
: Facsimile: [phone]
ATTORNEYS FOR PETITIONER
• • CERTIFICATE OF SERVICE BY UNITED STATES MAIL
I hereby certify that I have this day served upon the following by hand delivery a true and
correct copy of the foregoing: (I) Docketing Statement; (2) Statement oflssues To Be Raised;
(3) Provisional Certificate of Petitioner as to Parties, Rulings, and Related Cases; and, (4)
Statement Concerning Deferred Appendix:
Carol M. Browner, Administrator
United States Environmental
Protection Agency
401 M Street S.W.
Washington, D.C. 20460
Timothy Fields, Jr., Assistant Administrator
Office of Solid Waste and
Emergency Response
United States Environmental
Protection Agency
Mail Code 5101
401 M Street S.W.
Washington, D.C. 20460
Gary S. Guzy, General Counsel
United States Environmental
Protection Agency
1200 Pennsylvania Avenue N.W.
Mail Code 23 IO-A
Washington, D.C. 20460
Bill Holman, Secretary
North Carolina Department
ofNatural Resources
I 60 I Mail Service Center
Raleigh, North Carolina 27699-1601
Janet Reno
Attorney General of the United States
United States Department of Justice
Tenth Street and Constitution Avenue N.W.
Washington, D.C. 20530
OPPENHEIMER WOLFF
DONNELLY & BA YH LLP
1350 Eye Street N.W.
_Suite 200
·washington, D.C. 20005-3324
Telephone: [phone]
Dated at Washington, D.C. this 22nd day of
February 2000.
• •
RESPONSE ACTION CONTRACT
FOR REMEDIAL, ENFORCEMENT OVERSIGHT, AND NON-TIME
. CRITICAL REMOVAL ACTIVITIES AT SITES OF RELEASE OR
THREATENED RELEASE OF HAZARDOUS SUBSTANCES
IN EPA REGION IV
U.S. EPA CONTRACT NO. 68-WS-0022
Draft Final Problem Formulation
MAR 09 2000
SUPERFUND SECTION
Lower Roanoke River Site
Work Assignment No.: 030-RICO-041B
Document Control No.: 3280-030-RT-RISK-07131
February 21, 2000
Prepared by CDM Federal Programs
Atlanta, Georgia
For US EPA, Region IV
(Draft Preliminary Problem Formulation Prepared by:
Mark D. Sprenger
U.S. EPA
Edison, NJ
and
Nancy Finley
U.S. FWS
Edison, NJ
April 6, 1999)
• •
TABLE OF CONTENTS
LIST OF TABLES ............................................................. 3
LIST OF ACRONYMS ......................................................... 4
1.0 INTRODUCTION ....................................................... 5
I.I PURPOSE AND OVERVIEW ....................................... 5
1.2 ORGANIZATION OF THE DOCUMENT ............................. 6
2.0 PROBLEM FORMULATION ............................... , .............. 6
2.1 SITE BACKGROUND ............................................. 7
2.1.1 Weyerhaeuser Company Site ................................... 8
2.1.2 Georgia-Pacific Corporation Hardwood Sawmill Site ................ 9
2.2 SUMMARY OF THE SCREENING LEVEL ECOLOGICAL
RISK ASSESSMENT ............................................. 11
2.3 ECOTOXICITY .................................................. 12
2.3.1 Metals .................................................... 12
2.3.2 Organics .................................................. 21
2.4 EXPOSURE PATHWAYS ......................................... 25
2.5 IDENTIFICATION OF ASSESSMENT AND MEASUREMENT
ENDPOINTS .................................................... 28
2.5.1 Assessment Endpoint No. I -Protection of Soil Invertebrates ........ 30
2.5.2 Assessment Endpoint No. 2 -Protection of Worm-eating Birds ....... 30
2.5.3 Assessment Endpoint No. 3 -Protection of Insectivorous Mammals ... 31
2.5.4 Assessment Endpoint No. 4 -Protection of Insectivorous Birds ....... 31
2.5.5 Assessment Endpoint 5 -Protection of Carnivorous Birds .......... 32
2.5.6 Assessment Endpoint 6: Protection of Benthic Macro invertebrate
Communities .............................................. 33
2.5.7 Assessment Endpoint 7: Protection of Fish Communities ............ 33
2.5.8 Assessment Endpoint 8: Protection of Omnivorous Bird
Communities ............................................. ·. 34
2.5.9 Assessment Endpoint 9: Protection of Piscivorus Bird
Communities .............................................. 35
2.5.10 Assessment Endpoint I 0: Protection of Omnivorous Mammal
Communities .............................................. 35
3.0 FIELD INVESTIGATION .. : ............................................. 36
4.0 LITERATURE CITED .................................................. 36
• •
LIST OF TABLES
Table I: Literature-Derived LOAELs and NOAELs for Mammalian Endpoints
Table 2: Literature-Derived LOAELs and NOAELs for Avian Endpoints
BERA
CERCLA
COPCs
ERT
ES!
HQ
Kow
LOAEL
MSL
NOAEL
NPDES
OU
PCB
SAP
SERA
SSI
TCE
•
LIST OF ACRONYMS
Baseline Ecological Risk Assessment
Comprehensive Environmental Response, Compensation and Liability Act
Chemicals of Potential Concern
Environmental Response Team
Expanded Site Inspection
Hazard Quotient
Octanol/Water Partition Coefficient
Lowest Observed Adverse Effects Level
Mean Sea Level
No Observed Adverse Effects Level
National Pollution Discharge Elimination System
Operable Unit
Polychlorinated Biphenyl
Sampling and Analysis Plan
Screening-Level Ecological Risk Assessment
Screening Site Inspection
Trichloroethene
• •
1.0 INTRODUCTION
1.1 'PURPOSE AND OVERVIEW
Numerous tasks have been completed to date regarding the evaluation of potential ecological
risks associated with contamination for operable unit 2 (OU2) of the Weyerhaeuser Site,
otherwise known as the Lower Roanoke River Site, and its adjacent wetlands. These include the
development of a preliminary screening-level ecological risk assessment (US EPA,
Environmental Response Team [ERT] 1998), the development of a problem formulation
document (ERT 1999) to focus the implementation of a baseline ecological risk assessment
(BERA), implementation of a field reconnaissance sampling program in March 1999, and
ecological and media sampling in support of a baseline ecological risk assessment, conducted in
September 1999.
In conducting these tasks, numerous EPA groups and contractors have been involved in the
preparation of documents and implementation of field programs. The purpose of this document
is to finalize the problem formulation document for the BERA for the Lower Roanoke River Site,
and its adjacent wetlands. This document was originally drafted by Mark Sprenger, US EPA,
ERT, Edison, NJ, and Nancy Finley, US Fish and Wildlife Service (US FWS), Edison, NJ, and
has been updated by COM Federal Programs at the direction of EPA Region JV.
This Problem Formulation document will provide an overall structure to the ecological risk
evaluations and data collection efforts for the Georgia-Pacific Corporation Site and the
Weyerhauser Company Site in Plymouth, NC. These two sites are in close proximity, adjacent to
the Roanoke River, and have numerous contaminants of potential concern (CO PCs) in common
between the two sites. It therefore follows that an overall design to the ecological risk
assessments and data needs within the Roanoke River 'is appropriate to ensure that redundant
sampling and effort are not done.
5
• •
The EPA's Ecological Risk Assessment Guidance for Superfund: Process for Designing and
Conducting Ecological Risk Assessments (Process Document) (EPA I 997) was used in the
development of this Problem Formulation document. The Process Document provides the latest
EPA guidance on the steps for designing and conducting technically defensible ecological risk
assessments for the Superfund Program. This guidance consists of a series of eight steps and
several scientiti'c/management decision points (SMDPs), or meetings, between the risk manager
and the risk assessment team to evaluate and approve or redirect the work up to that point.
Step I, Screening-Level Problem Formulation and Ecological Effects Evaluation, and Step 2,
Screening-level Preliminary Exposure Estimate and Risk Calculation, were performed for this
site in a screening-level ecological risk assessment (SERA) (ERT 1998). The results of the
SERA indicated the potential for ecological risks, and it was determined that the risk assessment
should continue to the problem formulation and study design phases (i.e., steps 3 and 4) of a
BERA. This document presents the results of steps 3 and 4 of the 8-step process.
1.2 ORGANIZATION OF THE DOCUMENT
This document presents a discussion of the environmental setting, a summary of the screening-
level ecological risk assessment results that led to the decision to conduct a BERA, a discussion
of the contaminants of potential concern (COPCs) detected in river sedii11ents and wetland soils,
a discussion of potential exposure pathways to ecological receptors, and the identification of
assessment and measurement endpoints.
2.0 PROBLEM FORMULATION
Step 3 of the ERA process, BERA problem formulation, refines and expands on information
presented in the SERA screening-level problem fornrnlation. This is a planning step that
identifies the major ecological issues at the site, and establishes the goals and focus of the BERA.
Results of the problem formulation provide a foundation for the BERA, and ensure that the
6
• •
product of the assessment will support environmental decisions made by the risk manager. The
following sections discuss the environmental setting, results of the SERA, ecotoxicity of the
CO PCs, identified exposure pathways, and identified assessment and measurement endpoints.
2.1 SITE BACKGROUND
The lower Roanoke River is listed as sub-basin 09 in the coastal plain ecoregion by the North
Carolina Department of Environment, Health, and Natural Resources (NCDEHNR 1996).
Williamston and Plymouth are the two largest towns in the sub-basin that consists primarily of
agriculture and forest land-use. The area can be characterized as flat, low-lying topography, with
an elevation of 5 feet above mean sea level (MSL). The surrounding area ranges in elevation
from 5 feet above MSL to 15 feet above MSL.
The primary sources of contamination in the Lower Roanoke River are suspected to be the
Weyerhaeuser Company Paper Mill and the Georgia-Pacific Corporation Hardwood Sawmill.
No other source areas were identified or sampled in previous investigations of this reach of the
Roanoke River. Sediment samples from the Roanoke River in close proximity to the
Weyerhaeuser site were found to have higher concentrations of metals (i.e., aluminum, cadmium,
chromium, copper, lead, mercury, and zinc) and organics (i.e., polychlorinated biphenyls [PCBs],
dioxins and furans) than those taken from upstream and downstream locations. Numerous fish
samples were collected and analyzed in relation to the Weyerhaeuser National Pollution
Discharge Elimination System (NPDES) permit. Data suggest that fish tissues have elevated
concentrations of metals (i.e., cadmium, chromium, copper, lead, mercury, and zinc) and
organics (i.e., PCBs, dioxins, and furans). Two reports on the effects of dioxins and furans on
wood ducks and osprey were also completed (Beeman and Augspurger 1996; Augspurger et al.,
1996). Wood duck eggs were found to have elevated concentrations of dioxins and furans, as did
eggs of osprey. Osprey eggs were also found to be contaminated with mercury. These results led
to the initiation of the ecological risk evaluation for the Lower Roanoke River. A summary of
7
• •
industrial processes and investigation history at Weyerhaeuser and Georgia-Pacific is provided
below.
2.1.1 Weyerhaeuser Company Site
' The Weyerhaeuser Company/Plymouth site is an active wood and paper products mill located on
State Road 1565, Martin County, NC. The site was operated by Kieckhefer-Eddy Co. from 1937
until its merger with Weyerhaeuser Co. in 1957. Paper bleaching operations began in the mid-
1940s. Current operations at the facility include those of Weyerhaeuser Paper Company and the
Weyerhaeuser Forest Products Division. The Weyerhaeuser Paper Co. Produces wood pulp,
finished paper, and paperboard. The Forest Products Division produces finishes lumber and
plywood from raw pine and hardwoods (RMT 1998).
No wood treating took place prior to 1979, and no creosote or pentachlorophenol has been used in
the wood treating process. Since 1979, a chromated copper arsenate process has been used for
wood treating, producing approximately 1,500 pounds of treatment sludge per quarter (RMT 1998).
These waste solutions and sludge are captured and transported off-site to an approved Resource
Conservation and Recovery Act (RCRA) disposal facility. Originally, untreated process wastewater
from the paper products division was discharged to the Roanoke River. From the early 1960s to
1988, all untreated process wastewater was discharged to Welch Creek rather than the Roanoke
River. Since 1988, all wastewater except cooling water has been treated at an on-site secondary
treatment facility prior to discharge. The wastewater is first passed through two settling ponds
where solids are removed for incineration in the plant's steam boiler. Wastewater is then directed to
an aeration basin and finally through a serpentine retention pond approximately 750 acres in size.
Between 1968 and 1988, wastewater was discharged into Welch Creek following this treatment
process. Since 1988, the discharge point is into the Roanoke River, approximately ½-mile
downstream of the facility. The Weyerhaeuser Paper Company's current NPDES Permit
(#0000680) allows discharge of treated wastewater, non-contact cooling water, and storm water
runoff to the Roanoke River. This permit sets a discharge limit of 1.3 picograms per liter (pg/L) of
dioxin, with quarterly sampling required (Rumford 1996).
8
• •
There was a mercury cell chlorine plant operating at the site from approximately 1952 to 1965.
Spent graphite electrodes and marble cells, having absorbed mercury during the chlorine production
process, were disposed of in an on-site landfill. The Weyerhaeuser Company estimates that
somewhere between 60 pounds and 11,000 pounds of mercury were deposited in the landfill during
the plant's operation. Spilled processing fluids were collected by a series of drains in the floor that
emptied into a trench, ultimately discharging to the Roanoke River. In 1987, the chlorine
production plant was dismantled and approximately 1,300 tons of mercury-contaminated soil and
debris was removed and taken to the GSX hazardous waste landfill in Pinewood, South Carolina.
The area was then backfilled with "clean" soil and capped with asphalt. Mercury contaminated
soils remain at a depth of 4.5 feet below the surface. Three shallow (12 feet) monitoring wells
were placed in a triangular pattern around the area formerly occupied by the chlorine production
plant. Groundwater samples from these wells have yielded greater than background concentrations
of mercury (Rumford 1996).
The North Carolina Solid and Hazardous Waste Management Branch/Comprehensive
Environmental Response, Compensation, and Liability Act (CERCLA) Unit conducted a Site
Inspection (SJ) in 1985, however, no sampling was done during the inspection. Fish tissue samples
collected from the Roanoke River and Welch Creek in 1988 led to the issuance of a fish
consumption advisory by the NC Division of Environmental Management based on elevated dioxin
concentrations. In June of 1995, a Site Inspection Prioritization (SIP) for the Weyerhaeuser
Company/Plymouth site was conducted by the NC Solid and Hazardous Waste Management
Branch/CERCLA Unit. Sampling during the SIP concentrated on sediment and surface water
samples collected from the Roanoke River and Welch Creek. Analyses of the samples suggest that
mercury has been translocated from the chlorine production site and that detectable concentrations
of dioxin/furan isomers exist in both sediment and fish tissues (Rumford 1996).
2.1.2 Georgia-Pacific Corporation Hardwood Sawmill Site
The Georgia-Pacific Corporation Hardwood Sawmill site is an inactive sawmill, on 24 acres of
flat low-lying property, on Plywood Drive, Plymouth, Washington County, NC. The site is ·
9
• •
within the city limits of Plymouth, North Carolina. The Roanoke River, Plymouth High School,
and a residential area border the property. It was operated by Atlas Plywood Co. prior to 1950
when it was purchased by Georgia-Pacific Corporation. Operational history and waste-
management of the mill is unknown for the period of operation under Atlas Plywood Company.
Georgia-Pacific Corporation utilized the facility for sawing, planing, and treatment of rough
hardwood lumber and timber from logs, from the time of purchase until 1983. The facility was
closed in 1983 as a direct result of a devastating fire. Georgia-Pacific Corporation sold the
property to Decatur Partnerships in 1985, who in turn leased it to Outerbanks Contractors.
Outerbanks Contractors used a portion of the site as an asphalt mixing plant. Currently the site is
idle and unoccupied (Rumford 1997).
During operation under the Georgia-Pacific Corporation, process wastes primarily included spent
oil, halogenated and non-halogenated degreasing solvents, and sludge from the treatment of
wastewater from the wood preserving process. The pesticidal treatment of wood incorporated a
mixed solution of pentachlorophenate, sodium metaborate, lindane, and other chlorophenol
compounds. Wastes were either incinerated on-site or transported to the county landfill
(Rumford 1997).
A conveyer system was utilized to pass rough lumber through a dip vat for wood preservative
application. Spillage and leakage of the treatment solution have been suggested to cause area
'
soils to be contaminated with wood preservative/insecticidal compounds. In addition, it was
standard practice to allow treated wood to drip excess solution directly onto the ground. An on-
site machine shop and transformer station are suspects in soil contamination with oils, solvents,
and PCBs (Rumford 1997).
Several investigations of the Georgia-Pacific Corporation Hardwood Sawmill site have been
conducted. They include the following: Preliminary Assessment (NCDHS 1985), Phase I
Screening Site Inspection (SSI) (NUS Corp 1989), Phase II Screening Site Inspection (SSI)
(Greenhorne & O'Mara Inc 1991), SIP (Dynamac Corp 1994), and an Expanded Site Inspection
• •
(ES!) (Rumford 1997). Analytical data from samples collected during these investigations
suggest that soils are contaminated with metals (aluminum, arsenic, barium, cobalt, chromium,
copper; iron, lead, and manganese), organochlorine compounds (a-BHC, P-BHC, lindane,
TCDD, TCDF, HCDD, OCDD, PCDD, and DOD), and PCBs (Arochlor 1254). Sediments were
found to have a similar contaminant constituency. Samples from shallow groundwater wells
exceeded background concentrations in metals (arsenic, barium, beryllium, lead, manganese,
mercury, and nickel), organochlorine compounds (a-BHC, P-BHC, Ll-BHC, and lindane), and
trichloroethene (TCE).
2.2 SUMMARY OF THE SCREENING LEVEL ECOLOGICAL RISK ASSESSMENT
A screening ecological risk assessment (SERA) was conducted to determine the potential for
adverse ecological effects associated with the exposure of biota to contaminants in the Lower
Roanoke River. This included a literature search to locate site background information, identify
contaminants associated with the site, describe potential exposure pathways, and identify
potential ecological receptors. This information was used to identify preliminary assessment
endpoints, select the screening-level toxicological benchmarks used, and calculate ecological
risks using the hazard quotient (HQ) method of comparing maximum detected concentrations in
media to the screening-level toxicological benchmarks.
Based on the results of the screening ecological risk assessment, a variety of metals and organic
compounds were identified as contaminants of potential concern. Those chemicals in sediments
having HQ values greater than one included chromium, copper, lead, manganese, mercury,
nickel, and zinc. Other constituents that were detected in sediments and fish tissue have no
published screening level benchmark values, and were therefore recommended for inclusion in
additional evaluations in the BERA. These included aluminum, barium, magnesium, vanadium,
PCBs (particularly Arochlor 1254), beta-BHC, gamma-BHC (lindane), TCDD and TCDF.
11
•
2:3 ECOTOXICITY
An understanding of the mode of action or toxic mechanisms of the CO PCs is necessary to select
the assessment endpoints to be evaluated at a site. Table I summarizes toxicological benchmarks
for mammals, and Table 2 summarizes toxicological benchmarks for birds, that are
recommended for use in the BERA. A discussion of the toxic mechanisms for CO PCs detected
at the Lower Roanoke River Site is provided below.
2.3.1 Metals
Aluminum
Because of its strong reactivity, aluminum (Al) is not found as a free metal in nature. Aluminum
has only one oxidation state(+ 3), thus its behavior in the environment depends on its ordination
chemistry and the surrounding conditions. In soils, a low pH generally results in an increase in
aluminum mobility (A TSDR 1990).
The nervous system may be a target area for effects from aluminum exposure. Aluminum may
also interact with neuronal DNA to alter gene expression and protein formation. Mammalian
studies do not indicate that aluminum affects reproduction although some developmental effects
have been reported in mammals (A TSDR 1990).
Plants vary in their ability to remove aluminum from soils, although bioconcentration factors for
plants are generally less than one. Biomagnification of aluminum in terrestrial food chains does
not appear to occur.
Barium
Barium (Ba) is used in various alloys, in paints, soap, paper, and rubber, and in the manufacture
12
• •
of ceramics and glass. Barium fluorosilicate and carbonate have been used as insecticides.
Barium is relatively abundant in nature and is found in plants and animal tissue. Average
surficial soil concentrations are near 500 mg/kg in the United States. Plants accumulate barium
from the soil. Some water contains barium from natural sources.
The toxicity of barium compounds depends on their solubility. The soluble compounds are
absorbed and may be stored in the skeleton. It may be excreted in urine but it is reabsorbed by
the renal tubules. The feces is the major route of excretion.
Chromium
Chromium can exist in oxidation states ranging from -2 to +6, but is most frequently converted to
the relatively stable trivalent (+3) and hexavalent (+6) oxidation states (Eisler 1986). In soils, the
solubility and bioavailability of Cr are governed by soil pH and organic complexing substances,
although organic complexes play a more significant role (James and Bartlett 1983a; James and
Bartlett I 983b).
The trivalent state is the form usually found in biological materials. This form functions as an
essential element in mammals by maintaining efficient glucose, lipid, and protein metabolism
(Stevens et al. 1976). Chromium is beneficial but not essential to higher plants (Eisler 1986).
The biomagnification and toxicity of Cr+3 is low relative to Ct6 because of its low membrane
permeability and its noncorrosivity. However, a large degree of accumulation by terrestrial
plants and animals in the lower trophic levels has been documented (Eisler 1986), although, the
mechanism of accumulation remains largely unknown.
13
• •
Chromium is mutagenic, carcinogenic, and teratogenic, with Cr+6 exhibiting the greatest toxicity;
relatively less is known about the toxicity of Cr+3_ At high concentrations, Ct6 is associated with
abnormal enzyme activity, altered blood chemistry, lowered resistance to pathogenic organisms,
behavioral modifications, disrupted feeding, histopathology, osmoregulatory upset, alterations in
population structure, and inhibition of photosynthesis.
Rabbits fed dietary Cr accumulated hyaluronates, chondroitin sulfates, and neutral
mucopolysaccharides in the soft tissues, causing pericapillary sclerosis (Kucher and Shabanov
1967). This accumulation blocked blood tissue barriers, which are permeable under normal
conditions, preventing the normal transport of metabolites. One manifestation of this condition
was the inhibition of insulin production in the pancreatic islets due to damage to the beta-cells
contained therein.
Chromium also leads to nephron damage via swelling and loss of microvilli, the formation of
intracellular vacuoles, mitochondrial swelling, and cytoplasmic liquefication and loss of cells
lining the nephron surface (Evan and Dail 1974).
Copper
Copper does not appear to have mutagenic properties, but it is a teratogen (RTECS 1991) and a
possible carcinogen (V enugopal and Luckey 1978). Copper is caustic, and acute toxicity is
primarily related to this property (Hatch 1978).
Copper is an essential element for animals and is a component of many metalloenzymes and
respiratory pigments (Demayo et al. 1982). It is also essential to iron utilization and functions in
enzymes for energy production, connective tissue fomrntion, and pigmentation (Venugopal and
Luckey 1978). Excess copper ingestion leads to accumulation in tissues, especially in the liver.
High levels of copper modify hepatic metabolism (Brooks 1988), which may lead to inability of
the liver to store and excrete additional copper. When liver concentration exceeds a certain level,
14
• •
the metal is released into the blood, causing hemolysis and jaundice. High copper levels also
inhibit essential metabolic enzymes (Demayo et al. 1982). Toxic symptoms appear when the
liver accumulates 3 to 15 times the normal level of copper (Demayo et al. 1982).
Although the exact mechanism of toxicity is not known, the. following mechanisms have been
proposed: Formation of stable inhibitory complexes with cytochrome P-450 (Wiebe I et al. 1971);
impairment of function ofNADPH-cytochrome c reductase and alteration of mixed function
oxidations (Reiners et al. 1986); arid inhibition of heme biosynthesis (Martell 1981 ).
Intranuclear inclusions may act as a detoxifying mechanism where copper is complexed by
protein ligands, protecting cytoplasmic organelles (Demayo et al. 1982).
Lead
Lead does not biomagnify to a great extent in food chains, although accumulation by plants and
animals has been extensively documented (Wixson and Davis 1993, Eisler 1988b). Older
organisms typically contain the highest tissue lead concentrations, with the majority of the
accumulation in the bony tissue of vertebrates (Eisler 1988b ).
Predicting the accumulation and toxicity of lead is difficult since its effects are influenced to a
very large degree, relative to other metals, by interactions among physical, chemical, and
biological variables. In general, organolead compounds are more toxic than inorganic lead
compounds, and young, immature organisms are most susceptible to its effects (Eisler 1988b). In
plants, lead inhibits growth by reducing photosynthetic activity, mitosis, and water absorption.
The mechanism by which photosynthetic activity is reduced is attributed to the blocking of
sulfhydryl groups, inhibiting the conversion of coproporphyrinogen to proporphyrinogen (Holl
and Hampp 1975).
The toxic effects of lead on aquatic and terrestrial organisms are extremely varied and include
mortality, reduced growth and reproductive output, blood chemistry alterations, lesions, and
15
• •
behavioral changes. However, many effects exhibit general trends in their toxic mechanism.
Generally, lead inhibits the formation of heme, adversely affects blood chemistry, and
accumulates at hematopoietic organs (Eisler 1988b ). At high concentrations near levels causing
mortality, marked changes to the central nervous system occur prior to death (Eisler 1988b).
Plants can uptake lead through surface deposition in rain, dust, and soil, or by uptake through the
roots. The ability of a plant to uptake lead from soils is inversely related to soil pH and organic
matter content. Lead can inhibit photosynthesis, plant growth, water absorption.
Magnesium
Magnesium (Mg) is used in lightweight alloys, as an electrical conductive material, and for
incendiary devices such as flares. It is also an essential nutrient whose deficiency causes
neuromuscular irritability, calcification, and cardiac and renal damage. Magnesium is a cofactor
of many enzymes; it is apparently associated with phosphate in these functions. The average
drinking water contains about 6.5 mg/L, but varies considerably.
Magnesium salts are poorly absorbed from the intestine. Magnesium is absorbed mainly in the
small intestine. Calcium and magnesium are competitive with respect to their absorptive sites,
and excess calcium may partially inhibit the absorption of magnesium. Urine is the major route
of excretion under normal conditions.
It is reported that particles of magnesium in the subcutaneous tissue produce lesions that resist
healing. In animals, magnesium subcutaneously or intramusc·ularly administered produces gas
gangrene as a result of int_eraction with body fluids and subsequent generation of hydrogen and
magnesium hydroxide. The symptoms of acute exposure include a sharp drop in blood pressure
and respiratory paralysis due to central nervous system depression.
16 ·
• •
Manganese
Manganese (Mn) does not occur as a free metal in the environment but is a component of
numerous minerals. Elemental manganese and inorganic manganese compounds have negligible
vapor pressures, but may exist in air as suspended particulate matter derived from industrial
emissions or the erosion of soil. Removal from the atmosphere is mostly through gravitational
settling. The tendency of soluble manganese compounds to adsorb to soils depends mainly on
the cation exchange capacity and the organic composition of the soil. Biomagnification in the
food chain may not be significant (A TSDR 1990).
The amount of manganese absorbed across the gastrointestinal tract is variable. There does not
appear to be a marked difference between manganese ingested in food or in water. One of the
key determinants of absorption appears to be dietary iron intake, with low iron levels leading to
increased manganese absorption. This is probably because both iron and manganese arc
absorbed by the same transport system in the gut (A TSDR 1990).
Mercury
Mercury may be present in the environment in a number of forms. In all inorganic forms, Hg2' is
the toxic species. The most toxic and bioavailable form of mercury is methylmercury, which is
highly stable and lipophilic, accumulating in food chains. Mercury can become methylated
biologically or chemically. Microbial methylation of mercury occurs most rapidly under
anaerobic conditions, common in wetlands and aquatic sediments: The majority of mercury
detected ,n biological tissues is present in the form ofmethylmercury (Huckabee et al. 1979).
Mercury has no known biological function, and its presence in biological systems appears to
result in undesirable effects. A number of toxic responses have been reported for mercury
exposure. Eisler (I 987a) reports that juvenile life stages are most susceptible to acute effects of
mercury exposure. In fish, acute exposure results in impaired respiration, sluggishness, and loss
17 .. •
• •
of equilibrium (Armstrong 1979).
Mercury is a potent neurotoxin, resulting in impaired muscular coordination, weight loss, and
apathy in birds, mammals, and fish (Eisler 1987a). Other reported effects include
histopathological changes, changes in enzyme activity levels, mutagenicity, teratogenicity, and
reproductive impairment. Mercury, especially methylmercury, is known to concentrate in
biological tissues and magnify through the food chain.
Mercury can exist in 3 oxidation states: elemental mercury (Hg0), mercurous ion (Hg,'+), and
' mercuric ion (Hg2+). The mercuric ion is the most toxic inorganic chemical form (Clarkson and
Marsh 1982). Methylmercury (MeHg) is the most hazardous form of mercury due to its high
stability, its lipid solubility, and the ability to penetrate membranes in living organisms (Beijer
and Jemalov 1979).
Mercury in soils is generally not available for uptake by plants, due to the high binding capacity
to clays and other charged particles (Beauford et al. 1977). Mercury levels in plant tissues
increase as soil levels increase, however 95 percent of the accumulation and retention of mercury
is in the root system (Beauford et al. 1977), Cocking et al. 1991 ).
All mercury compounds interfere with thiol metabolism in organisms, causing inhibition or
inactivation of proteins containing thiol ligands and ultimately leading to mitotic disturbances
(Das et al. 1982, Elhassani 1983). Mercury also binds strongly with sulfhydryl groups, Phenyl-
and methylmercury compounds are among the strongest known inhibitors of cell division (Birge
et al. 1979). In mammals, methylmercury irreversibly destroys the neurons of the central nervous
system.
For all organisms tested, early developmental stages are most sensitive to toxic effects of
'
mercury. Organomercury compounds, especially methylmercury, are more toxic than inorganic
forms. In aquatic organisms, mercury adversely affects reproduction, growth, behavior,
18 .
• •
osmoregulation and oxygen exchange. At comparatively low concentrations in birds and
mammals, mercury adversely affects growth and development, behavior, mator coordination,
vision, hearing, histology, and metabolism. In mammals, the fetus is the most sensitive life stage
(Eisler 1987).
Nickel
Pure nickel is a hard, white metal that is usually used in the formation of alloys (such as stainless
steel) and nickel combined with other elements is found in all soils. Nickel is the 24th most
abundant element and is found in the environment as oxides or sulfides. Nickel may be released
into the environment through mining, oil-burning power plants, coal-burning power plants, and
incinerators. Nickel will attach to soil or sediment particles, especially those containing iron or
manganese. Under acidic conditions, nickel may become more mobile and seep into the
groundwater. The typical nickel concentration reported in soils is from 4 -80 mg/kg. The
speciation and physiochemical state of nickel is important in considering its behavior in the
environment and its availability to biota.
The most probable exposure routes of nickel is through dermal contact and ingestion of nickel-
contaminated soil and food. Animals exposed to nickel through oral exposure were noted to
have lethargy, ataxia, irregular breathing, salivation, and squinting (A TSDR 1996).
Vanadium
\
Vanadium (V) is a ubiquitous element. It is a by-product of petroleum refining, and vanadium
pentoxide is used as a catalyst in the various chemicals including sulfuric acid. It is also used in
the hardening of steel, pigment manufacturing, photography, and insectides.
Average concentrations in public water supplies range between I and 6 µg/L. Use of petroleum
products or oil refineries are suspect for sources of airborne vanadium. Vanadium has strong·
19
• •
affinity for fats and oils. Within the body, fat is the compartment with the largest stores of
vanadium. The principal route of excretion is in urine. When excess concentrations are taken in,
vanadium can be found in high concentrations in the red blood cells (Klaassen et al I 986).
The toxic action of vanadium is largely confined to the respiratory tract because inhalation is the
most common route of exposure. Ingestion of vanadium compounds (V 20 5) may lead to acute
poisoning characterized by marked effects on the nervous system, hemorrhage, paralysis,
convulsions, and respiratory depression. It has been suggested that subacute exposures at high
concentrations may adversely affect the liver, adrenals, and bone marrow (Klaassen el al 1986).
Zinc
Zinc (Zn) is -essential for normal growth and reproduction in plants and animals and is regulated
by metallothioneins. Metallothioneins act as temporary zinc storage sites and aid in reducing the
toxicity of zinc to both vertebrates and invertebrates (Olsson et al. 1989). Zinc is not known to
bioaccumulate in food chains, because it is regulated by the body and excess zinc is eliminated.
Zinc has its primary metabolic effect on zinc-dependant enzymes that regulate the biosynthesis
and catabolic rate of RNA and DNA. High levels of zinc induce copper deficiency and interfere
with metabolism of calcium and iron (Goyer 1986). The pancreas and bone seem to be the
primary targets of zinc toxicity in birds and mammals. Pancreatic effects include cytoplasmic
vacuolation, cellular atrophy, and cell death (Lu and Combs 1988; Kazacos and Van Vleet 1989).
Zinc preferentially accumulates in bone, and induces osteomalacia, a softening of bone caused by
a deficiency of calcium, phosphorus and other minerals (Kaji et al. 1988). Gill epithelium is the
primary target site in fish. Zinc toxicosis results in destruction of gill epithelium and tissue
hypoxia (Spear 198 I).
20 .
• •
2.3.2 Organics
Dioxiris/Furans (PCDDs/PCDFs)
There are 75 dioxin isomers, the most toxic of which is the chlorinated 2,3,7,8-TCDD isomer.
Dioxins are found in chlorophenols, certain pesticides, and in polychlorinated biphenyls.
Dioxins enter the environment through accidental release during chlorophenol production, aerial
application of herbicides, from combustion in municipal and industrial incinerators, and in the
effluents of kraft bleach paper mills (Eisler 1988c).
PCDDs are resistant to biological breakdown, concentrated in fat, not readily excreted, and
extremely toxic to some animals. The.cumulative effects of small doses to animals and humans
is of primary concern (Eisler 1988c ).
TCDD is a persistent, hydrophobic non-polar organic chemical. Its method of toxicity is through
binding to the cystolic aryl hydrocarbon (Ah) receptor. After the initial binding, the ligand
receptor complex is translocated to the nucleus of the cell where it becomes associated with
DNA thereby causing initiation of transcription of one or more target genes. The physiological
effects ofTCDD exposure may include weight loss, decreased immunocompetence,
subcutaneous edema, reproductive effects, alterations in lipid metabolism and gluconeogenesis,
thymic atrophy, and induction of certain enzyme systems (cytochrome P4501Al). A
characteristic ofTCDD toxicity is delayed mortality. These contaminants accumulate in fish in
proportion to the body lipid content and the age of the animal (U.S. EPA 1993).
An estimate of the long-term toxicities of the CDDs/CDFs can be expressed in terms ofan
equivalent amount of2,3,7,8-TCDD [using toxicity equivalents (TEQs)]. The TEQs can be
generated by using a toxicity equivalency factor (TEF) to convert the concentrations of a given
CDD/CDF into an equivalent concentration of2,3,7,8-TCDD (U.S. EPA 1989a). For the
purposes of this risk assessment, the 2,3,7,8-TCDD values are reported as total equivalence
21 .
• •
values and any discussion of dioxin implies that total equivalents are used.
PCBs ·
The PCBs are a group of 209 synthetic halogenated aromatic hydrocarbons that are extremely
stable, bioaccumulate, and are resistant to most chemical and biological degradation processes
(Eisler 1986; Hornshaw et al. 1983). The persistence and stability of PCBs in the environment
are due to chemical properties such as their lipophilicity and stable carbon-halogen bonds
(Risebrough et al. 1968). Polychlorinated biphenyls have low aqueous solubility (Chou and
Griffin 1986) and have a maximum solubility in water of about 200 parts per billion (ppb) at 25
degrees Celsius (°C) (U.S. EPA 1976).
Upon entering an aquatic system, PCBs may partition between the water, sediment, air,
particulate matter, and biota (Koslowski et al. 1994). Optimum accumulation of PCBs by
aquatic biota occurs when planar molecules are substituted with 5 to 7 chlorine atoms (Shaw and
Connell 1984). In terrestrial systems, the PCBs are not readily leachable in soils and strongly
sorb to soil constituents (Chou and Griffin 1986; Strek and Weber 1982). Their level in soil is
proportional to the organic matter and clay content of the soil (Chou and Griffin 1986).
The uptake of PCBs from soils by terrestrial plants is very low (Iwata et al. 1974; Iwata and
gunther 1976; Weber and Mrozek 1979). Plants do not readily accumulate PCBs from the soil,
however, PCBs do settle on and adhere to the outside surfaces of plants (Horn et al. 1979; Ruelle
1986). The uptake of PCBs by aquatic plants has been reported (Moza et al. 1974) indicating
that these compounds can be translocated to plants from both aquatic and terrestrial
environments, although at low levels.
The PCBs are extremely lipid-soluble and tend to accumulate in the lipid component, internal
organs, and mesenteric fat of organisms (Eisler 1986; Ruelle 1986). The more lipophilic and
hydrophobic a substance, the more concentrated it will be in the sediment and phytoplankton of
22
• •
an aquatic system (Loizeau and Menesguen 1993). The bioaccumulated PCBs in lower trophic
level organisms readily biomagnify to higher trophic level organisms. Subsequently, high
residue levels have been detected in fish, mammals, and birds worldwide (Olafsson et al. 1983;
Storm et al. 1981 ). Some organisms are capable of storing extremely high concentrations of
PCBs in their fat without any apparent detrimental effect (Olaffson et al. 1983).
Much of the toxicity caused by PCBs has been attributed to the planar congeners that resemble
2,3,7,8-tetrachlorodibenzo-p-dioxin (2,3,7,8-TCDD) (Geisy et al. 1994). The toxic nature of
some prepared PCB mixtures may be associated with trace levels of compounds having four or
more _chlorine atoms at both the para and meta positions (Koslowski et al. 1994; Tanabe et al.
1987); the biphenyl structure may be substituted with one to ten chlorine atoms. These
isostereomers of 2, 3, 7, 8-TCDD are known to elicit toxic biological responses in animals such
as hepatic damage, weight loss, thymic atrophy, dermal disorder, reproductive toxicity,
immunosuppresion, teratogenicity, and functional effects to the spleen, adrenal and testis (Batty
1990; Sanders et al. 1974; Tanabe et al. 1987).
The general sub lethal effect of PCBs to plants is reduced growth via a reduction in
photosynthetic activity as a result of diminished chlorophyll content of the plant (Strek and
Weber 1982; Iwata et al. 1974; Iwata et al. 1976; Weber and Mrozek 1979; Maza et al. 1974;
Mahanty 1973).
The primary biochemical effect of PCBs in animals is to induce hepatic mixed function oxidase
systems, increasing an organisms capacity to biotransfom1 or detoxify xenobiotic chemicals.
Enzymes in this system are sometimes referred to as drug-metabolizing enzymes (DMEs) (Kluwe
et al. 1979). Although the increased capacity to detoxify xenobiotic chemicals may appear to
benefit an organisms, the metabolism of the foreign chemicals often produces metabolites that
are more toxic than the parent compound (Mitchell et al. 1976). In addition, PCB-induced
changes in enzyme activity may also alter enzyme substrate concentrations in other metabolic
23
• •
pathways (Montz et al. 1982). The PCBs also induce microsomal hepatic enzyme systems that
metabolize naturally occurring steroid hormones (Peakall I 975). The degree of this enzyme
system·response has been found to be positively dose-related (Linzey 1987). Polychlorinated
bi phenyl-induced effects to these hepatic enzyme systems results in increased liver weight, fatty
degeneration, hyalin degeneration, necrosis, hepatocyte formation, and increased hormone
metabolism in animals (Batty et al. 1990; Lincer and Peakall 1970; Sanders and Kirkpatrick
1977; Sanders et al. 1974; Stotz and Greichus I 978; Vos I 972; Welsch 1985).
Chlorinated hydrocarbons such as PCBs have been implicated as a cause of reproductive
dysfunction and mortality in wildlife species (Heaton et al. 1995; Hoffman et al. 1986; Langford
1979). Exposure to PCBs have been found to reduce litter sizes at birth, number of litters, and
longer birthing intervals in mice (Linzey 1987; Merson and Kirkpatrick 1976) and reduce plasma
concentrations of estradiol and progesterone in female rats (Johnson et al. 1976). Transplacental
movement of PCBs has been reported for humans, rabbits, monkeys, and rats (Storm et al. 1981)
causing a dose-dependent reduction in the body weights and survival of pre-natally, as well as
post-natally, exposed mammalian offspring (Barsotti et al. 1976; Brezner et al. 1984; Fein et al.
1984; Heaton et al. 1995; Wren et al. 1987a,b). There is also some evidence of PCB transfer to
young via mother's milk (Wren et al. 19987a). Polychlorinated biphenyls have been implicated
as the cause of low embryonic weight in black-crowned night herons (Nycticorax nycticorax)
(Hoffman et al. 1986). Persistence in courtship behavior was reduced in PCB-fed mourning
doves (Zenaida macroura) (Tori and Peterle 1983). Reduced sperm concentration, thin-shelled
eggs, poor hatching success, and offspring born with teratogenic abnormalities have also been
reported (Abrahamson and Allen 1973; Bird et al. 1983; Lowe and Stendell 1991; Scott 1977).
Adverse reproductive effects from PCB exposure are likely to be correlated with hepatic
microsomal enzyme system effects (Tanabe 1988).
BHC (alpha-, beta-, delta-, gamma-)
Lindane, or gamma-BHC, is used as an insecticide for field crops such as corn and wheat, for
24 .
• •
ornamentals, for pasture and forage crops, for forestry and timber protection, for soil and seed
treatment and viticulture, in medications, and in baits for rodent control. When released into
water, lindane is not expected to volatilize significantly. It is also not expected to hydrolyze in
acidic or neutral water, but in basic water, hydrolysis might be significant. Lindane has also been
reported to photodegrade, but this is not expected to be a significant fate process. When released
into soil, lindane will most likely volatilize and slowly leach into the groundwater. Lindane will
also biodegrade moderately under aerobic conditions and significantly under anaerobic
conditions. With a log Kow of3.72, lindane is expected to bioconcentrate slightly. Measured
bioconcentration factors range from 63 in grass shrimp to I 613 in northern brook silverside
(HSDB 1997).
The mechanism of toxicity oflindane is unknown. However, it is thought that lindane might
interact with pores of the lipoprotein structure of insect nerve causing distortion and consequent
excitation of nerve impulse transmission. The main metabolites of lindane found in human urine
have been 2,4,6,,,2,3,5,,, and 2,4,5,,trichlorophenol. These metabolites have also been found
either free or as conjugates in the urine of rats after i.p. injection. In mice, urinary metabolites
consisted mostly of the glucuronide and sulfate conjugates of2,4,6;;trichlorophenol and
2,4;;dichlorophenol after i.p. injection. After oral ingestion of lindane by rats,
3,4;;dichlorophenol, 2,4,6,,trichlorophenol, 2,3,4,5,, and 2,3,4,6,,tetrachlorophenol, and
2,3,4,5,6,,pentachloro,,2,,cyclohexene,, l ,,o I were excreted in urine (HSDB 1997).
2.4 EXPOSURE PATHWAYS
The exposure characterization for the aquatic system of the Lower Roanoke River study area was
developed in the SERA to illustrate the site dynamics. This characterization relied on existing
data, habitat and receptors, contaminant sources and fate and transport mechanisms, exposure
concentrations, and exposure routes. From this synthesis, exposure pathways critical to the
assessment endpoints were identified. The primary contaminant source is the waste generated
and deposited throughout the river during the past operation of a paper mill and a sawmill that
25
• •
treated rough hardwood lumber and timber. The habitats in the study area consist of the Roanoke
River and its associated wetlands. These areas have historically or are suspected to have received
direct contamination or runoff from the site.
Organisms at the site may absorb contaminants through dermal contact with sediments, from
sediment ingestion, from water ingestion, or secondarily through food chain accumulation.
Direct contact with the whole sediment burden incorporates the contaminant fraction adsorbed to
the solid phase as well as contaminants dissolved in the liquid interstitial phase. Food chain
transfer or ingestion of contaminated food items represents the dominant exposure route for
upper trophic levels.
A number of chemical factors affect the rate of dermal absorption including concentration,
molecular size, water and lipid solubility, extent of ionization, and hydrolysis of the chemical at
the pH of the epidermis and dermis. Additionally, transfer of chemicals across a dermal
membrane during burrowing and other activities is a function of the amount of exposed dermis in
contact with the contaminated media. Benthic invertebrates intimately contact the sediment and
are directly exposed to contaminants and direct contact is therefore considered to be a significant
route of exposure for invertebrates.
The following potential exposure pathways are linear representations of complex interactions
regarding site dynamics of contaminant movement through the ecosystem.
Linear Representations:
Benthic Invertebrate
direct contact with water
direct contact with sediment
ingestion of sediment
26
Fish
•
direct contact with water
direct contact with sediments
ingestion of water
incidental ingestion of sediment
ingestion of prey species
Omnivorous Bird
direct contact with water
direct contact with sediment
ingestion of water
incidental ingestion of sediments
ingestion of benthic invertebrates
Piscivorous Bird
direct contact with water
direct contact with sediment
ingestion of water
incidental ingestion of sediment
ingestion of fish
Soil Invertebrate
direct contact with soil
ingestion of soil
Worm-eating Bird
Incidental ingestion of soil
ingestion of earthworms
27
•
•
Insectivorous Bird
ingestion of emergent insects
Carnivorous Bird
incidental ingestion of soil
ingestion of small mammals
Insectivorous Mammal
direct contact with soil
incidental ingestion of soil
ingestion of soil invertebrates
Omnivorous Mammal
direct contact with water
direct contact with sediment
ingestion of water
incidental ingestion of sediment
ingestion ofbenthic invertebrates and fish
•
Based on these exposure concerns, ten assessment endpoints were selected, as discussed in the
following section.
2.5 IDENTIFICATION OF ASSESSMENT AND MEASUREMENT ENDPOINTS
Assessment endpoints are explicit expressions of the actual environmental values (e.g.,
ecological resources) that are to be protected at the site. Valuable ecological resources include
those without which ecosystem function would be significantly impaired, those providing critical
resources ( e.g., habitat), and those perceived as valuable by humans ( e.g., endangered species and
other issues addressed by legislation). Assessment endpoints are selected based on key
28
• •
ecosystem, community, or ecological functions, the contaminants present, the extent and
magnitude of contamination, mechanisms of toxicity, susceptibility to the toxicity of the CO PCs,
and potential exposure pathways. Because assessment endpoints focus the risk assessment
design, sample collection, and data analysis, appropriate selection and definition are critical to
the utility of a risk assessment. They are the focus of the risk assessment and form a link
between the measurement endpoints and the risk management process. Individually, each
assessment endpoint revolves around a key ecological receptor, community, or critical ecological
function. Collectively, the assessment endpoints are broadly representative of the aquatic and
wetland ecosystems present in the Lower Roanoke River basin. Assessment endpoints selected
and used in the risk assessment represent worst-case scenarios and are meant to be broadly
protective of biota not specifically mentioned.
Ten assessment endpoints were developed in the SERA to evaluate the potential for ecological
risks from exposure to contaminants in the Lower Roanoke River Basin. Following the site
reconnaissance in March 1999, the assessment endpoints were refined based on site-specific
observations of habitat use by ecological receptors. Each of the assessment endpoints is listed
below followed by a summary of the types of data that were collected during the September 1999
sampling to generate the information required for use in the BERA. Each assessment endpoint
may have more than one measurement endpoint. For those assessment endpoints having multiple
measurement endpoints, a weight-of-evidence approach allows the results of the measurement
endpoints to be integrated into a single conclusion. A weight-of-evidence evaluation implies that
there are multiple lines-of-evidence, but not all lines-of-evidence necessarily have equal strength.
When multiple lines of evidence for a particular assessment endpoint lead to the same
conclusion, there is an implied weighting and the level of confidence increases in the risk
estimate. If multiple lines generate apparent conflicts, then the weights relative to the
mechanisms of toxicity will be used in evaluating the level of confidence in the risk estimate.
29
• •
2.5.1 Assessment Endpoint No. 1 -Protection of Soil Invertebrates
This assessment endpoint provides for the protection of the soil invertebrate community to insure
that exposure to soil contaminants does not have a negative impact on growth, survival, or
reproduction of the soil invertebrate community. There are two types of data collected for this
endpoint, including an earthworm toxicity/bioaccumulation bioassay, and chemical analysis of
wetland soils. The earthworm (Eisenia sp.) was selected as a representative species.
This assessment endpoint will help define potential risks from the upland areas of the site, not
only to soil invertebrates, but also to worm-eating birds and insectectivorous mammals. Wetland
soil samples were collected from five locations just inland of the river sediment samples
collected along the Roanoke River (greater detail is provided in the SAP [COM 1999]). At each
location, a sufficient amount of soil was collected for both chemical analysis and an earthworm
toxicity test/bioaccumulation study. For the assay, the response oflaboratory-supplied worms to
contaminants in the wetlands soil was monitored over a 28-day period. At the completion of the
test, the earthworms were removed from the contaminated soil and placed on clean, moist paper
towels. The digestive tract was allowed to clear for approximately 24 hours. The wom1s were
then analyzed for TAL metals, BNAs, PCB/pesticides, dioxin/furan, percent moisture, and
percent lipids. The results of the toxicity evaluation portion of this study will be compared to
soil analytical results to determine if wetland soils have an adverse impact on the growth or
survival of the soil invertebrate community. The results of the tissue concentration analysis (i.e.,
the bioaccumulation portion of the test) will be used for input into food chain models for higher
trophic level receptors.
2.5.2 Assessment Endpoint No. 2 -Protection of Worm-eating Birds
This assessment endpoint provides for the protection of worm-eating birds to insure that
ingestion of contaminants in earthworms does not have a negative impact on growth, survival,
and reproductive success. The American robin (Turdus migratorius) was selected as a
30 .
• •
representative species. The conceptual model for this endpoint is ingestion of earthworms and
incidental ingestion of wetland soil from each area tested, by a worm-eating bird. There are two
types of data collected for this endpoint, soil analytical data and earthworm bioaccumulation
bioassay results. These data will be input into a food chain exposure model to estimate exposure
to the robin to estimate risks to worm-eating birds. Using the analytical results (both maximum
per location sampled and a site mean concentration) the estimated daily dose to the robin will be
compared to data from existing laboratory studies [body-burden no observed apparent effect
levels (NOAELs) and low observed apparent effect level (LOAELs)] to determine if the
population of worm-eating birds is at risk.
2.5.3. Assessment Endpoint No. 3 -Protection of insectivorous mammals
This assessment endpoint provides for the protection of insectivorous mammals to insure that
ingestion of contaminants in prey does not have a negative impact on growth, survival, and
reproductive success. The short-tailed shrew (Blarina brevicata) was selected as a representative
species. The conceptual model for this endpoint is the ingestion of earthworms and the
incidental ingestion of wetland soil by an insectivorous mammal. There are two types of data
collected for this endpoint, soil analytical data and earthworm bioaccumulation bioassay results.
These data will be input into a food chain exposure model to estimate exposure to the shrew to
estimate risks to insectivorous mammals.
Using the analytical results (both maximum per location sampled and a site mean concentration)
the estimated daily dose to the shrew will be compared to data from existing laboratory studies
[body-burden no observed apparent effect levels (NOAELs) and low observed apparent effect
level (LOAELs)] to determine if the population of insectivorous mammals is at risk.
2.5.4 Assessment Endpoint No. 4 -Protection of insectivorous birds
This assessment endpoint provides for the protection of insectivorous birds to insure that
31
• •
ingestion of contaminants in emergent aquatic invertebrates does not have a negative impact on
growth, survival, and reproductive success. Insectivorous birds are important in the control of
populations of emerging aquatic insects. The barn swallow (Hirundo rustica) was selected as a
representative species.
For one of the measurement endpoints, sediment samples were collected from five locations
along the Roanoke River (greater detail is provided in the SAP [COM 1999]). At each location, a
sufficient amount of sediment was collected for chemical analysis, a bioaccumulation test using
mayfly larvae (Hexagenia), and for a toxicity test using Hyalella. Once the sediment was
received by the laboratory, it was determined that the test species (Hexagenia) would be replaced
by an aquatic worm (Lumbricu/us).
The conceptual model for this endpoint is ingestion of emergent insects by insectivorous birds,
using Lumbricu/us as a surrogate species. The tissue concentrations of Lumbricu/us will be input
into a food chain exposure model to estimate exposure to the barn swallow to estimate risks to
insectivorous birds. Using the analytical results (both maximum per location sampled and a site
mean concentration) the estimated daily dose to the barn swallow will be compared to data from
existing laboratory.studies [body-burden no observed apparent effect levels (NOAELs) and low
observed apparent effect level (LOAELs)] to determine if the population of insectivorous birds is
at risk.
2.5.5 Assessment Endpoint 5 -Protection of Carnivorous Birds
This assessment endpoint provides for the protection of carnivorous birds to insure tliat ingestion
of contaminants in prey and incidental ingestion of contaminants in soil do not have a negative
impact on growth, survival, and reproductive success. The red-tailed hawk (Buteo jamaicensis)
was selected as a representative species. The conceptual model for this 'endpoint is the ingestion
of small mammals and the incidental ingestion of soil by a carnivorous bird.
• •
The analytical results of the earthworm bioaccumulation assay will be used to generate modeled
body burdens to small mammals, which will be input into a food chain exposure model to
estimate exposure to the red-tailed hawk to estimate risks to carnivorous birds. Using the
analytical results (both maximum per location sampled and a site mean concentration) the
estimated daily dose to the red-tailed hawk will be compared to data from existing laboratory
studies [body-burden no observed apparent effect levels (NOAELs) and low observed apparent
effect level (LOAELs)) to determine if the population of carnivorous birds is at risk.
2.5.6 Assessment Endpoint 6: Protection of Bent hie Macroinvertebrate Communities
This assessment endpoint provides for the protection of the benthic invertebrate communities
that inhabit the Lower Roanoke River to insure that contact with river sediments does not have a
negative impact on growth, survival, and reproductive success. Sediment samples were collected
and analyzed for CO PCs. A split sediment sample from each location was submitted to a
laboratory for a bioaccumulation study using Hexagenia. In addition, a split sediment sample
from each location was submitted to a laboratory for a toxicity test using Hyalel/a azteca. The
results of the toxicity test will be analyzed to determine if survival, growth, or reproduction is
adversely affected following exposure to river contaminants. The results will then be correlated
to the measured concentrations of the CO PCs in the sediment to determine if a dose-response
relationship existed between the observed toxicity and any of the COPCs.
2.5.7 Assessment Endpoint 7: Protection of Fish Communities
This assessment endpoint provides for the protection of fish communities that inhabit the Lower
Roanoke River to ensure that contact with contaminated sediments does not have a negative
impact on growth, survival, and reproductive success. During the ecological sampling, redear
sunfish (Lepomis microlophus) and largemouth bass (Micropterus sa/moides) were collected at
several locations along the river and analyzed for CO PCs. The results will be correlated to the
33
• •
measured concentrations of the CO PCs in the sediment collected near the same sampling
locations.
To evaluate potential ecological risks to fish receptors, food chain accumulation models will be
employed using site specific data (sediment, invertebrate, and fish contaminant concentrations)
to evaluate the exposure of fish to bioaccumulative CO PCs. Using the sediment and fish tissue
analytical results (both maximum per location sampled and a site mean concentration) the
estimated daily dose to fish will be compared to data from existing laboratory studies [body-·
burden no observed apparent effect levels (NOAELs) and low observed apparent effect level
(LOAELs)) to determine if the fish population is at risk.
2.5.8 Assessment Endpoint 8: Protection of Omnivorous Bird Communities
This assessment endpoint provides for the protection of omnivorous birds to insure that ingestion
of contaminants in prey does not have a negative impact on growth, survival, and reproductive
success. The wood duck (Aix sponsa) was selected as a representative species. The conceptual
model for this endpoint is the ingestion of benthic invertebrates and the incidental ingestion of
sediment by omnivorous birds. There is one line of evidence for this endpoint which is a food
chain exposure model.
There are two types of data collected for this endpoint, soil analytical data and Lumbricu/11s
bioaccumulation bioassay results. These data will be input into a food chain exposure model to
estimate exposure to the wood duck to estimate risks to omnivorous birds. Using the analytical
results (both maximum per location sampled and a site mean concentration) the estimated daily
dose to the wood duck will be compared to data from existing laboratory studies [body-burden no
observed apparent effect levels (NOAELs) and low observed apparent effect level (LOAELs)) to
determine if the population of omnivorous birds is at risk.
34
• •
2.5.9 Assessment Endpoint 9: Protection of Piscivorus Bird Communities
This assessment endpoint provides for the protection of piscivorus birds to insure that ingestion
of contaminants in prey does not have a negative impact on growth, survival, and reproductive
success. The osprey (Pandion ha/iae/us) and great blue heron (Ardea herodias) were selected as
representative species. The conceptual model for this endpoint is the ingestion of fish and the
incidental ingestion of sediment by a piscivorus bird. There are two types of data collected for
this endpoint, sediment analytical data and fish tissue data.
These data will be input into a food chain exposure model to estimate exposure to the osprey and
great blue heron to estimate risks to piscivorous birds. Using the analytical results (both
maximum per location sampled and a site mean concentration) the estimated daily dose to the
osprey and great blue heron will be compared to data from existing laboratory studies [body-
burden no observed apparent effect levels (NOAELs) and low observed apparent effect level
(LOAELs)) to determine if the population of piscivorous birds is at risk.
2.5:IO Assessment Endpoint 10: Protection of Omnivorous Mammal Communities
This assessment endpoint provides for the protection of omnivorous mammals to insure that
ingestion of contaminants in prey docs not have a negative impact on growth, survival, and
reproductive success. The river otter (Lutra canadensis) and raccoon·(Procyon lo/or) were
selected as representative species. The conceptual model for this endpoint is the ingestion of
contaminated prey and the incidental ingestion of sediment by an omnivorous mammal.
There are three types of data collected for this endpoint, fish tissue data, Lumbriculus from the
sediment bioaccumulation bioassay, and sediment data. These data will be input into a food
chain exposure model to estimate exposure to the river otter and raccoon to estimate risks to
omnivorous mammals. Using the analytical results (both maximum per location sampled and a
35
• •
site mean concentration) the estimated daily dose to the river otter and raccoon will be compared
to data from existing laboratory studies [body-burden no observed apparent effect levels
(NOAELs) and low observed apparent effect level (LOAELs)] to determine if the population of
omnivorous mammals is at risk.
3.0 FIELD INVESTIGATION
As part of step 4 ofEPA's 8 step process for conducting ecological risk assessments, a SAP and
QAPP were prepared to define the Data Quality Objectives (DQOs) and sampling and analysis
methodologies for the ecological sampling. A field investigation was subsequently conducted in
September 1999 to collect the site specific information described above for use in the baseline
ecological risk assessment. This investigation involved the collection of sediment, soil, and biota.
Selected samples were not only analyzed for chemical composition, but were also split for
various bioassays.
A SMDP meeting is planned for February 2000 to discuss the results of the analytical sampling
and the data usability for conducting the BERA. At that time, data review and preparation of the
BERA will be initiated.
4.0 LITERATURE CITED
Armstrong, F.A. J. 1979. Effects of Mercury Compounds in Fish. In: The Biogeochemistry of
Mercury in the Environment. Nriagu, J.O. (Ed.) Elsevier/North-Holland Biomedical Press.
New Your. Pp. 657-670.
ATSDR. (Agency for Toxic Substances and Disease Registry). 1996. Toxicological Profile for
Nickel. Report Prepared by the Research Triangle Institute for the U.S. Department of
Health and Human Services, Agency for Toxic Substances and Disease Registry. Atlanta,
GA.
36
• •
ATS DR. I 990. Toxicological Profile for Aluminum. Report Prepared by the Research
Triangle Institute for the U.S. Department of Health and Human Services, Agency for
Toxic Substances and Disease Registry. Atlanta, GA.
ATSDR. I 990. Toxicological Profile for Manganese. Report Prepared by the Research Triangle
Institute for the U.S. Department of Health and Human Services, Agency for Toxic
Substances and Disease Registry. Atlanta, GA.
Augspurger, T., J. Holloman, and M. Canada. 1996. Productivity and contaminant assessment
of ospreys from western Albemarle Sound, North Carolina. Poster presentation:
Seventeenth Annual Meeting of the Society of Environmental Toxicology and Chemistry
(SETAC). Washington, DC.
Beeman, D.K., and T. Augspurger. 1996. Dioxins and furans in wood duck eggs from the lower
Roanoke River, North Carolina. U.S. Fish and Wildlife Service. 94-4N38.
Beijer, K. And A. Jernalov. I 979. Methylation of Mercury in Natural Waters. In: The
Biogeochemistry of Mercury in the Environment. Nriagu, J.O. (Ed.) Elsevier/North-
1-Iolland Biomedical Press. New Your. Pp. 201-210.
Beauford, W.J., J Barber, and A.R. Barringer. 1977. Uptake and Distribution of Mercury Within
Higher Plants. Physiol. Plant 39: 261-265.
Birge, W.J., J.A. Black, and A.G. Westerman. I 979. Evaluation of Aquatic Pollutants using
Fish and Amphibian eggs as bioassay Organisms. In: Animals as Monitors of
Environmental Pollutants. National Academy of Science, Washington D.C. Pp. 108-118.
Bode, R.W. 1988. Quality Assurance Workplan for Biological Stream Monitoring in New York
37
• •
State. New York State Department of Environmental Conservation, Albany, New York.
Brooks; 1988. Citation not provided in Preliminary Ecological Risk Assessment Report for the
Lower Roanoke River. ERT. 1998. August.
COM. 1999. Final Sampling and Analysis Plan for Ecological Sampling. Roanoke River Site,
Plymouth, North Carolina. August 17.
Chou, S.F.J, and R.A. Griffen. 1986. Solubility and Soil Mobility of PCBs. Pages 101-120 in
"PCBs and the Environment, Volume!". (J.S. Waid, ed.). CRC Press, Boca Raton, Florida.
228 p.
Clarkson, T.W. and D.O Marsh. 1982. Mercury Toxicity in Man. In: Clinical, Biochemical, and
Nutritional Aspects of Trace Elements, Volume 6. Prasad, A.S. (Ed.), Alan R. Liss, Inc.,
New York. pp. 49-468.
Cocking, D., R. Hayes, M. L. King, M.J. Rohrer, R. Thomas, and D. Ward. 1991.
Compartmentalization of mercury in biotic components of terrestrial floodplain ecosystems
adjacent t the South River and Waynesboro, VA. Water, Air, and Soil Pollution 57-58: I 59-
170.
Das, S.K., A. Sharma, and G. Talukder. 1198;2. Effects of Mercury on Cellular Systems in
Mammals - a Review. Nucleus (Calcutta) 25: 193-230.
DeMayo et al., 1982. Citation not provided in Preliminary Ecological Risk Assessment Report
for the Lower Roanoke River. ERT. 1998. August.
Eisler, R. 1986. Chromium Hazards to Fish, Wildlife, and Invertebrates: a Synoptic Review.
U.S. Fish and Wildlife Service Biological Report, 85(1.86). 60p.
38
• •
Eisler, R. 1986. Polychlorinated Biphenyl hazards to Fish, Wildlife, and Invertebrates: a
Synoptic Review. U.S. Fish and Wildlife Service Biological Report, 85(1.7). 72p.
Eisler, R. 1987. Mercury Hazards to Fish, Wildlife, and Invertebrates: a Synoptic Review. U. S.
Fish and Wildlife Service Biological Report, 85 (1.10) 90 p.
Eisler, R. 1988b. Lead Hazards to Fish, Wildlife, and Invertebrates: A Synoptic Review. U.S. Fish
and Wildlife Service Biological Report, 85(1.14). 134 p.
Eisler, R. 1988c. Dioxin Hazards to Fish, Wildlife, and Invertebrates: A Synoptic Review. U.S.
Fish and Wildlife Service Biological Report, 85(1.8).
ERT. 1998. Preliminary Ecological Risk Assessment. Lower Roanoke River, Plymouth, Martin,
and Washington Counties, NC. August.
ERT. 1999. Draft Preliminary Problem Formulation. April.
Evan and Dail. I 974. Citation not provided in Preliminary Ecological Risk Assessment Report
for the Lower Roanoke River. ERT. 1998. August.
Geisy, J.P., et al., 1994.
Goyer, R.A. 1986. Toxic Effects of Metals, pages 582-635. In: Klaassen et al., 1993. Casarett and
Doull's Toxicology, Third Edition. In. Eisler 1993. Zinc Hazards to Fish, Wildlife, and
Invertebrates: A Synoptic Review. U.S., Fish and Wildlife Service Report No 26. 106p.
Hatch 1978. Citation not provided in Preliminary Ecological Risk Assessment Report for the
Lower Roanoke River. ERT. 1998. August.
Holl, W. And R. I-Iampp. 1975. Lead and Plants. Residue Rev., 54:79-111.
39
• •
Horn, E.G., et al., 1979. The Problem of PCBs in the Hudson River System. New York Acad Sci.
320:591-609. In: Ruelle, R., 1986. Indicator Organisms as Evaluators of PCB Migrations
· from a Superfund Site. Hazardous Materials spills Conference.
Hornshaw, T.C., R.J. Aulerich, H.E. Johnson. 1983. Feeding Great Lakes Fish to Mink: Effects on
Mink and Accumulation and Elimination of PCBs by Mink. J. Toxicol. Environ. Health.
11 :933-946.
Huckabee, J.W., J.M. Elwood, and S.G. Hildebrand. 1979. Accumulation of Mercury in
Freshwater Biota. In: The Biogeochemistry of Mercury in the Environment. Nriagu, J.O.
(Ed.) Elsevier/North-Holland Biomedical Press. New Your. Pp. 277-302.
Iwata, Y., et al., 1974. Uptake of a PCB (Aroclor 1254) from Soil into Carrots Under Field
Conditions. Bull. Environ. Contam. Toxicol. 11 :523-528.
Iwata, Y., and F.A. Gunther. 1976. Translocation of the PCB Aroclor 1254 from Soil Into Carrots
Under Field Conditions. Arch. Environ. Contam. Toxicol. 4:44-59.
James, B.R., and R.J. Bartlett. 1983a. Behavior of Chromium in Soils: V. Fate of Organically
Complexed Cr(III) added to Soil. J. Environ. Qua!., 12:169-172. In: Eisler, R. 1986.
James, B.R., and R.J. Bartlett. 1983b. Behavior of Chromium in Soils: VI. Interactions
Between Oxidation-Reduction and Organic Complexation. J. Environ Qua!., 12: 169-172.
In Eisler 1986.
Kaji, T., R. Kawatani, et al., 1988. The Effects of Cadmium, Copper, or Zinc on Formation of
Embryonic Chick Bone in Tissue Culture. Toxicology 50:303-316. In: Eisler 1993. Zinc
Hazards to Fish, Wildlife, and Invertebrates: A Synoptic Review. U.S., Fish and Wildlife
Service Report No 26. 106p.
40
•
Kazacos, E.A., and J. F. Van Vleet. 1989. Sequential Ultrastructural Changes of the Pancreas in
Zinc Toxicosis in Ducklings. American J. Of Pathology. 134:5810595. ln:Eisler, 1993,
· Zinc Hazards to Fish, Wildlife, and Invertebrates: A Synoptic Review. U.S., Fish and
Wildlife Service Report No 26. I 06p.
Klaassen, C.D., M.O. Amdur, and J. Dou!!. 1986. Casarett and Doull's Toxicology: The Basic
Science of Poisons. Third Edition, Macmillan Publishing Co. New York, p. 628.
Koslowski,S.E., et al., 1994. The Distribution of 42 PCB, including Three Coplanar Congeners, in
the food Web of the Western Basin of Lake Erie. J. Great Lakes Res. 20:260-270.
Kucher and Shabanov I 967. Citation not provided in Preliminary Ecological Risk Assessment
Report for the Lower Roanoke River. ERT. I 998. August.
Loizeau, V. And A. Menesguen. 1993. A Steady-state model of PCB Accumulation is Dab Food
Web. Oceanologica Acta. 16:633-640.
Lu, J. And G.F. Combs. 1988. Effects of Excess Dietary Zinc on Pancreatic Exocrine Function in
the Chick. J. Nutrition 118:681-689. In: Eisler, 1993. Zinc Hazards to Fish, Wildlife, and
Invertebrates: A Synoptic Review. U.S., Fish and Wildlife Service Report No 26. 106p.
Martell, A.E. I 981. Chemistry and Metabolism of Metals Relevant to their Carcinogenicity.
Environmental Health Perspectives. 40: 27-34.
Merrit, R.W. and K.W. Cummins, eds. 1984. An Introduction to the Aquatic Insects of North
America. Second Edition. Kendall/Hunt Publishing Co., Dubuque, Iowa, USA.
Moza et al., 1974. Citation not provided in Preliminary Ecological Risk Assessment Report for
the Lower Roanoke River. ERT. 1998. August.
41
• •
North Carolina Department of Environment, Health, and Natural Resouces. 1996. Roanoke
River Basinwide Water Quality Management Plan, NCDEHNR, Division of Water
Quality, Raleigh, NC.
Olafsson, P.G., et al., I 983. Snapping Turtles - a Biological Screen for PCBs. Chemosphere
!2:1525-1532.
Olsson, P.E., M. Zafarullh, and L. Gedamu. 1989. A Role ofMetallothionen in Zinc Regulation
after Oestradiol Induction ofVitellogenin Synthesis in Rainbow Trout, Sa/mo gairdneri.
Biochemical Journal 257:555-559. In: Eisler 1993, Zinc Hazards to Fish, Wildlife, and
Invertebrtates: A Synoptic Review. U.S. Fish and Wildlife Service Reprot No. 26. 106
p.
Reiners et al., 1986. Citation not provided in Preliminary Ecological Risk Assessment Report for
the Lower Roanoke River. ERT. 1998. August.
Risebrough, R. W., P. Rieche, D.B. Peakall, et al., 1968. Polychlorinated Biphenyls in the Global
Ecosystem. Nature 220:1098-1102. In: Kluwe, W.M, et al., 1979. Effects of Dietary
Polychlorinated Biphenyls and Polybrominated Biphenyls on the Renal and Hepatic
Toxicities of Several Chlorinated Hydrocarbon Solvents in Mice. J. Toxicol Envioron.
Health. 5:605-615.
RMT, Inc. 1998. Site Inspection Prioritization. Volume 1, Attachment 2. Prepared for
Weyerhaeuser Company. April.
RTECS. (Registry of Toxic Effects of Chemical Substances). 1991. Published y the National
Institute for Occupational Safety and Health (NJOSH).
Ruelle,R. 1986. Indicator Organisms as Evaluators of PCB Migrations from a Superfund Site.
42
• •
Hazardous Materials Spills Conference.
Rumford, G.D. 1996. Revised Site Inspection Prioritization: Weyerhaeuser Co./Plymouth Wood
Treating. North Carolina Department of Environment, Health, and Natural Resources;
Division of Solid Waste Management; Superfund Section, 12 pp.
Rumford, G.D. 1997. Expanded Site Inspection: Georgia-Pacific Corp. Hardwood Sawmill. North
Carolina Department of Environment, Health, and Natural Resources; Division of Solid
Waste Management; Superfund Section, 29 pp.
Shaw, G.R., and D. W. Connell. 1984. Physicochemical Properties Controlling PCB
Concentrations in Aquatic Organisms. Environ. Sci. Technol. 18:23-31. In: Koslowski
et al, 1994.
Spear, 1981. Citation not provided in Preliminary Ecological Risk Assessment Report for the
Lower Roanoke River. ERT. 1998. August.
Stevens et al., 1976. Citation not provided in Preliminary Ecological Risk Assessment Report
for the Lower Roanoke River. ERT. 1998. August.
Storm,J.E. et al., 1981. Behavior of Mice after Pre-and Post-natal Exposure to Aroclor1254.
Neurobhav. Toxicol. Terato. 3:5-9.
Strek and Weber 1982. Citation not provided in Preliminary Ecological Risk Assessment Report
for the Lower Roanoke River. ERT. 1998. August.
U.S. Environmental Protection Agency. 1997. Ecological Risk Assessment Guidance for
Superfund: Process for Designing and Conducting Ecological Risk Assessments. U.S.
Environmental Protection Agency, Environmental Response Team Center, Edison, NJ.
43
• •
U.S. Environmental Protection Agency. 1993. Interim Report on Data and Methods for
Assessment of 2,3, 7,8-Tetrachlorodibenzo-p-dioxin risks to aquatic life and associated
· Wildlife. Office of Research and Development. Washington, DC. EPA/600/R-93/055.
U.S. Environmental Protection Agency. 1990. Quality Assurance/Quality Control Guidance for
Removal Activities. Sampling QA/QC Plan and Data Validation Procedures. U.S.
Environmental Protection Agency, Office of Emergency and Remedial Response,
Washington, D.C. EP A/540/O-90/004.
U.S. Environmental Protection Agency. 1989a. Interim Procedures for Estimating Risks
Associated with Exposures to Mixtures of chlorinated dibenzo-p-dioxins and
dibenzofurans (CDDs and CDFs) and 1989 Update. U.E. Environmental Protection
Agency, Washington DC. EPA/625/3-89/016.
U.S. Environmental Protection Agency. 1989b. Protocols for Short Term Toxicity Screening of
Hazardous Waste Sites. U.S. Environmental Protection Agency. Environmental Research
Lab. Corvallis, OR. February 1989. EP A/600/3-88/029.
U.S. Environmental Protection Agency. 1976. Quality Criteria for Water, US EPA,
Washsington, DC. 256 pp. In: Ruelle, 1986. Indicator Organisms as Evaluators of PCB
Migrations from a Superfund Site. Hazardous Materials Spills Coriference.
Venugopal and Luckey 1978. Citation not provided in Preliminary Ecological Risk Assessment
Report for the Lower Roanoke River. ERT. 1998. August.
Weber, JB, and E. Mrozek. 1979. PCBs: Absorption and Translocation by Plants and
Inactivation by Activated Carbon. Bull. Environ. Contam. Toxicol. 23:412-417.
Weibel, F.J., L.C. Leutz, L. Diamond and H.V. Gelboin. 1971. Ary! Hydrocarbon
44
I • •
(benzo(a)pyrene)hydroxylase in microsomes from rat tissues: differential Inhibition and
Stimulation by Benzoflavones and organic solvents. Arch. Biochm Biophys., 144:78-86.
Wixson and Davis, 1993. Citation not provided in Preliminary Ecological Risk Assessment
Report for the Lower Roanoke River. ERT. 1998. August.
45
Table1 I
Literature-derived NOAELs and LOAELs for Mammalian Endooints
I I
' i
Ecolo_glcal Test Route of Test NOAEL ! Duration Endoolnt LOAEL Duration EndDolnt Citation Source
COPC form Exoosure Soecles ma/ka/dl! fma/ka/di
Metals I
Aluminum AICl3 oral in water mouse 1.93 j3 generations reproduction 19.3 3 generations reproduction Ondreicka et al .. 1968 ws
Barium chloride oral in water rat 5.1 / 16 months IarowtM,unar1ension Perru et al.. 1983 ws
Chromium a· oral in water ,at 3.28 !1 year weight loss, food consum Mackenzje et al., 1958 ws
Col'Y'let sulfate !oral in diet mink 11.71 [(vear ~~roduction 15.14 1 Y.:ear ~eproduction Aulerich et al.. 1982 ws
M;Snesium no info fourid '
.
.... '
~-~noanese oxide oral in diet ,at 88 1224 da~~_gestation reoroduction 284 224 days, gestation roduction Laskev etal., 1982 ws
Mercurv methv!.. ··--·-oral in diet mink . o.~-~-~-_m 193 davs ffiortalltv 0.15 (~J.. 93 davs . ffiortalitv Wobeser et al., 1976 ws
Nickel sulfate oral in diet ,at 40 1.~ .. generations ~-~roduction 80 ?._generations r_~roduction Ambrose et al., 1976 ws
....... -....
Nickel oral mouse I 2.3 re.Froduction A
Nickel oral ~.Q.9 25 ! ~~temic A
Vanadium Navo, oral intubation rat 0.21 !so days plus gestation reproduction 2.1 60 days plus gestation reproduction Domingo et al., 1986 ws
Zinc oxide oral in diet ral 160 (oestation reoroduction 320 oestation roduction Schlicker and Cox 1968 ws
l
Oraanlcs ' 80ta BHC NA oral in diet ral 0.4 l13 weeks growth, blood, oraans 2 13 weeks Arowth, blood, omans Van Velsen et al., 1986 s
Gamma • BHC llindanel lindane oral in diet ral 8 !3 generations reornduction ND Palmer et al., 1978 s
Arochlor 1254 NA oral in diet mouse 0.068 !12 months reoroduction 0.68 12 months reoroduction McCov et al., 1995 s
TCOO/TCDF NA oral in diet rat 0.000001 13 oenerations ' duction 0.00001 3 aenerations roduction Murrav et al., 1979 s
~A c not apolicable
ND :. not determined
{~\ Estimated NOAEL: subchronic factor of 10 lied
t?J From USEPA 1993 I
3) Estimated NOAEL: LOAEL to NOAEL factor of 0.1 al'Y'llied
{4) Estimated LOAEL: NOAEL to LOAEL factor of 10 aDJlUed
I I
I I I ;
Source Codes: W S: from Weverhaeuser ERA Studv Desian and SAP (AMT 1999)
S: from Oak Rid_g_!._~~~-~~!!-I Laboratory.~~!Jcolooical Benchmarks for Wildlife, 1996 Revision (Samele 1996}
A: ATSDR 1992 Draft Toxicoloaical Profile for Nickel, Februarv 18 I •
Table 2
Literature-derived NOAELs and LOAELs for Avian End:x>ints
Ecoloalcal Test Route of Test NOAEL Duration Endpoint LOAEL Duration EndDOlnt Citation Source
COPC form Ex,.,.sure Species malka/d) fma/ka/dl
Metals
Aluminum Al2(504h oral in diet ,!ringed dove 109.7 4 months reproduction 1097(4) 4 months reproduction Carriere et el. 1986 ws
Barium hvdroxide oral in diet !dav-old chicks 20.811} 4 weeks mortality 41.7 (1) 4 weeks mortality Johnson et al., 1960 ws
Chromium Ci'' oral in diet [black duck 1 10 months ronroduction 5 10 months reoroduction Haseltine et al., Unnubl data_ ws
~.QJ?Pl!f oxide oral in diet [chicken 47 10 wee~-· 9rowthlmortalitv 61.7 10weeks arowthhnortalitv Mehrino et al., 1960 s
~.':':9nesium no info found .......
~~.riganese oxide oral in diet !i~.~D.~.~.~-.9~1:1.il 977 75 davs 9~.~-~•g·gressiveness 9770 l~L 75 davs 9~.~~9.gressiveness Laskev and Edens, 1985 ws
Mercury methvl oral in diet ! mallard duck 0.0064 l!l 3 .. 9.en ·-·--· r_~production 0.064 3 gen·-·-·--~~reduction Heinz 1979. ws
·····-·-........... Cain and Pafford 1981
Nickel sulfate oral in diet ! mallard duck 77.4 90 days mortalitv/arowth/behavior 107 90 days mortallivmrowth/behavior ws
Vanadium vanadyl sulfate oral in diet i mallard duck 11.4 12 weeks mortalitVioodv wt/blood 114 (4) 12weeks mortalitvlbodv wt/blood White and Dieter 1978 ws
Zinc zinc sulfa1e· · oral in diet [chicken 14.5 44 weeks ~~reduction 130.9 44 weeks reoroduction Stahl et al., 1990 ws •
q_~g8f11Cs
Beta BHC no info found···
Gamma -BHC (lindane) .. lindens oral intubation ;'mallard duck 2 8 weeks -.~duction 20 8 weeks reproduction Chakravartv and Lahiri 1986 s
Arochlor 1254 NA weeklr_ oral_._ J~!!g-necked Pheasant 0.18 17 weeks ~~roduction 1.8 17weeks rearoduction Oahlnren et al., 1972 ws
TCOOITCOF NA wkly ip iniact !rinn-necked aheasant -0.000014 10 weeks reoroduction 0.00014 10 weeks r roduction Nosek et al., 1992 ws
'
' I
(1 Estimated NOA EL: subchronic factor of 1 O applied
2 From USEPA 1993 I I ' (3 Estimated NOAEL: LOAEL to NOAEL factor of 0.1 lied
4 Estimated LOAEL: NOAEL to LOAEL factor of 10 lied
•
Tab1e1
Literature-derived NOAELs and LOAELs tor Mammalian Endrviints
Ecolo_glcal Test Route of Test NOAEL Duration Endpoint LOAEL Duration Endpoint Citation Source
COPC form Exposure Snecies ma/ka/dli lmnlknldl
Metals
Aluminum AICJ3 oral in water mouse 1.93 (3 generations reproduction 19.3 3 generations reproduction Ondreicka et al .• 1968 ws
Ban'um chloride oral in water rat 5.1 )16 months larowtMwaertension Perrv et al., 1983 ws
Chromium er'· oral in water rat 3.28 \tvear weiaht loss, food consum Mackenzie et al., 1958 ws
~P.W!'' sulfate loral in diet mink 11.71 L1...vear 1r_~roduction 15.14 )_vear ~roduction Au1erich et al., 1982 WS
Maanesium no info found
. ··•--·-·--·-·-
Miinaanese oxide oral in diet rat 88 [224 da~. _gestation rPnroduction 284 224 da~. gestation ,_,roduction Laskey et al., 1982 ws
M0TCurv methyl ·-·-·---oral in diet mink 0.015 (lj..)93 davs rriortalitv 0.15(~. 93 days mortalitv Wobeser et al., 1976 ws
Nickel sulfate oral in diet rat 40 \3 oenerations reuroduction 80 ?_generations reproduction Ambrose et al., 1976 ws
Nickel oral mouse 2.3 -roduction A
Nickel oral ~og 25 ~~temic A •
Vanadium NaVO, oral intubation ,at 0.21 )60 days plus gestation reproduction 2.1 60 days plus gestation reproduction Domingo et al., 1986 ws
Zinc oxide oral in diet rat 160 ioestation ronroduction 320 aestation reoroduction Schlicker and Cox 1968 ws
Oraanlca
Beta BHC NA oral in diet rat 0.4 113 weeks growth, blood, omans 2 13 weeks 'Qrowth, blood, omans Van Velsen et al .. 1986 s
Gamma -BHC 1indane) lindane oral in diet rat 8 ]3 oenerations ' duction ND Palmer et al., 1978 s
Arochlor 1254 NA oral in diet mouse 0.068 !12 months duction 0.68 12 months ' reduction McCo.-et al., 1995 s
TCOOfTCDF NA oral in diet rat 0.000001 !3 aenerations tl'Ol'\mduction 0.00001 3 aenerations ' roduction Murray et al., 1979 s
;
~A .. not api:ilicable
ND : not determined
(~I Estimated NOAEL: subchronic factor of 10 lied
(~ From USEPA 1993 t I '
(;!) Estimated NOAEL: LOAEL to NOAEL factor of 0.1 Ann1ied
(41 Estimated LOAEL: NOA EL to LOAEL factor of 10 annlied
t t I
I t I
Source Codes: W S: rrom Weyerhaeuser ERA Study Desian and SAP IAMT 1999)
S: from Dak Ridge Natlonat LaboratO!)'., Toxicoloaical Benchmarks tor Wildlife, 1996 Revision /Sample 1996)
A: ATSOR 1992 Draft Toxicoloaical Profile for Nickel, FebruAN 18 I •
Table 2
Literature-derived NOAEls and LOAELs for Avian Endooints
!
Ecol lcal Tesl Route of ' Test NOAEL Duration EndDolnt LOAEL Duration EndDOlnl Cllallon Source
COPC form Ex..,..sure ! SDecles lmo/kaJdl fmaJka/dl
Metals I
Aluminum Al,i(SO4h oral in diet /ringed dove 109.7 4 months reproduction 1097(4) 4 months reproduction Carriere et al. 1986 ws
Barium hvdroxide oral in diet !dav-old chicks 20.8 fl) 4 weeks mortalitv 41.7 fl) 4weeks mortalitv Johnson et al., 1960 ws
Chromium C~' oral in diet iblack duck 1 10 month.~ .. ~~reduction 5 10 months ~~roduction Haseltine et el., Unpubl data ws
Corine,· oxide
............ oral in diet "ichicken 47 10 weeks growth/mortali!Y_ 61.7 10 weeks growthlmorta!itv Mehrino et al., 1960 s
M'aQnesium no info found ;
~~~ganese oxide oral in diet :j~oanese ouail 977 75 davs 9!!?.~.~~-g_gressiveness 9110 ,~I -75 davs g~-~-~ggressiveness Laskev and Edens. 1985 ws
Mercurv methtl oral in diet !mallard duck o.oos41n 3. 9_en -···--· r_eoroduction 0.064 ·-
3 gen·-·--~!!eroduction Heinz 1979 ws
Nickel sulla!e oral in diet !mallard duck 77.4 90 days '!!Q..~11Y.~rowthlbehavior 107 90 davs mortalirvmrowth/behavior Gain and Pafford 1981 ws
Vanadium vanadyl sulfate oral in die! imallard duck 11.4 12 weeks mortalitv/bodv wt/blood 1141~L .. 12 weeks mortalitilbodv wt/blood White and Dieter 1978 ws
Zinc zinc suifa1e·····""' oral in diet (chicken 14.5 44 weeks r,~oroduction 130.9 44weeks reoroduction Stahl et ar.; 1990 ws •
i I
Oraanlcs ' 881a BHC no info found I
Gamma -BHC jlindane)_ lindane oral intubation /mallard duck 2 8 weeks renmduction 20 8weeks reproduction Chaktavartv and Lahiri 1986 s
Arochlor 1254 NA _weekl.Y,_oral .. ,_,_.jrin_g-necked oheasant 0.18 17 weeks !~roduction 1.8 17weeks LBDtoduction Dahtgmn et al., 1972 ws
TCDD/TCDF 111A wk.Iv ip inject ,ring-necked Dheasam 0,000014 10 weeks reoroduction 0.00014 10weeks roduction Nosek et al., 1992 ws
I
!
!
!
(1 Estimated NOAEL: subchronic factor of 10 aoolied !
2 From USEPA 1993 I
(3 Estimated NOAEL: LOAEL to NOAEL factor of 0.1 a[]( lied
4 Estimated LOAEL: NOA EL to LOAEL factor of 10 a lied
•
I