EPA
        United States
        Environmental Protection
        Agency	
            Solid Waste and
            Emergency Response
            (5305W)
EPA530-D-99-001C
  November 1999
 www.epa.gov/osw
Screening Level
Ecological Risk
Assessment Protocol
For Hazardous Waste
Combustion Facilities
Volume Three
Appendices B-H
           Peer Review Draft
                           IWSROSSAIfNUE
                Printed on paper that contains at least 30 percent postconsumer fiber

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                          APPENDIX B




ESTIMATING MEDIA CONCENTRATION EQUATIONS AND VARIABLE VALUES




               Screening Level Ecological Risk Assessment Protocol



                            August 1999

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Screening Level Ecological Risk Assessment Protocol
Appendix B: Estimating Media Concentration Equations  	August 1999


                               APPENDIX B


                           TABLE OF CONTENTS


TABLE                                                              PAGE

SOIL INGESTION EQUATIONS


B-l-1  SOIL CONCENTRATION DUE TO DEPOSITION 	B-l


B-l-2  COPC SOIL LOSS CONSTANT DUE TO ALL PROCESSES  	B-10


B-l-3  COPC LOSS CONSTANT DUE TO SOIL EROSION  	B-14


B-l-4  COPC LOSS CONSTANT DUE TO RUNOFF	B-20


B-l-5  COPC LOSS CONSTANT DUE TO LEACHING	B-25


B-l-6  COPC LOSS CONSTANT DUE TO VOLATILIZATION	B-31



SURFACE WATER AND SEDIMENT EQUATIONS


B-2-1  TOTAL COPC LOAD TO WATER BODY	B-37


B-2-2  DEPOSITION TO WATER BODY  	B-41


B-2-3  DIFFUSION LOAD TO WATER BODY	B-44


B-2-4  IMPERVIOUS RUNOFF LOAD TO WATER BODY	B-48


B-2-5  PERVIOUS RUNOFF LOAD TO WATER BODY 	B-51


B-2-6  EROSION LOAD TO WATER BODY	B-56


B-2-7  UNIVERSAL SOIL LOSS EQUATION (USLE) 	B-62


B-2-8  SEDIMENT DELIVERY RATIO	B-67


B-2-9  TOTAL WATER BODY CONCENTRATION	B-71


B-2-10 FRACTION IN WATER COLUMN AND BENTfflC SEDIMENT	B-75


B-2-11 OVERALL TOTAL WATER BODY DISSIPATION RATE CONSTANT  	B-80


B-2-12 WATER COLUMN VOLATILIZATION LOSS RATE CONSTANT 	B-82


B-2-13 OVERALL COPC TRANSFER RATE COEFFICIENT	B-86


U.S. EPA Region 6                                                  U.S. EPA
Multimedia Planning and Permitting Division                                   Office of Solid Waste
Center for Combustion Science and Engineering                                            B-i

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Screening Level Ecological Risk Assessment Protocol
Appendix B; Estimating Media Concentration Equations	August 1999

                                APPENDIX B

                            TABLE OF CONTENTS

TABLE                                                                PAGE

B-2-14 LIQUID-PHASE TRANSFER COEFFICIENT 	B-90

B-2-15 GAS-PHASE TRANSFER COEFFICIENT	B-95

B-2-16 BENTfflC BURIAL RATE CONSTANT	B-99

B-2-17 TOTAL WATER COLUMN CONCENTRATION	B-104

B-2-18 DISSOLVED PHASE WATER CONCENTRATION	B-108

B-2-19 COPC CONCENTRATION IN BED SEDIMENT	B-lll


TERRESTRIAL PLANT EQUATIONS

B-3-1  PLANT CONCENTRATION DUE TO DIRECT DEPOSITION	B-l 15

B-3-2  PLANT CONCENTRATION DUE TO AIR-TO-PLANT TRANSFER 	B-125

B-3-3  PLANT CONCENTRATION DUE TO ROOT UPTAKE 	B-130
U.S. EPA Region 6                                                  U.S. EPA
Multimedia Planning and Permitting Division                                   Office of Solid Waste
Center for Combustion Science and Engineering                                            B-ii

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Screening Level Ecological Risk Assessment Protocol
Appendix B; Estimating Media Concentration Equations
                                                             August 1999
Pa
P»
e
a
A
A,
b
BD
BCFr

BS
Bs
Bv
c
C
Cd
Chv
Cs
Cyp
Cyv
Cywv
                   APPENDK B

    LIST OF VARIABLES AND PARAMETERS

Empirical constant (unitless)
Dimensionless viscous sublayer thickness (unitless)
Viscosity of air (g/cm-s)
Viscosity of water corresponding to water temperature (g/cm-s)
Density of air (g/cm3 or g/m3)
Density of water corresponding to water temperature (g/cm3)
Temperature correction factor (unitless)
Bed sediment porosity (L volume/L sediment)—unitless
Soil volumetric water content (mL water/cm3 soil)

Empirical intercept coefficient (unitless)
Surface area of contaminated area (m2)
Impervious watershed area receiving COPC deposition (m2)
Total watershed area receiving COPC deposition (m2)
Water body surface area (m2)

Empirical slope coefficient (unitless)
Soil bulk density (g soil/cm3 soil)
Plant-soil biotransfer factor (mg COPC/kg DW plant)/(mg COPC/kg
soil)—unitless
Benthic solids concentration (g sediment/cm3 sediment)
 Soil bioavailability factor (unitless)
Air-to-plant biotransfer factor (mg COPC/kg DW plant)/(mg COPC/kg
air)—unitless

Junge constant =  l.TxlO"4 (arm-cm)
USLE cover management factor (unitless)
Drag coefficient (unitless)
Dissolved phase water concentration (mg COPC/L water)
Unitized hourly air concentration from vapor phase (ng-s/g-m3)
Unitized hourly air concentration from particle phase (ug-s/g-m3)
COPC  concentration in soil (mg COPC/kg soil)
COPC  concentration in bed sediment (mg COPC/kg sediment)
Total COPC concentration in water column (mg COPC/L water column)
Total water body COPC concentration including water column and bed sediment
(g COPC/m3 water body) or (mg/L)
Unitized yearly average air concentration from particle phase (ug-s/g-m3)
Unitized yearly average air concentration from vapor phase (ug-s/g-m3)
Unitized yearly average air concentration from vapor phase (over water body or
watershed)  (ug-s/g-m3)

Diffusivity  of COPC in air (cm2/s)
Depth of upper benthic sediment layer (m)
U.S. EPA Region 6
Multimedia Planning and Permitting Division
Center for Combustion Science and Engineering
                                                        U.S. EPA
                                                        Office of Solid Waste
                                                                     B-iii

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Screening Level Ecological Risk Assessment Protocol
Appendix B;  Estimating Media Concentration Equations
                                                              August 1999
Ds
dwc
Dw
Dydp
Dytwp

Dywp
Dywv
Dywwv
ER
Ev

/*.
Fd
Fw
Jwc
H

I

k
K



Kds
kp
ks
kse
ksg
ksl
ksr
ksv
Deposition term (mg COPC/kg soil-yr)
Depth of water column (m)
Diffusivity of COPC in water (cm2/s)
Unitized yearly average dry deposition from particle phase (s/m2-yr)
Unitized yearly average total (wet and dry) deposition from particle phase (over
water body or watershed) (s/m2-yr)
Unitized yearly average wet deposition from particle phase (s/m2-yr)
Unitized yearly average wet deposition from vapor phase (s/m2-yr)
Unitized yearly average wet deposition from vapor phase (over water body or
watershed) (s/m2-yr)
Total water body depth (m)

Soil enrichment ratio (unitless)
Average annual evapotranspiration (cm/yr)

Fraction of total water body COPC concentration in benthic sediment (unitless)
Fraction of diet that is soil (unitless)
Fraction of COPC wet deposition that adheres to plant surfaces (unitless)
Fraction of total water body COPC concentration in the water column (unitless)
Fraction of COPC air concentration in vapor phase (unitless)

Henry's Law constant (atm-m3/mol)

Average annual irrigation (cm/yr)

Von Karman's constant (unitless)
USLE erodibility factor (ton/acre)
Benthic burial rate constant (yr"1)
Bed sediment/sediment pore water partition coefficient
(cm3 water/g bottom sediment or L water/kg bottom sediment)
Soil-water partition coefficient (cm3 water/g soil)
Suspended sediment-surface water partition coefficient
(L water/kg suspended sediment)
Gas phase transfer coefficient (m/yr)
Liquid phase transfer coefficient (m/yr)
Soil organic carbon-water partition coefficient (mL water/g soil)
Octanol-water partition coefficient
(mg COPC/L octanol)/(mg COPC/L octanol)—unitless
Plant surface loss coefficient (yr !)
COPC soil loss constant due to all processes (yrn)
COPC loss constant due to soil erosion (yr"1)
COPC loss constant due to biotic and abiotic degradation (yr !)
COPC loss constant due to leaching (yrn)
COPC loss constant due to surface runoff (yr :)
COPC loss constant due to volatilization (yr"1)
Water column volatilization rate constant (yr l)
Overall COPC transfer rate coefficient (m/yr)
Overall total water body dissipation rate constant (yr *)
 U.S. EPA Region 6
 Multimedia Planning and Permitting Division
 Center for Combustion Science and Engineering
                                                         U.S. EPA
                                                         Office of Solid Waste
                                                                       B-iv

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Screening Level Ecological Risk Assessment Protocol
Appendix B;  Estimating Media Concentration Equations	August 1999
LDEP           =      Total (wet and dry) particle phase and wet vapor phase COPC direct deposition
                      load to water body (g/yr)
LKf           =      Vapor phase COPC diffusion (dry deposition) load to water body (g/yr)
LE             =      Soil erosion load (g/yr)
LR             =      Runoff load from pervious surfaces (g/yr)
LKI            =      Runoff load from impervious surfaces (g/yr)
LT             =      Total COPC load to the water body (including deposition, runoff, and erosion)
                      (g/yr)
LS             =      USLE length-slope factor (unitless)

OCsed          =      Fraction of organic carbon in bottom sediment (unitless)

p °L            -      Liquid phase vapor pressure of chemical (atm)
p °s            =      Solid phase vapor pressure of chemical (atm)
P              =      Average annual precipitation (cm/yr)
PF            =      USLE supporting practice factor (unitless)
Pd             =      Plant concentration due to direct deposition (mg COPC/kg DW)
Pr             =      Plant concentration due to root uptake (mg COPC/kg DW)
Pv             =      Plant concentration due to air-to-plant transfer (|ig COPC/g DW plant tissue or
                      mg COPC/kg DW plant tissue)

Q              =      COPC-specific emission rate (g/s)

r              —      Interception fraction—the fraction of material in rain intercepted by vegetation
                      and initially retained (unitless)
R              =      Universal gas constant (atm-m3/mol-K)
RO            =      Average annual surface runoff from pervious areas (cm/yr)
RF            =      USLE rainfall (or erosivity) factor (yr'1)
Rp             =      Interception fraction of the edible portion of plant (unitless)

SD            =      Sediment delivery ratio (unitless)
ASf           =      Entropy of fusion [ASf/R = 6.79 (unitless)]
SF             =      Slope factor (mg/kg-day)'1
ST             =      Whitby's average surface area of particulates (aerosols)
                             = 3.5x10"6 cnrVcm3 air for background plus local sources
                             = l.lxlO"5 cnrYcm3 air for urban sources

Ta             =      Ambient air temperature (K)
Tj             =      Tune period at the beginning of combustion (yr)
T2             =      Length of exposure duration (yr)
tD             =      Time period over which deposition occurs (or time period of combustion) (yr)
Tm             =      Melting point of chemical (K)
Tp             =      Length of plant exposure to deposition per harvest of edible portion of plant (yr)
TSS           =      Total suspended solids concentration (mg/L)
Twk             =      Water body temperature (K)
t1/2             =      Half-time of COPC (days)
U.S. EPA Region 6                                                                  U.S. EPA
Multimedia Planning and Permitting Division                                             Office of Solid Waste
Center for Combustion Science and Engineering                                                          B-v

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Screening Level Ecological Risk Assessment Protocol
Appendix B;  Estimating Media Concentration Equations
                                                                                     August 1999
                       Current velocity (m/s)

                       Dry deposition velocity (cm/s)
                       Average volumetric flow rate through water body (mVyr)

                       Average annual wind speed (m/s)

                       Unit soil loss (kg/m2-yr)

                       Dry harvest yield = 1.22xlOH kg DW, calculated from the 1993 U.S. average
                       wet weight Yh of 1.35xlOn kg (USDA 1994b) and a conversion factor of 0.9
                       (Fries 1994)
                       Harvest yield of fth crop (kg DW)
                       Yield or standing crop  biomass of the edible portion of the plant (productivity) (kg
                       DW/m2)
Vdv
Vfx

W

xe

Yh
Yht
Yp
0.01
10'6
10-6
0.31536
365
907.18
0.1
0.001
100
1000
4047
IxlO3
3.1536xl07
                       Soil mixing zone depth (cm)
                       Units conversion factor
                       Units conversion factor
                       Units conversion factor
                       Units conversion factor
                       Units conversion factor
                       Units conversion factor
                       Units conversion factor
                       Units conversion factor
                       Units conversion factor
                       Units conversion factor
                       Units conversion factor
                       Units conversion factor
                       Units conversion factor
(kg cm2/mg-m2)
(kg/mg)
(m-g-s/cm-ug-yr)
(days/yr)
(kg/ton)
(g-kg/cm2-m2)
(kg-crrrVmg-m2)
(mg-cm2/kg-cm2)
(mg/g)
(m2/acre)
(g/kg)
(s/yr)
U.S. EPA Region 6
Multimedia Planning and Permitting Division
Center for Combustion Science and Engineering
                                                                                 U.S. EPA
                                                                                 Office of Solid Waste
                                                                                              B-vi

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The following uncertainty is associated with this variable:
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originally cited in Hoffman and Baes (1979). U.S. EPA (1994c) recomm
a mean value for loam soil that was obtained from Carsel, Parrish, Jones,
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The following uncertainty is associated with this variable:
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variable is COPC-specific and should be determined from the COPC tables in Appendix A-
:nted in U.S. EPA (1993), RTI (1992), and NC DEHNR (1997) based on the work of Bidler
EPA(1994c).
Following uncertainty is associated with this variable:
It is based on the assumption of a default ST value for background plus local sources, rathe
urban sources. If a specific site is located in an urban area, the use of the latter ST value mi
Specifically, the ST value for urban sources is about one order of magnitude greater than th
local sources, and it would result in a lower calculated Fv value; however, the Fv value is li
percent lower.
According to Bidleman (1988), the equation used to calculate Fv assumes that the variable
constant for all chemicals. However, the value of c depends on the chemical (sorbate) mol
surface concentration for monolayer coverage, and the difference between the heat of deso:
the particle surface and the heat of vaporization of the liquid-phase sorbate. To the extent i
COPC-specific conditions may cause the value of c to vary, uncertainty is introduced if a c
of c is used to calculate Fv.
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y organic COPC with a low Henry's Law Constant.
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TABLE B-1-1




SOIL CONCENTRATION DUE TO DEPOSITION
(SOIL EQUATIONS)


ral Soils." Journal of Contaminant Hydrology. Vol. :
3
3
(Page 8 of 9)
sel, R.F., R.S. Parrish, R.L. Jones, J.L. Hansen, and R.L. Lamb. 1988. "Characterizing the Uncertainty of Pesticide Leaching in Agrk
Pages 11-24.
£3
U


This reference is cited by U.S. EPA (1994b) as the source for a mean soil bulk density value of 1.5 g/cm3 for loam soil.




lei, D. 1980. Fundamentals of Soil Physics. Academic Press, Inc. New York.
*^*
a
seness or compaction of the soil, depending on the
o
_o
This document is cited by U.S. EPA (1990a) for the statement that dry soil bulk density, BD, is affected by the soil structure, such as
water and clay content of the soil.


Radionuclides. ORNL/NOREG/TM-882.
^

. EPA. 1 990a. Interim Final Methodology for Assessing Health Risks Associated with Indirect Exposure to Combustor Emissions. Er
Research and Development. EPA 600-90-003. January.
1/1
3
:curs (time period for combustion ), tD, be
8 .
n ™
This document is a reference source for the equation in Table B-1-1, and it recommends that (1) the time period over which depositk
represented by periods of 30, 60, and 100 years, and (2) undocumented values for soil mixing zone depth, Z,, for tilled and untilled si


•king Group Recommendations. Office of Solid
1
. EPA. 1 993. Addendum to the Methodology for Assessing Health Risks Associated with Indirect Exposure to Combustor Emissions .
Waste. Office of Research and Development. Washington, D.C. September 24.
c^
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fraction of COPC air concentration in vapor phase) ii
M
§
This document is a reference for the equation in Table B-1-1. It recommends using a deposition term, Ds, and COPC-specific F, val
the Cs equation.


Attachment C, Draft Exposure Assessment Guidanc
I .
. EPA 1994a. Revised Draft Guidance for Performing Screening Level Risk Analyses at Combustion Facilities Burning Hazardous Wa
for RCRA Hazardous Waste Combustion Facilities. Office of Emergency and Remedial Response. Office of Solid Waste. April 15,
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EPA/600/6-88/005Cc.
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Waste. December 14.
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asition velocity for HNO3 from a U.S. EPA database
alue should be applicable to any organic compound h
following:
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alue for dry deposition velocity is based on median dry de
lered the most similar to the constituents covered and the
mendation was not cited. This document recommends thi
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1998. "Human Health Risk Assessment Protocol for Hazi
30-D-98-001A. July.
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REFERENCES AND DISCUSS!
















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*e Risk Assessments for Hazardous Wa.
s
to
Protocol for Performing Indirect Expo,
NCDEHNR

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1
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! onto the site and away from the site.
(4_ QU
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-003. November 10.
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arch and Development. EPA-600-AP-1
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tachment C, Draft Exposure Assessment
>er 14.
*•* JJ
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. Office of Solid Wasi
f /?wA: Analyses at Combustion Facilitie
of Emergency and Remedial Response
S 8
Guidance for Performing Screening Le
ous Waste Combustion Facilities. Offi
evised Draft >
CRA Hazard
as a;

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compounds.
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£ -8
reference documents for the equations
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is one of the
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EPA (1994b), U.S.

med for kse is zero
value a
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Varies (calculated - Table B-2-7)
This variable is site-specific and is calculated by using the equation in Table B-2-7.
The following uncertainty is associated with this variable:
(1) All of the equation variables are site-specific. Use of default values rather than site-specific vi
these variables will result in unit soil loss (X,) estimates that are under- or overestimated to so:
default values, Xe estimates can vary over a range of less than two orders of magnitude.
is,
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Varies (calculated - Table B-2-8)
This value is site-specific and is calculated by using the equation in Table B-2-8.
Uncertainties associated with this variable include the following:
(1) The recommended default values for the empirical intercept coefficient, a, are average values
of sediment yields from various watersheds. Therefore, those default values may not accurate
watershed conditions. As a result, use of these default values may under- or overestimate SD.
(2) The recommended default value for the empirical slope coefficient, b, is based on a review of
various watersheds. This single default value may not accurately represent site-specific water
result, use of this default value may under- or overestimate SD.
I
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variable is affected by the soil structure, such as loosi
ent of the soil (Hillel 1980), as summarized in U.S. El
Baes (1979). U.S. EPA (1994) recommends a default
taken from Carsel, Parrish, Jones, Hansen, and Lamb
itively narrow range" for BD of 1.2 to 1.7 g/cm3 (U.S.
following uncertainty is associated with this variable:
The recommended range of soil dry bulk density val
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EPA OSW recommends the following values for this
Soil Depth (cm)
Untilled 1
Tilled 20
following uncertainty is associated with this variable:
For soluble COPCs, leaching might lead to mov<
This uncertainty may overestimate kse.
Deposition to hard surfaces may result in dust re
with in-situ materials), in comparison to that of (
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TABLE B-1-3








mj
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H
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ONSTANT DUE T
(SOIL EQUATIO
U
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-------


TABLE B-1-3





Z
O
N*N
8
COPC LOSS CONSTANT DUE TO SOIL EK







(SOIL EQUATIONS)







©

w>
£







REFERENCES AND DISCUSSION





g in Agricultural Soils." Journal of Contaminant Hydrology. Vol
c
., R.S. Parish, R.L. Jones, J.L. Hansen, and R.L. Lamb. 1988. "Characterizing the Uncertainty of Pesticide Lez
ages 11-24.
u_ a.
oi .
CO
=
u

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document is cited by U.S. EPA (1994) as the source for a mean soil bulk density, BD, value of 1.5 g/cm3 for lot
_«
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1980. Fundamentals of Soil Physics. Academic Press, Inc. New York.

Q
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o
1
a
1
CO
a"
3
3
document is cited by U.S. EPA (1990) for the statement that dry soil bulk density, BD, is affected by the soil st:
r and clay content of the soil.
« 
-------



TABLE B-1-3























OIL EROSION
)SS CONSTANT DUE TO S
(SOIL EQUATIONS)
^
J
^
PH
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Attachment C, Draft Exposure Assessment Guidance J

ng Hazardous Wastes.
(Page 6 of 6)
'lyses at Combustion Facilities Burni
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U.S. EPA (1993).
for tilled and untilled soil, as cited in
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ite. December 14.
3 M
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se. Office of Solid Wi
/ /?wfc Analyses at Combustion Facili
of Emergency and Remedial Respon
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This variable depends on the available water and on soil structure; i
be estimated as the midpoint between a soil's field capacity and wil
of 0.2 mL/cm3 as a default value. This value is the midpoint of the
which is recommended by U.S. EPA (1993) (no source or reference
EPA(1994b).
The following uncertainty is associated with this variable:
(1) The default &„, values may not accurately reflect site-specific
overestimated to a small extent, based on the limited range of
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U.S. EPA OSW recommends the following values for this variable:
Soil Depth (cm)
Untilled 1
Tilled 20
The following uncertainty is associated with this variable:
(1) For soluble COPCs, leaching might lead to movement to belo\
uncertainty may overestimate ksr.
(2) Deposition to hard surfaces may result in dust residues that ha
in-situ materials), in comparison to that of other residues. Thi

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The following uncertainty is associated with this variable:
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ap
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-------


TABLE B-1-4






COPC LOSS CONSTANT DUE TO RUNOFF
(SOIL EQUATIONS)






(Page 4 of 5)
REFERENCES AND DISCUSSION




Itural Soils." Journalof Contaminant Hydrology. Vol
3
U
'&
.F., R.S. Parrish, R.L. Jones, J.L. Hansen, and R.L. Lamb. 1988. "Characterizing the Uncertainty of Pesticide Leaching in Ai
'ages 11 -24.
a- &.
I"05
55
U


document is cited by U.S. EPA (1994) as the source of a mean soil bulk density, BD, value of 1.5 g/cm3 for loam soil.
t/;
1


i
><
1
|
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1
J.J., D.W. Miller, F. Van der Leeden, and F.L. Troise. 1973. Water Atlas of the United States. Water Information Center,
>,
1)
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off, R. This reference provides maps with isolines of
^ interflow, and ground water recharge. Because these
te surface runoff.
C > TO
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document is cited by U.S. EPA (1993), U.S. EPA (1994c), and NC DEHNR (1997) as a reference to calculate average annus
lal average surface water runoff, which is defined as all flow contributions to surface water bodies, including direct runoff, sh
ss are total contributions, and not only surface runoff, U.S. EPA (1994c) recommends that they be reduced by 50 percent to e
•1 3 2
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1980. Fundamentals of Soil Physics. Academic Press, Inc. New York.
Q
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£
oseness or compaction of the soil, depending on the
Cfl
CS
document is cited by U.S. EPA (1990) for the statement that dry soil bulk density, BD, is affected by the soil structure, such
r and clay content of the soil.
« o
£ 1


e ofRadionuclides. ORNL/NUREG/TM-882.
1
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P.O., and C.F. Baes. 1979. A Statistical Analysis of Selected Parameters for Predicting Food Chain Transport and Interna
c
ta
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document presents a soil bulk density, BD, range of 0.83 to 1.84.
vi
S


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nj
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^IR. 1997. NC DEHNR Protocol for Performing Indirect Exposure Risk Assessments for Hazardous Waste Combustion Uni
*—<
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document also recommends the following:
VD CO
II


eden, and Troise 1973) or site-specific procedures,
the use of the CNE
3<8
J- u
• Estimation of annual current runoff, RO (cm/yr), by using the Water Atlas of the United States (Geraghty, Miller, Van d<
such as using the U.S. Soil Conservation Service curve number equation (CNE) (U.S. EPA [1985]) is cited as an examp]
Default value of 0.2 mL/cm3 for soil volumetric water content (
-------


TABLE B-1-4










RUNOFF
O
IS CONSTANT DUE T
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(SOIL EQUATIONS)












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calculate average annual runoff
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dy soils) to 0.3 (heavy loam/c
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ange of soil volumetric water content, 0^ values
ange (2 to 280,000 mL/g) of Kd, values for inorga
; of the Water Atlas of the United States (Geraght
- *• >- s
< < < ID

• • • •


ires. External Review Draft. Office of Research and Development.
•a
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D.C. EPA/600/6-88/005Cc. June.
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u
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Office of Solid Waste. December 14.
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1, D. 1980. Fundamentals of Soil Physics. Academic Press, Inc. New, New York.
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in Transport and Internal Dose of Radionuclides. ORNL/NUREG/TM-882.
ing Food Cha\
nan, P.O., and C.F. Baes. 1979. A Statistical Analysis of Selected Parameters for Predict
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This document presents a soil bulk density, BD, range of 0.83 to 1.84.


es", In: Pollutants in a Multimedia Environment. Yoram Cohen, Ed. Plenum
i waste faciliti
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Publishing Corp. New York.
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—
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recommends the following:


: values are not identified.
sources of these values are not identified.

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TABLE B-1-6







JZATION
M
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C LOSS CONSTANT DUE TO
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star Emissions. External Review Draft. Office of Research and
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REFERENCES AND DISCUSSION

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Science and Technology. Volume 22. Number 4. Pages 3i
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Bxposure Risk Assessments for Hazardous Waste Combusl
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Risks Associated with Indirect Exposure to Combustor En\
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id Waste. December 14.
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Level Risk Analyses at Combustion Facilities Burning Ha
Office of Emergency and Remedial Response. Office of !
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Organic COPCs: 3
COPC enrichment occurs because lighter soil particles erode more than heavier sc
of organic COPCs which is a function of organic carbon content of sorbing media
eroded material than in-situ soil (U.S. EPA 1993). In the absence of site-specific
a default value of 3 for organic COPCs and 1 for inorganic COPCs. This is consi
guidance (1993), which recommends a range of 1 to 5 and a value of 3 as a "reasc
range has been used for organic matter, phosphorus, and other soil-bound COPCs
no sources or references were provided for this range. ER is generally higher in s
loamy soils (U.S. EPA 1993).
The following uncertainty is associated with this variable:
(1) The default ER value may not accurately reflect site-specific conditions; the
underestimated to an unknown, but relatively small, extent.
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This value is COPC-and site-specific and should be calculated using the equation
Cs in watersheds, the maximum or average of air parameter values at receptor grii
watershed may be used (see Chapter 4). Uncertainties associated with this variab!
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(1) Uncertainties associated with this parameter will be limited if Kd, values an
Appendix A-2.
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(Page 5 of 6)
REFERENCES AND DISCUSSION



in Agricultural Soils." Journal of Contaminant Hydrology.
.5
IS
.F., R.S. Parrish, R.L. Jones, J.L. Hansen, and R.L. Lamb. 1988. "Characterizing the Uncertainty of Pesticide
ume2. Pages 11-24.
oi "3
"o
»
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i document is the source for a mean soil bulk density of 1.5 cm3 for loam soil.
1




1980. Fundamentals of Soil Phys ics. Academic Press, Inc. New York.
Q
s
—
ffi
such as looseness or compaction of the soil, depending on the
structure,
i document is cited by U.S. EPA (1990) for the statement that dry soil bulk density, BD, is affected by the soil
sr and clay content of the soil.
II


malDose ofRadionuclides. ORNL/NUREG/TM-882.
n and Inte
P.O., and C.F. Baes. 1979. A Statistical Analysis of Selected Parameters for Predicting Food Chain Transpoi
c
ca
1
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E


i document presents a soil bulk density, BD, range of 0.83 to 1.84 g/cm3.
s


>,
1
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1
mbustion
••JR. 1 997. NC DEHNR Protocol for Performing Indirect Exposure Risk Assessments for Hazardous Waste Co
a
w
Q
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water content.
\
1
document is cited as one of the sources for the range of BD and Kd, values, and the default value for the volui
W2
1


ns. Environmental Criteria and Assessment Office. Office of
tr Emissio
. 1 990. Interim Final Methodology for Assessing Health Risks Associated with Indirect Exposure to Combush
;arch and Development. EPA 600-90-003. January.
•^ CO
^ 3
w °*
c/i
3
oseness or compaction of the soil, depending on the water and
JO
M
a
1
V3
document cites Hillel (1980) for the statement that dry soil bulk density, BD, is affected by the soil structure,
content of the soil.
'£ S
H "3


ssions. External Review Draft. Office of Research and
ustor Emii
1993. Addendum to the Methodology for Assessing Health Risks Associated with Indirect Exposure to Comb
elopment. Washington, D.C. November 1993.

l&
tn
H>
jsed for organic matter, phosphorous, and other soil-based
ecause lighter soil particles erode more than heavier soil
e, concentrations of organic COPCs, which are a function of the
SB!
Ill
£ ° H
document is the source of the recommended range of COPC enrichment ratio, ER, values. This range, 1 to 5,
'Cs. This document recommends a value of 3 as a "reasonable first estimate," and states that COPC enrichmer
cles. Lighter soil particles have higher surface-area-to-volume ratios and are higher in organic matter content.
nic carbon content of sorbing media, are expected to be higher in eroded material than in in-situ soil.

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imends the use of current j
specific values for this var
), was based on a soil orga
Vhelan 1989), and chosen
" "O ^J"
iP H5 •-< ca
This value is site-specific. U.S. EPA OSW i
1997; U.S. EPA 1985) in determining water!
default value of 0.36, as cited in U.S. EPA (
Strenge, Buck, Hoopes, Brockhaus, Walter, i




























variable:
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VERSAL SOIL LOSS EQUATIC
(SOIL EQUATIONS)
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(Page 4 of 5)
REFERENCES AND DISCUSSIO



ental Pollutant Assessment System (MEPAS) Application
i. December.
timedia Environm
hland, Washingtol
, M.B. Walter, and G. Whelan. 1989. Mult
'.meters. Pacific Northwest Laboratory. Ric
ppo, J.G. Jr., D.L. Strenge, J.W. Buck, B.L. Hoopes, R.D. Brockhaus
Guidance: Volume 2 -Guidelines for Evaluating MEPAS Input Para
2
Q
value of 0.36, based on a soil organic matter content of
erodibility factor
3
1
o
•o
i
8
09
8
g
1
1
This document is cited by U.S. EPA 1994 and NC DEHNR 1997 as
1 percent.


c
CS
e Combustion Uni
sure Risk Assessments for Hazardous Wast
DEHNR. 1997. NC DEHNR Protocol for Performing Indirect Expo
U
z



This document recommends the following:


ientative of a whole watershed, not just an agricultural field.
of 0. 1 to be repres
§
1
I
u
"O
cfl
T3
§
t-l
O
CQ
2
• A USLE erodibility factor, K, value of 0.36 ton/acre
• A USLE length-slope factor, LS, value of 1.5 (unitless)
A range of USLE cover management factor, C, values of 0
• A USLE supporting practice factor, P, value of 1


rsal Soil Loss Equation (RUSLE). Agricultural Research
the Revised Unive
r: A Guide to Conservation Planning With
. Department of Agriculture. 1997. Predicting Soil Erosion by Wate,
Service, Agriculture Handbook Number 703. January.
CO
D
CO*
f
a
O
1
S
o
I
i
1
1
face and Ground
**•
e
1
|
u
1
L
. EPA. 1985. Water Quality Assessment: A Screening Procedure foi
EPA/600/6-85/002a.
GO
3


lid Waste. Washington, D.C. April.
.EPA. 1988. Superfund Exposure Assessment Manual. Office of Sol
CO
D
of 1.5. This value reflects a variety of possible distance and
ilope factor value
the reference source for the USLE length-!
tershed, not just an agricultural field.
This document is cited by U.S. EPA 1994 and NC DEHNR 1997 as
slope conditions and was chosen to be representative of a whole wa


Working Group Recommendations. Office of Solid Waste
>ustor Emissions.
Associated with Indirect Exposure to Coml
mber 24.
EPA. 1993a. Addendum: Methodology for Assessing Health Risks .
and Office of Research and Development. Washington, D.C. Septe:
GO
ID
en
3
i
o
e
CS
CO
CO
u
I
1
2
i
1
a
55
C
C3
1
W
I
•o
§
average annual USLE rainfall factors, RF,
This document cites Wischmeier and Smith (1978) as the source of
United States to greater than 300 for the southeast.





This document also recommends the following:



ntrol measures
and agricultural crops
ssumed absence of any erosion or runoff co:
• A USLE cover management factor, C, of 0.1 for both grass
A USLE supporting practice factor, P, of 1, based on the a


52
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ION (USLE)
'ect Exposure to Combustion Emissions. Office of Health and Environmental
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Office of Research and Development. EPA-600-A
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i is influenced by vegetative cover and cropping practices, such as planting
;s greater than 0.1 but less than 0.2 are appropriate for agricultural row crops,
R X
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3 >
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nt discusses the USLE cover management factor. 1
rather than up and down slope. This document disc
if 1 is appropriate for sites mostly devoid of vegetat
0) ~ "
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o- K w
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•.ardous Wastes. Office of Emergency and Remedial Response. Office of Soli
K
Facilities Burning Hi
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1
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Guidance for Performing Screening Level Risk Ana
mber 14.
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LTER AND SEDIM
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NC DEHNR (1997). U.S. EPA
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; sediment delivery ratios vary approxima
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REFERENCES AND DISCUSSION







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'rming Indirect Exposure Risk Assessments for Hazardous Waste Combustion
DEHNR Protocol for Perfo
O
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ited as one of the reference
Formation.
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ons. External Review Draft. Office of Research and
8
• Assessing Health Risks Associated with Indirect Exposure to Combustor Emi
ium to the Methodology for
shington, D.C. November.
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w. Attachment C, Draft Exposure Assessment Guidance for
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s. April 15.
Guidance for Performing S
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7M51 Wasfe*. Attachment C, Draft Exposure Assessment
IVaste. December 14.
"2 -a
arming Screening Level Risk Analyses at Combustion Facilities Burning Haza
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id Draft Guidance for Perfi
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the -(1/8) power of the drainage ratio.
(!!§
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:s document concludes that the sediment delivery ratios vary approximately wi
ited by U.S. EPA (1993) as
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especially for those water bodies for which flow rate information is not readily available. There
values may contribute to the under- or overestimation of total water body COPC concentration,
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following uncertainty is associated with this variable:
The default values for the variables in the equation in Table B-2-10 may not accurately represei
- specific conditions. However, the range of several variables— including dbs, CBS, and 6b— is re
Other variables, such as d^ and dz, can be reasonably estimated on the basis of generally avails
The largest degree of uncertainty may be introduced by the default medium-specific organic cai
content values. Because OC content values may vary widely in different locations in the same i
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of these variables will contribute to the under- or overestimation of Cmat The degree of uncerti
the variable k,, is expected to be under one order of magnitude and is associated largely with the
soil loss, X,, values for the variables fm, k,, and/,,, are dependent on medium-specific estimates i
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three may be significant in specific instances.
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TOTAL WATER BODY CONCENTRATION
RFACE WATER AND SEDIMENT EQUATIONS
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(Page 4 of 4)
REFERENCES AND DISCUSSION





















^3 o
TWeRM Assessments for Hazardous Waste Combustion Uni
ments for the default depth of upper benthic layer value The def
r the range of values for the depth of the upper benthic lay™
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alue is the midpoint of an acceptable range. Th
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for the default depth of the upper benthic layer value The defau
the range of values for the depth of the upper benthic layer.
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Varies (see Appendix A-2
variable is COPC-specific and should be determined from the COPC t
Following uncertainty is associated with this variable:
The Kdm values in Appendix A-2 are based on default OC contents f<
default values may not accurately reflect site- and water body-specifi
actual Kdw values. Uncertainty associated with this variable will be i
estimates are used to calculate Kd^,.
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variable is site-specific. U.S. EPA OSW recommends the use of site-
:sentative of long-term average annual values for the water body of cor
by NC DEHNR (1997), U.S. EPA (1993a), and U.S. EPA (1993b) in 1
Following uncertainty is associated with this variable:
Limitation on measured data used for determining a water body speci
accurately reflect site- and water body-specific conditions long term.
under-or overestimation of fm.
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variable is site-specific and should be an average annual value.
Following uncertainty is associated with this variable:
Use of default depth of water column, dm, values may not accurately
those water bodies for which depth of water column information is ui
dvc values may contribute to the under- or overestimation of total wat
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variable is site-specific. U.S. EPA OSW recommend
stent with U.S. EPA (1994) and NC DEHNR (1997) ;
ference was cited for this range.
bllowing uncertainty is associated with this variable:
Use of default depth of upper benthic layer, dbs, valu
conditions. However, any uncertainly introduced is
range.
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variable is site-specific. U.S. EPA OSW recommend
depth, consistent with NC DEHNR (1997):
dt = d^ + d^
bllowing uncertainty is associated with this variable:
Calculation of this variable combines the concentrati
summed. Because most of the total water body dept
uncertainties associated with dwc are not expected to
variable, dt, are also not expected to be significant.
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variable is site-specific. U.S. EPA OSW recommend
i that this value should be reasonable for most applica
U.S. EPA (1993b and 1994) and NC DEHNR (1997]
bllowing uncertainty is associated with this variable:
The recommended default value may not accurately
the variable/^ may be under- or overestimated; the
based on the narrow recommended range.
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is consistent with other U.S. EPA (1993b and 1994) guidance.
1















following uncertainty is associated with this variable:
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calculation. To the extent that the recommended default values of BS and
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'ERENCES AND DISCUSSION
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$
1
ba
ssessments for Hazardous Waste Combustion Unit
.. 1997. NC DEHNR Protocol for Performing Indirect Exposure Risk A
K
§

W
Q
U
Z
en
CB
T3
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'o
lent is also
sediment, respectively. This docurr
1
53
sumed OC values of 0.075 and 0.04 for surface wal
ocument is cited as one of the sources of the range of Kd, values and ass
•o
CO
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£'!l
:al water bo
is documen
yer. Thede
:e of the equation for calculating tot
alue for bed sediment porosity. Th
ue for depth of the upper benthic la;
Hi
a-Sl
:e of information. This document is also cited as tl
as one of the reference source documents for the d
one of the reference source documents for the defi
the sources of TSS. This document cites U.S. EPA (1993b) as its sourc
No source of this equation was identified. This document is also cited
PA ( 1 993b) as its source of information. This document is also cited as
^- - rrj
O -C

1993b) as its source of information for the range oi
t bed sediment concentration.
is the midpoint of an acceptable range. This document cites U.S. EPA (
tent is also cited as one of the reference source documents for the defaul
0 fc
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earch and
ternal Review Draft. Office of Res
£
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'ated with Indirect Exposure to Combustor Emissic
993a. Addendum to the Methodology for Assessing Health Risks Associ
3pment. Washington, D.C. November 1993.
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1 H £ § § ,
I ss § '1 1 5
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sediment, respectively. The generic
value; however, OC is medium-spe
Y 7.5 and 4, because the OC values
ent porosity ( 6bs); no source of this
range was identified. Finally, this
10 to 20 be specified in streams an
•o ,a * a .a -g
g S K =5 •£ o
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iumed OC values of 0.075 and 0.04 for surface wat
follows: Kd,j = Koc * OC,. Koc is a chemical-s
d,,, values were estimated by multiplying the Kd, v
iment also presents the equation for calculating be*
nthic solids concentration (BS); no original source
to 10 be specified for parks and lakes, and a TSS \
ocument is cited as one of the sources of the range of Kd, values and ass
jting partition coefficients (soil, surface water, and bed sediments) is as
, values was based on an assumed OC value of 0.01 for soil. Kd^, and K
diment are 7.5 and 4 times greater than the OC value for soil. This doci
led. This document was also cited as the source for the range of the be
mends that, in the absence of site-specific information, a TSS value of 1
-o — 13 o sr c
-1 1 * -S § 1
f 13 <4- c £ H
H o o « .2 "



a
w
I
of Solid W
» Group Recommendations. Office
1
with Indirect Exposure to Combustor Emissions. )
993b. Addendum: Methodology for Assessing Health Risks Associated
of Research and Development. Washington, D.C. September 24.
— o
O

.S. EPA (1994) as the source of the
he depth of the upper benthic layer
P s
"S"3
!&
This document is also cited by NC DEHNR (1997;
fault bed sediment concentration value, and the rar
ocument is cited by NC DEHNR (1997) as the source of the TTS value.
:nt porosity value and the equation used to calculate the variable, the de:
•o £
& .£
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4
f Guidance.
nent C, Draft Exposure Assessment
•5
5
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Combustor Facilities Burning Hazardous Wastes.
994. Draft Guidance for Performing Screening Level Risk Analyses at i
Hazardous Waste Combustion Facilities. April 15.
•<
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n U
Si °<
W
CO
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ibrmation. '
.S. EPA (1993b) as its source of ini
D
CO
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It value for bed sediment porosity. This document
ocument is cited as one of the reference source documents for the defau
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SB
H
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alue is the midpoint of an acceptab
iment is also cited as one of the reft
*• 5
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t value for depth of the upper benthic layer. The d
values for the depth of the upper benthic layer. Tl
icnt is also cited as one of the reference source documents for the defaul
tent cites U.S. EPA (1993b) as its source of information for the range of
icnts for the default benthic solids concentration.
SEE
333
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WATER BODY
WATER AND S
LL TOTAL
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Varies (calculated - Table B-2-13)
ariable is COPC- and site-specific, and is calculated by using the equation i
ated with this variable include the following:
All of the variables in Table B-2-13 are site-specific. Therefore, the use o
variables could contribute to the under- or overestimation of kv.
The degree of uncertainty associated with the variables dt and TSS is expe<
information necessary to estimate these variables is generally available or
narrow.
Values for the variable k, and Airfw are dependent on medium-specific estii
content can vary widely for different locations in the same medium, uncer
variables may be significant in specific instances.
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Varies (calculated - Table B-2-10)
ariable is COPC- and site-specific, and is calculated by using the equation :
tainties associated with this variable include the following:
The default variable values recommended for use in the equation in Table
site-specific water body conditions. However, the range of several variabi
relatively narrow; therefore, the degree of uncertainty associated with thes
small. Other variables, such as d^ and dt, can be reasonably estimated on
information.
The largest degree of uncertainty may be introduced by the default mediur
content values are often not readily available and can vary widely for diffe
Therefore, the degree of uncertainty may be significant in specific instanci
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Varies (calculated - Table B-2-16)
ariable is COPC- and site-specific, and is calculated by using the equation :
tainties associated with this variable include the following:
All of the variables in Table B-2-16 are site-specific. Therefore, the use o
values, for any or all of these variables, will contribute to the under- or ovi
The degree of uncertainty associated with each of these variables is as foil
magnitude at most, (2) BS, dbr Vfff TSS, and Aw— limited because of the ni
variables or because resources to estimate variable values are generally av
site-specific and degree of uncertainty unknown.
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or the variable

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Varies (calculated - Table B-2-13)
variable is COPC- and site-specific, and is calculated by using the equation
rtainties associated with this variable include the following:
All of the variables in Table B-2-13— except R, the universal gas constant,
Therefore, the use of default values, for any or all these variables, could co
Kv.
The degree of uncertainty associated with the variables H and Twk is expect
well-established, and average water body temperature, Twk, will likely vary
The uncertainty associated with the variables KL and KG is attributable larg
content. Because OC content values can vary widely for different location
values may generate significant uncertainty in specific instances. Finally, 1
unknown; therefore, the degree of associated uncertainty is also unknown.
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fS ;§ S S S
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Varies (site-speciflc)
variable is site-specific and should be an average annual value.
following uncertainty is associated with this variable:
Use of default values for depth of water column, d^., may not accurately r<
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d^. values may contribute to the under- or overestimation of total water hot
degree of under- or overestimation is not expected to be significant.
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bllowing uncertainty is associated with this variable:
The values contained in Appendix A-2 for Kd^, are calculated on the basis of default
soil. Kd^ values based on default values may not accurately reflect site-and water bo
under- or overestimate actual Kdm values. Uncertainty associated with this variable \
medium-specific OC estimates are used to calculate Kdm.
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REFERENCES AND DISCUSSION












Working Group Recommendations. Office of Solid Waste
tn
9r Emission,
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Draft Guidance for Performing Screening
CRA Hazardous Waste Combustion Facility
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range of windspeeds at a single location may be more significant
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REFERENCES AND DISCUSSION





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1

Exposure Risk Assessments for Hazardous Waste Combustion
1 for Performing Indirect 1
NC DEHNR Protoco
DEHNR. 1997.
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, ft, 4, and //„ values of 1.2 x Itf3, 0.4, 4, and 1.81 E-04, respi
rce of information for k and Af
sources of the variables pt
.S. EPA (1993a) as its soui
is cited as one of the
: paw&jua, and(2)U
This document
information foi


ns. Working Group Recommendations. Office of Solid Waste,
Ci
isks Associated with Indirect Exposure to Combustion Emissit
September 24.
'gyfor Assessing Health R
ment. Washington, D.C.
ddendum: Methodolo
Research and Develop
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7rf) value of 0.001 1, (2) the recommended von Karman's constani
hese variable values are not identified.
w —
1997) as the source of (1) the recommended drag coefficient (
us sublayer thickness ( A.^ value of 4. The original sources of
(1994) and NC DEHNR (
ended dimensionless visco
is cited by U.S. EPA
, and (3) the recommi
This document
(A:) value of 0.4


ms. External Review Draft. Office of Solid Waste, and Office
.s
Risks Associated with Indirect Exposure to Combustor Emissi
10.
logy for Assessing Health
hington, D.C. November
ddendum to Methodo
j Development. Was
, EPA. 1993b. A
of Research am
C/3
b
onstant (K), and (3) a value of 4 for the dimensionless viscous
U
coefficient (Cd) variable, (2) a value of 0.4 for von Karman's
riable values are not identified.
lue of 0.0011 for the drag
; original sources of the va
recommends (1) a va
ess (AJ variable. Th<
This document
sublayer thickn


'ous Wastes . Attachment C, Draft Exposure Assessment
Waste. December 14.
^s T:
Level Risk Analyses at Combustion Facilities Burning Hazar
Office of Emergency and Remedial Response. Office of Soli
for Performing Screening
te Combustion Facilities.
vised Draft Guidance
CRA Hazardous Was
EPA. 1994. Re
Guidance for R
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3
lively. This document cites (1) Weast (1979) as its source of
U
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is cited as one of the
^and//a, and(2)U.
This document
information for


s the source of#, pw, and//,, variables of 1.2 x 103, 1, and 1.69 x
C3
;d. CRC Pres, Inc. Cleveland, Ohio. This document is cited ;
mistry and Physics. 60th e
RC Handbook of Che
ly.
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(Page 4 of 4)
2RENCES AND DISCUSS!
b








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'aste Combust
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NC DEHNR Protocol for Performing Indirect Exposure Risk A
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Asians. External Review Draft. Office of Research and
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to Combusto
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ddendum to the Methodology for Assessing Health Risks Assoc
Washington, D.C. November.
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5 that values from 0.01 to 0.05 meter would be appropriate.
= 1
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•.. Attachment C, Draft Exposure Assessment Guidance for
HJ
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Combustor Facilities Burnin
•aft Guidance for Performing Screening Level Risk Analyses at
us Waste Combustion Facility. April 15.
Q|
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ended value is the midpoint of an acceptable range. This
and db! is expected to be minimal either because informatil
;iated with the variables /^ and Cwo/ is largely associated
ium, use of default medium-specific values can result in
E jj 5 "g
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32 D. a
depth of upper benthic layer
of uncertainty associated wil
for a variable (dj,,) is narrow
iry widely in different locatio
is cited as one of the reference sources for the default value for
U.S. EPA (1993a) as the source of its information. The degree
hese variables is generally available (d^) or the probable range
default OC content values. Because OC content is known to va
:rtainty in some instances.
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variable is COPC- and site-specific, and is calculated by using the equation in Table B-2-1'
following uncertainty is associated with this variable:
All of the variables in Table B-2-17 are COPC- and site-specific. Therefore, the use of def
specific values, for any or all of these variables, will contribute to the under- or overestimal
The degree of uncertainty associated with the variables dm and dh, is expected to be minimi
for estimating a variable (d^) is generally available or because the probable range for a vai
uncertainty associated with the variables fm and Cwtol is associated with estimates of OC co
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uncertainty in specific cases.
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DISSOLVED PHASE WATER CONCENTRATION
(SURFACE WATER AND SEDIMENT EQUATIONS
(Page 3 of 3)




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REFERENCES AND DISCUSSION
NC DEHNR Protocol for Performing Indirect Exposure Risk Assessments for Hazardous Waste Combustion Uni
DEHNR 1997. .
U
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) as its sources of information regarding TSS, and
J3
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is cited as one of the sources for Kd, values and a default TSS value of 10. This document cites (1) U.S. EPA (1
as its source regarding Kd,.
This document
(2) RTI (1992)


ng Group Recommendations. Office of Solid
3
1
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.0
ddendum to the Methodology for Assessing Health Risks Associated with Indirect Exposure to Combustor Emiss,
ce of Research and Development. Washington, D.C. September 24.
^ £
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W &
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lie of 0.075 for surface water. The generic
ecific value; however, OCis medium-specific.
Kd, values by 7.5, because the OC value for
s source of the recommended TSS value.
•a g- o -s
> _i •£ x
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is cited by U.S. EPA (1994) and NC DEHNR (1997) as one of the sources of the range ofKd, value and the assu
Iculating partition coefficients (soil, surface water, and bed sediments) is as follows: Kdv = Kxj * OC,. Kx is a
'd, values was based on an assumed OC value of 0.01 for soil. Therefore, the Kdm values were estimated by mull
> 7.5 tunes greater than the OC value for soil. This document is also cited by U.S. EPA (1994) and NC DEHNR
This document
equation for ca
The range of A
surface water if


view Draft. Office of Research and
u
rv!
External 1
ddendum: Methodology for Assessing Health Risks Associated with Indirect Exposure to Combustor Emissions.
November.
EPA. 1993b. A
Development.
yi
b
le of 0.075 for surface water. The generic
Ecific. The range of Kd, values was based on an
ir surface water is 7.5 times greater than the OC
•a S"2
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•o ^ d
•o o u 3
1 SO 5
is cited by U.S. EPA (1994) and NC DEHNR (1997) as one of the sources of the range ofA^, value and the assui
Iculating partition coefficients is as follows: Kdv = Kxj * OC,. Kx is a chemical-specific value; however, OC is
ilue of 0.01 for soil. Therefore, the Kdm values were estimated by multiplying the Kd, values by 7.5, because the
Fhis document is also cited by U.S. EPA (1994) and NC DEHNR (1997) as the source of the recommended TSS i
This document
equation for cal
assumed OC va
value for soil. '


f C, Draft Exposure Assessment Guidance for
s
.«
1
"5
aft Guidance for Performing Screening Level Risk Analyses at Combustion Facilities Burning Hazardous Waste.
us Waste Combustion Facilities. April 15.
EPA. 1994. Dn
RCRA Hazardo
CO
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is cited as one of the sources of the range of Kd, values, citing RTI (1992) as its source of information.
This document



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variable is COPC- and site-specific, and is calculated by using the equal
following uncertainty is associated with this variable:
The default variable values recommended for use in the equation in Tal
-specific water body conditions. The degree of uncertainty associated i
to be limited either because the probable ranges for these variables are i
estimates is generally available.
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be significant in specific instances. Uncertainties associated with the v;
because of the summation of many variable-specific uncertainties.
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variable is COPC-specific, and should be determined from the COPC ta
following uncertainty is associated with this variable:
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variable is site-specific. U.S. EPAOSW recommends a default bed sedi
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eb, = i -BS /p,
is consistent with other U.S. EPA (1993b and 1994) guidance.
following uncertainty is associated with this variable:
To the extent that the recommended default values of BS and p, do not
body-specific conditions, 6bs will be under- or overestimated to some d
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0.5 to 1.5
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, U.S. EPA OSW recommends a default value of 1
tie reasonable for most applications. No reference
S. EPA (1993b and 1994) guidance.
associated with this variable:
ault value for BS may not accurately represent site
Csed may be under- or overestimated to a limited
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associated with this variable:
;s may not accurately reflect site-specific conditioi
- or overestimation of the variable Cscd. However,
TOW recommended range of default values.
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DISCUSSION
REFERENCES AND




zardous Waste Combustion Units. January.
DEHNR. 1997. NC DEHNR Protocol for Performing Indirect Exposure Risk Assessments for Ha.
U
z
993a; 1993b) as its source of
t value is the midpoint of an
lyer. This document is also cited as
_H *-H fc«
ro 3 ~^
liment porosity ( 6bs). This document cites U.S. EPA 1
t value for depth of the upper benthic layer. The defa
the range of values for the depth of the upper benthic
This document is cited as one of the reference source documents for the default value for bed sed
infonnation. This document is also cited as one of the reference source documents for the defaul
acceptable range. This document cites U.S. EPA (1993a; 1993b) as its source of information for
one of the reference source documents for the default benthic solids concentration ( BS).


•raft. Office of Research and
u
Exposure to Combustor Emissions. External Review
. EPA. 1993a. Addendum to the Methodology for Assessing Health Risks Associated with Indirect
Development. Washington, D.C. November 1993.
cr>
S
ir sediment. The generic equation for
1 is medium-specific. The range of
OC value for sediment is four times
lis equation was identified. This
<£
range of Kd, values and an assumed OC value of 0.04
This document is cited by U.S. EPA (1994) and NC DEHNR (1997) as one of the sources of the


y u
•43
'x * OC,. Kx is a chemical-specific value; however, O
imated by multiplying the Kd, values by 4, because th
alculating bed sediment porosity ( 6bs). No source of
source of this range was identified.
calculating partition coefficients (soil, surface water, and bed sediments) is as follows: Kdu = K
Kd, values was based on an assumed OC value of 0.01 for soil. Therefore, the Kdb, value was est


greater than the OC value for soil. This document is also cited as the source of the equation for c
document was also cited as the source for the range of the benthic solids concentration (BS). No


mendations. Office of Solid Waste
e
>sure to Combustor Emissions. Working Group Recoi
EPA. 1993b. Addendum: Methodology for Assessing Health Risks Associated with Indirect Expc
and Office of Research and Development. Washington, D.C. September 24.
CO
S
U
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1
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73
>ed sediment porosity value (6bs), the default benthic s
This document is cited by NC DEHNR (1997) and U.S. EPA (1994) as the source of the default I
range for depth of upper benthic layer (dbt) values.


posure Assessment Guidance for
t3
es Burning Hazardous Wastes. Attachment C, Draft 1
EPA. 1994. Draft Guidance for Performing Screening Level Risk Analyses at Combustor Faciliti
RCRA Hazardous Waste Combustion Facilities. April 15.
CO
S
as its source of information
lent cites U.S. EPA ( 1993a; 1993W
s- c
of 0.04 for sediment. This document cites RTI (1992
fault value for bed sediment porosity ( 6L). This docu
This document is cited as one of the sources of the range of Kd, values and an assumed OC value
regarding Kd, values. This document is cited as one of the reference source documents for the de


lit value is the midpoint of an
yer. This document is also cited as
.« «
t value for depth of upper benthic layer ( dbs). The def
the range of values for the depth of the upper benthic 1
as its source. This document is also cited as one of the reference source documents for the defaul
acceptable range. This document cites U.S. EPA (1993a; 1993b) as its source of information for I
one of the reference source documents for the default benthic solids concentration (BS).



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Cations and most Organics: 0.6
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Consistent with U.S. EPA (194b; 1995) in evaluating aboveground forage, U.S. EPA OSW recommends using tl
value of 0.2 for anions and 0.6 for cations and most organics. These values are the best available information, bi
on a review of the current scientific literature, with the following exception: U.S. EPA OSW recommends using
Fw value of 0.2 for the three organic COPC that ionize to anionic forms. These include (1) 4-chloroaniline, (2) i
nitrosodiphenylamine, and (3) n-nitrosodi-n-proplyamine (see Appendix A-2).
The values estimated by U.S. EPA (1994b; 1995) are based on information presented in Hoffman, Thiessen, Frai
and Blaylock (1992), which presented values for a parameter (r) termed the "interception fraction." These value
were based on a study in which soluble radionuclides and insoluble particles labeled with radionuclides were
deposited onto pasture grass (specifically a combination of fescues, clover, and old field vegitation) via simulate
rain. The parameter (r) is defined as "the fraction of material in rain intercepted by vegetation and initially retail
or, essentially, the product of Rp and Fw, as defined for use in this guidance:
r = Rp • Fw
The r values developed by Hoffman, Thiessen, Frank, and Blaylock (1992) were divided by an Rp value of 0.5 fi
forage (U.S. EPA 1994b). TheFw values developed by U.S. EPA (1994b) are 0.2 for anions and 0.6 for cations
insoluble particles. U.S. EPA (1994b; 1995) recommended using the Fw value calculated by using the r value fr
insoluble particles to represent organic compounds; however, no rationale for this recommendation is provided.
Uncertainties associated with this variable include the following:
(1) Values of r developed experimentally for pasture grass (specifically a combination of fescues, clover, and i
field vegitation) may not accurately represent all forage varieties specificto a site.
(2) Values of r assumed for most organic compounds, based on the behavior of insoluble polystryene
microspheres tagged with radionuclides, may not accurately represent the behavior of organic compounds
under site-specific conditions.
Varies (modeled)
This variable is COPC- and site-specific, and is determined by air dispersion modeling (see Chapter 3).
Uncertainties associated with this variable are site-specific.
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U.S. EPA OSW recommends thefcp value of 18 recommended by U.S. EPA (1993; 1994b).
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ton
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the midpoint of a possible range of values. U.S. EPA (1990) identified several processes— il
water removal, and growth dilution— that reduce the amount of contaminant that has been de

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surface. The term kp is a measure of the amount of contaminant lost to these physical proce
EPA (1990) cited Miller and Hoffman (1983) for the following equation used to estimate kp

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kp = (In 21 tl/2) • 365 days/yr
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t1/2 = half-time (days)
Miller and Hoffman (1983) report half-time values ranging from 2.8 to 34 days for a variety
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herbaceous vegetation. These half-time values result in kp values of 7.44 to 90.36 yr '. U.S
recommend a kp value of 18, based on a generic 14-day half-time, corresponding to physica

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Uncertainties associated with this variable include the following:

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processes would decrease half-times and thereby increase kp values; plant concentratil
« =g
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(2) The half-time values reported by Miller and Hoffman (1983) may not accurately repre
COPCs on plants.
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(3) Based on this range (7.44 to 90.36), plant concentrations could range from about 1 .8 ti
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This variable is site-specific. U.S. EPA OSW recommends the use of these defauli
s
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1997) recommended
essive grazing.
site-specific information. U.S. EPA (1990), U.S. EPA (1994b), and NC DEHNR (
a constant, based on the average periods between successive hay harvests and succ<


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For forage, the average of the average period between successive hay harvests (60
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ulating the COPC co
These average periods are from Belcher and Travis (1989), and are used when calc
in cattle forage.






The following uncertainty is associated with this variable:

1
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(1) Beyond the time frame of about 3 months for harvest cycles, if the kp value r
Tp values will have little effect on predicted COPC concentrations in plants.
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TABLE B-3-1






SITION
8.
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T CONCENTRATION DUE TO DIRECT D
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2






tfi
(TERRESTRIAL PLANT EQUATION!








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REFERENCES AND DISCUSSION






'ronmentally Released Radionuclides through Agriculture .
1
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Q£
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^ 2
U o
tfi
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ca
n
;s. Class-specific estimates of the empirical constant, y> were
n estimates of Rp and Yp.
z g
CA 3
.3 E
e x
lip developed by Chamberlain (1970) for other vegetation
ough several points, including average and theoretical ma
it proposed using the same empirical relations!
forcing an exponential regression equation thr
c ^
CO >>
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o g.
•a 2,
01 O
JS %
H T3


irt on Sensitivity and Uncertainty Analysis for the Terrestrial Food
Oak Ridge National Laboratory. Oak Ridge, Tennessee.
&§
of ;a
; RURA and Municipal Waste Combustion Projects: Final
, Office of Risk Analysis, Health and Safety Research Div
C.C.Travis. 1989. "Modeling Support for tht
" Interagency Agreement No. 1824-A020-A1,

•o -3
§"8
^!l
-i %
J U O
u
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03

eb
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CS
i period between successive hay harvests and successive g:
t recommends Tp values based on the average
c
documei
c«
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Tt
tH
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oveml
Science and Technology. Volume 22. Pages 361-367. N
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IR (1997) as the source of the equations for calculating Fv.
t is cited by U.S. EPA (1994a) and NC DEHN
c
documei
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00
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:tive Aerosols by Vegetation." Atmospheric Environment.
1970. "Interception and Retention of Radioac

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= Empirical constant; range provided z
= Standing crop biomass (productivity

(£• x. -?•
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f Radioactive Contaminants Deposited on Pasture Grass by
o
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992. "Quantification of the Interception and Initial Reten
:3313to3321.
I. Thiessen, M.L. Frank, and E.G. Blaylock. 1
n." Atmospheric Environment. Vol. 26A. 18
>; •—
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gamma-emitting radionuclides and insoluble particles tagged
d field vegetation, including fescue) via simulated rain. The
5 product of Rp and Fw, as defined by this guidance:
| 05
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srmed "interception fraction," based on a study in which si
ture grass (specifically, a combination of fescues, clover, i
tercepted by vegetation and initially retained" or, essential
t developed values for a parameter (r) that it tf
mitting radionuclides were deposited onto pas
s defined as "the fraction of material in rain in
n ^ ""
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r values obtained include the following:

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for anions, U.S. EPA (1994a) used the highest geometric mean r
1
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uble radionuclide iodide-131 [131I]); when calculating Rp '
ge of 0.006 to 0.3 for anions (based on the sol
(0.08) observed in the study.
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U.S. EPA (1994a) used the highest geometric mean r

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(Page 9 of 10)
luclide beryllium-7 [7Be]; when calcu
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micrometers, labeled with cerium- 141 [ l41Ce], [9SN]b,
janiline; n-nitrosodiphenylamine; and n-nitrosodi-n-
ers. However, no rationale for this selection was
JL *^
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ing in diameter fron
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ith a diameter of 3 i
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the geometric mean r value for IPM w
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. EPA (1994a) i
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le cation 7Be and the IPMs, r depends more on
egetation surface has become saturated, and (2) the
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mount, whereas for
ved with the water t
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(1) the anionic 131I is essentially remo'
iurface. This discrepancy between the
ca <_, •"
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also concluded
tie out on, the pi
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Ith Physics. 45 (3): 731 to 744.
c
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2.8 to 34 d;
half-time values ranging from :
The study reports
90.36 yr1.

















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(1982).


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                    APPENDIX C




MEDIA-TO-RECEPTOR BIOCONCENTRATION FACTORS (BCFs)






         Screening Level Ecological Risk Assessment Protocol



                      August 1999

-------
Screening Level Ecological Risk Assessment Protocol
Appendix C;  Media-To-Receptor BCF Values	August 1999

                                APPENDIX C

                            TABLE OF CONTENTS

Section                                                                Page

C-1.0  GENERAL GUIDANCE	C-l

C-l.l  SOIL-TO-SOIL INVERTEBRATE BIOCONCENTRATION FACTORS 	C-2

C-1.2  SOIL-TO-PLANT AND SEDIMENT-TO-PLANT BIOCONCENTRATION
      FACTORS	C-2

C-l.3  WATER-TO-AQUATIC INVERTEBRATE BIOCONCENTRATION FACTORS	C-3

C-l.4.  WATER-TO-ALGAE BIOCONCENTRATION FACTORS	C-4

C-1.5  WATER-TO-FISH BIOCONCENTRATION FACTORS	C-4

C-l.6  SEDEMENT-TO-BENTfflC INVERTEBRATE BIOCONCENTRATION FACTORS	C-5

C-l.7  AIR-TO-PLANT BIOTRANSFER FACTORS  	C-5

REFERENCES: APPENDIX C TEXT	C-9

TABLES OF MEDIA-TO-RECEPTOR BCF VALUES 	C-13

REFERENCES: MEDIA-TO-RECEPTOR BCF VALUES	C-99
U.S. EPA Region 6                                                  U.S. EPA
Multimedia Planning and Permitting Division                                   Office of Solid Waste
Center for Combustion Science and Engineering                                            C-i

-------
Screening Level Ecological Risk Assessment Protocol
Appendix C: Media-To-Receptor BCF Values	August 1999
                                         APPENDIX C

                                 MEDIA-TO-RECEPTOR BCFs

Appendix C provides recommended guidance for determining values for media-to-receptor bioconcentration
factors (BCFs) based on values reported in the scientific literature, or estimated using physical and
chemical properties of the compound.  Guidance on use of BCF values in the screening level ecological risk
assessment is provided in Chapter 5.

Section C-1.0 provides the general guidance recommended to select or estimate BCF values.
Sections C-l.l through C-1.7 further discuss determination of BCFs for specific media and receptors.
References cited in Sections C-l.l through C-1.7 are located following Section C-1.7.

For the compounds commonly identified in risk assessments for combustion facilities (identified in Chapter
2), BCF values have been determined following the guidance in Sections C-l.l through C-1.7.  BCF values
for these limited number of compounds are included in this appendix in Tables C-l through C-7 to
facilitate the completion of screening ecological risk assessments. However, it is expected that additional
compounds may require evaluation on a site specific basis, and in such cases, BCF values for these
additional compounds could be determined following the same guidance (Sections C-l.l through C-1.7)
used in determination of the BCF values reported in this appendix. For reproducibility and to facilitate
comparison of new data and values as  they become available, all data reviewed in the selection of the BCF
values provided at the end of this appendix are also included in Tables C-l through C-7.  References cited
in Tables C-l through C-7 (Media-to-Receptor BCF Values) are located following Table C-7.

For additional discussion on some of the references and equations cited in Sections C-l.l through C-1.7,
the reader is recommended to review the Human  Health Risk Assessment Protocol (HHRAP) (U.S. EPA
1998) (see Appendix A-3), and the source documents cited in the reference section of this appendix.

C-1.0          GENERAL GUIDANCE

This section summarizes the recommended general guidance for determining compound-specific BCF
values (media-to-receptors) provided in Tables C-l through C-7.  As a preference, BCF values were
selected from empirical field and/or laboratory data generated from reviewed studies that are published in
the scientific literature.  Information used from these studies included calculated BCF values, as well as,
collocated media and organism concentration data from which BCF values could be calculated.  If two or
more BCF values, or two or more sets of collocated data, were available in the published scientific
literature, the geometric mean of the values was used.

Field-derived BCF values were considered more indicative of the level of bioconcentration occurring in the
natural environment than laboratory-derived values. Therefore, when available and appropriate,
field-derived BCF values were given priority over laboratory-derived values. In some cases, confidence in
the methods used to determine or report field-derived BCF values was less than for the laboratory-derived
values. In those cases, the laboratory-derived values were used for the recommended BCF values.

When neither  field or laboratory data were available for a specific compound,  data from a potential
surrogate compound were evaluated. The appropriateness of the surrogate was determined by comparing
the structures of the two compounds. Where an appropriate surrogate was not identified, a regression
equation based on the compound's log K^ value was used to calculate the recommended BCF value.


U.S. EPA Region 6                                                                 U.S. EPA
Multimedia Planning and Permitting Division                                            Office of Solid Waste
Center for Combustion Science and Engineering                                                        C-l

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With the exception of the air-to-plant biotransfer factors (Bv), recommended BCF values provided in the
tables at the end of this appendix are based on wet tissue weight and dry media weight (except for water).
As necessary, reported values were converted to these units using the referenced tissue or media wet weight
percentages. The conversion factors, equations, and references for these conversions are discussed in
Sections C-l.l through C-1.7 where appropriate, and are presented at the end of each table (Tables C-l
through C-7).

C-l.l   SOIL-TO-SOIL INVERTEBRATE BIOCONCENTRATION FACTORS

Soil-to-soil invertebrate BCF values (see Table C-l) were developed mainly from data for earthworms.
Measured experimental results were primarily in the form of ratios of compound concentrations in a
earthworm and the compound concentrations in the soil in which the earthworm was exposed. As
necessary, values were converted to wet tissue and dry media weight assuming a moisture content (by
mass) of 83.3 percent for earthworms and 20 percent for soil (Pietz et al. 1984).

Organics For organic compounds with no field or laboratory data available, recommended BCF values
were estimated using the following regression equation:

                     log BCF= 0.819 log Km -1.146                              Equation C-l-1

        •       Southworth, G.R., J.J. Beauchamp, and P.K. Schmieder.  1978. "Bioaccumulation
               Potential of Polycyclic Aromatic Hydrocarbons in Daphnia Pulex." Water Research.
               Volume 12.  Pages 973-977.

Inorganics For inorganic compounds with no field or laboratory data available, the recommended BCF
value is equal to the arithmetic average of the available BCF values for other inorganics as specified in
Table C-l.

C-1.2   SOIL-TO-PLANT AND SEDIMENT-TO-PLANT BIOCONCENTRATION FACTORS

Soil-to-plant BCF values (see Table C-2) account for plant uptake of compounds from soil.  Data for a
variety of plants and food crops were used to determine recommended BCF values.

Organics For all organics (including PCDDs and PCDFs) with no available field or laboratory data, the
following regression equation was used to calculate recommended values:

               log BCF =  1.588 - 0.578 log K^                                     Equation C-l-2

        •       Travis, C.C. and A.D. Anns. 1988. "Bioconcentration of Organics in Beef, Milk, and
               Vegetation." Environmental Science and Technology. 22:271-274.

Inorganics For most metals, BCF values were based on empirical data reported in the following:

        •       Baes, C.F., R.D. Sharp, A.L. Sjoreen, and R.W. Shor. 1984. "Review and Analysis of
               Parameters and Assessing Transport of Environmentally Released Radionuclides Through
               Agriculture." Oak Ridge National  Laboratory, Oak Ridge, Tennessee.

The scientific literature also was searched to identify studies. Although U.S. EPA (1995a) provides values
for certain metals calculated on the basis of plant uptake response slope factors, it is unclear how the BCF

U.S. EPA Region 6                                                              U.S. EPA
Multimedia Planning and Permitting Division                                           Office of Solid Waste
Center for Combustion Science and Engineering                                                        C-2

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Appendix C; Media-To-Receptor BCF Values	August 1999
values were calculated or which sources or references were used.  Therefore, values reported in
U.S. EPA (1995a) were not used.

C-1.3   WATER-TO-AQUATIC INVERTEBRATE BIOCONCENTRATION FACTORS

Experimental data for crustaceans, aquatic insects, bivalves, and other aquatic invertebrates were used to
determine recommended BCF values for water-to-aquatic invertebrate (see Table C-3).  Both marine and
freshwater exposures were reviewed.  As necessary, available results were converted to wet tissue weight
assuming that invertebrate moisture content (by mass) is 83.3 percent (Pietz et al. 1984).

Orsanics Reported field values for organic compounds were assumed to be total compound concentrations
in water and, therefore, were converted to dissolved compound concentrations in water using the following
equation from U.S. EPA (1995b):

               BCF (dissolved) = (BCF (total) / fffl) - 1                                Equation C-l-3

        where
               BCF (dissolved)        =      BCF based on dissolved concentration of compound in
                                            water
               BCF (total)             =      BCF based on the field derived data for total
                                            concentration of compound in water
               jja                     =      Fraction of compound that is freely dissolved in the water
        and,
               ft,                     =      l/[l + ((DOCxKow)/10) + (POCxKow)]
               DOC                  =      Dissolved organic carbon, kilograms of organic carbon /
                                            liter of water (2.0 x 10^* Kg/L)
               Km                   =      Octanol-water partition coefficient of the compound, as
                                            reported in U.S. EPA (1994a)
               POC                  =      Paniculate organic carbon, kilograms of organic carbon /
                                            liter of water (7.5 x lO"09 Kg/L)

Laboratory data were assumed to be based on dissolved compound concentrations.

For organic compounds with no field or laboratory data available, BCF values were determined from
surrogate compounds or calculated using the following regression equation:

               log BCF = 0.819 x  log KoW - 1.146                                   Equation C-l-4

        •      Southworth, G.R., J.J. Beauchamp, and P.K. Schmieder. 1978. "Bioaccumulation
               Potential of  Polycyclic Aromatic Hydrocarbons in Daphnia Pulex." Water Research.
               Volume 12.  Pages 973-977.

Inorganics For inorganic compounds with no field or laboratory data available, the recommended BCF
values were estimated as the arithmetic average of the available BCF values for other inorganics, as
specified in Table C-3.
U.S. EPA Region 6                                                                U.S. EPA
Multimedia Planning and Permitting Division                                            Office of Solid Waste
Center for Combustion Science and Engineering                                                       C-3

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C-1.4  WATER-TO-ALGAE BIOCONCENTRATION FACTORS

Experimental data for both marine and freshwater algal species were reviewed. As necessary, available
results were converted to wet tissue weight assuming that algae moisture content (by mass) is 65.7 percent
(Isensee et al. 1973).

Organics For organic compounds with no field or laboratory data available, BCF values were calculated
using the following regression equation:

               log BCF = 0.819 x log K™ -1.146                                   Equation C-l-5

       •       Southworth, G.R., J.J. Beauchamp, and P.K. Schmieder.  1978.  "Bioaccumulation
               Potential of Polycyclic Aromatic Hydrocarbons in Daphnia Pulex." Water Research.
               Volume 12.  Pages 973-977.

Inorganics For inorganics, available field or laboratory data were evaluated for each compound.

C-1.5  WATER-TO-FISH BIOCONCENTRATION FACTORS

Experimental data for a variety of marine and freshwater fish were used to determine recommended BCF
values (see Table C-5). As necessary, values were converted to wet tissue weight assuming that fish
moisture content (by mass) is 80.0 percent (Holcomb et al. 1976).

For both organic and inorganic  compounds, reported field values were considered bioaccumulation factors
(BAFs) based on contributions of compounds from food sources as well as media. Therefore, field values
were converted to BCFs based on the trophic level of the test organism using the following equation:

               BCF = (BAF^ I FCMjjJ - 1                                         Equation C-l-6

       where
                            =      The reported field bioaccumulation factor for the trophic level "n"
                                    of the study species.
                     ,       =      The food chain multiplier for the trophic level "n" of the study
                                    species.

Organics Reported field values for organic compounds were assumed to be total compound concentrations
in water and, therefore, were converted to dissolved compound concentrations in water using the following
equation from U.S. EPA (1995b):

               BAF(dissolved) = (BAF(total) lffd) -1                               Equation C-l-7

       where
               BAF (dissolved)        =      BAF based on dissolved concentration of compound in
                                           water
               BAF (total)            =      BAF based on the field derived data for total
                                           concentration of compound in water
               ffd                    =      Fraction of compound that is freely dissolved in the water

       and,

U.S. EPA Region 6                                                              U.S. EPA
Multimedia Planning and Permitting Division                                            Office of Solid Waste
Center for Combustion Science and Engineering                                                       C-4

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Appendix C; Media-To-Receptor BCF Values	August 1999
               fju                    =      1 / [1 + ((DOC x K^) / 10) + (POC x K.J]
              DOC                 =      Dissolved organic carbon, Kg of organic carbon / L of
                                           water (2.0 x lO"06 Kg/L)
              Kow                   =      Octanol-water partition coefficient of the compound, as
                                           reported in U.S. EPA (1994a)
              POC                 =      Paniculate organic carbon, Kg of organic carbon / L of
                                           water (7.5 x lO"09 Kg/L)

Laboratory data were assumed to be based on dissolved compound concentrations.

For organics for which no field or laboratory data were available, the following regression equation was
used to calculate the recommended BCF values:

              log BCF = 0.91 x log K^ -1.975 x log (6.8E-07 x K^ + 1.0) - 0.786     Equation C-l-8

       •      Bintein, S., J. Deviflers, and W. Karcher. 1993. "Nonlinear Dependence of Fish
              Bioconcentrations on n-Octanol/Water Partition Coefficients." SAR and QSAR in
              Environmental Research. Vol.1. Pages 29-39.

Inorganics For inorganic compounds with no available field or laboratory data, the recommended BCF
values were estimated as the arithmetic average of the available BCF values reported for other inorganics.

C-1.6  SEDEMENT-TO-BENTHIC INVERTEBRATE BIOCONCENTRATION FACTORS

Experimental data for a variety of benthic infauna, worms, insects, and other invertebrates were used to
determine the recommended BCF values for sediment-to-benthic invertebrate (see Table C-6). As
necessary, values were converted to wet tissue weight assuming that benthic invertebrate moisture content
(by mass) is 83.3 percent (Pietz et al. 1984).

Orsanics For organic compound (including PCDDs and PCDFs) with no available field or laboratory
data, the recommended BCF values were determined using the following regression equation:

              log BCF = 0.819 x log K^ - 1.146                                   Equation C-l-9

       •      Southworth, G.R., J.J. Beauchamp, and P.K. Schmieder.  1978. "Bioaccumulation
              Potential of Polycyclic Aromatic Hydrocarbons in Daphnia Pulex." Water Research.
              Volume 12. Pages 973-977.

Inorganics For inorganic compound with no available field or laboratory data, the recommended BCF
values were estimated as the arithmetic average of the available BCF values for other inorganics.

C-1.7  AIR-TO-PLANT BIOCONCENTRATION FACTORS

The air-to-plant bioconcentration (Bv) factor (see Table C-7) is defined as the ratio of compound
concentrations in exposed aboveground plant parts to the compound concentration in air.  Bv values in
Table C-7 are reported on dry-weight basis since the plant concentration equations (see  Chapter 3) already
include a dry-weight to wet-weight conversion factor.
U.S. EPA Region 6                                                               U.S. EPA
Multimedia Planning and Permitting Division                                            Office of Solid Waste
Center for Combustion Science and Engineering                                                       C-5

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Appendix C; Media-To-Receptor BCF Values	
                                               August 1999
Oreanics  For organics (excluding PCDDs and PCDFs), the air-to-plant bioconcentration factor was
calculated using regression equations derived for azalea leaves in the following documents:

       •       Bacci E., D. Calamari, C. Gaggj, and M. Vighi. 1990. "Bioconcentration of Organic
               Chemical Vapors in Plant Leaves:  Experimental Measurements and Correlation."
               Environmental Science and Technology.  Volume 24. Number 6. Pages 885-889.

               Bacci E., M. Cerejeira, C. Gaggi, G. Chemello, D. Calamari, and M. Vighi.  1992.
               "Chlorinated Dioxins: Volatilization from Soils and Bioconcentration in Plant Leaves."
               Bulletin of Environmental Contamination and Toxicology. Volume 48. Pages 401-408.

Bacci et al. (1992) developed a regression equation  using empirical data collected for the uptake of
1,2,3,4-TCDD in azalea leaves and data obtained from Bacci et al. (1990). The bioconcentration factor
obtained was included in a series of 14 different organic compounds to develop a correlation equation with
Kg* and H (defined below). Bacci et al. (1992) derived the following equations:
        log Bvol = 1.065 log Kow  - log
;—)  - 1.654
 RT
                           (r  = 0.957)     Equation C-l-10
                             Bv =
                                       Pair •
        \ol
                                         Equation C-l-11
                                                 orage
        where
               Bv
               Pair
               Pforage
               Jwaler

               H
               R
               T
Volumetric air-to-plant biotransfer factor (fresh-weight basis)
Air-to-plant biotransfer factor (dry-weight basis)
1.19g/L(Weastl986)
770 g/L (Macrady and Maggard 1993)
0.85 (fraction of forage that is water—Macrady and Maggard
[1993])
Henry's Law constant (atm-nrVmole)
Universal gas constant (atm-nrVmole °K)
Temperature (25 °C, 298 °K)
Equations C-l-10 and C-l-11 are used to calculate Bv values (see Table C-7) using the recommended
values of H and Kow provided in Appendix A at a temperature (T) of 25 °C or 298.1 K. The following
uncertainty should be noted with use of Bv values calculated using these equations:
U.S. EPA Region 6
Multimedia Planning and Permitting Division
Center for Combustion Science and Engineering
                                           U.S. EPA
                                           Office of Solid Waste
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Appendix C; Media-To-Receptor BCF Values	August 1999
        •       For organics (except PCDDs and PCDFs), U.S. EPA (1993) recommended that Bv values
               be reduced by a factor of 10 before use.  This was based on the work conducted by U.S.
               EPA (1993) for U.S. EPA (1994b) as an interim correction factor.  Welsch-Pausch,
               McLachlan, and Umlauf (1995) conducted experiments to determine concentrations of
               PCDDs and PCDFs in air and resulting biotransfer to welsh ray grass. This was
               documented in the following:

                      Welsch-Pausch, K.M. McLachlan, and G. Umlauf.  1995.  "Determination of the
                      Principal Pathways of Polychlorinated Dibenzo-p-dioxins and Dibenzofurans to
                      Lolium Multiflorum (Welsh Ray Grass)". Environmental Science and
                      Technology.  29: 1090-1098.

               A follow-up study based on Welsch-Pausch, McLachlan, and Umlauf (1995) experiments
               was conducted by Lorber (1995) (see discussion below for PCDDs and PCDFs). In a
               following publication, Lorber (1997) concluded that the Bacci factor reduced by a factor
               of 100 was close in line with observations made by him through various studies, including
               the Welsch-Pausch, McLachlan, and Umlauf (1995) experiments. Therefore, this
               guidance recommends that Bv values be calculated using the Bacci, Cerejeira, Gaggi,
               Chemello, Calamari, and Vighi (1992) correlation equations and then reduced by a factor
               of 100 for all organics, excluding PCDDs and PCDFs.

PCDDs and PCDFs  For PCDDs and PCDFs, Bv values, on a dry weight basis, were obtained from the
following:

        •       Lorber, M., and P.  Pinsky.  1999. "An Evaluation of Three Empirical Air-to-Leaf Models
               for Polychlorinated Dibenzo-p-Dioxins and Dibenzofurans." National Center for
               Environmental Assessment (NCEA). U.  S. EPA, 401 M St. SW, Washington, DC.
               Accepted for Publication in Chemosphere.

U.S. EPA (1993) stated that, for dioxin-like compounds, the use of the Bacci, Cerejeira, Gaggi, Chemello,
Calamari, and Vighi (1992) equations may overpredict Bv values by a factor of 40.  This was because the
Bacci, Calamari, Gaggi, and Vighi (1990) and Bacci, Cerejeira, Gaggi, Chemello, Calamari, and Vighi
(1992) experiments did not take photodegradation effects  into account.  Therefore, Bv values calculated
using Equations C-10 and C-l 1 were recommended to be reduced by a factor of 40 for dioxin-like
compounds.

However, according to Lorber (1995), the Bacci algorithm divided by 40 may not be appropriate because
(1) the physical and chemical properties of dioxin congeners are generally outside the range of the 14
organic compounds used by Bacci, Calamari, Gaggi, and Vighi (1990), and (2) the factor of 40 derived
from one experiment on 2,3,7,8-TCDD may not apply to  all dioxin congeners.

Welsch-Pausch, McLachlan, and Umlauf (1995) conducted experiments to obtain data on uptake of
PCDDs and PCDFs from air to Lolium Multiflorum (Welsh Ray grass). The data includes grass
concentrations and air concentrations for dioxin-congener groups, but not the invidual congeners. Lorber
(1995) used data from Welsch-Pausch, McLachlan, and Umlauf (1995) to develop an air-to-leaf transfer
factor for each dioxin-congener group.  Bv values developed by Lorber (1995) were about an order of
magnitude less than values that would have been calculated using the Bacci, Calamari, Gaggi, and Vighi
(1990; 1992) correlation equations.  Lorber (1995) speculated that this difference could be attributed to
several factors including experimental design, climate, and lipid content of plant species used.

U.S. EPA Region 6                                                                U.S. EPA
Multimedia Planning and Permitting Division                                             Office of Solid Waste
Center for Combustion Science and Engineering                                                        C-7

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Lorber (1999) conducted an evaluation of three empirical air-to-leaf models for estimating grass
concentraions of PCDDs and PCDFs from air concentrations of these compounds described and tested
against field data. Bv values recommended for PCDDs and PCDFs in this guidance were obtained from the
experimentally derived values of Lorber (1999).

Metals  For metals, no literature sources were available for Bv values. U.S. EPA (1995a) quoted from the
following document, that metals were assumed not to experience air to leaf transfer:

        •       Belcher, G.D., and C.C. Travis.  1989. "Modeling Support for the RURA and Municipal
               Waste Combustion Projects: Final Report on Sensitivity and Uncertainty Analysis for the
               Terrestrial Food Chain Model." Interagency Agreement No. 1824-A020-A1.  Office of
               Risk Analysis, Health and Safety Research Division. Oak Ridge National Laboratory.
               Oak Ridge, Tennessee. October.

Consistent with the above references, Bv values for metals (excluding elemental mercury) were assumed to
be zero (see Table C-7).

Mercuric Compounds  Mercury emissions are assumed to consist of both the elemental and divalent
forms. However,  only small amounts of elemental mercury is assumed to be deposited (see Chapter 2).
Elemental mercury either dissipates into the global cycle or is converted to the divalent form. Methyl
mercury is assumed not to exist in the stack emissions or in the air phase.  Consistent with various
discussions in Chapter 2 concerning mercury, (1) elemental mercury reaching or depositing onto the plant
surfaces is negligible, and (2) biotransfer of methyl mercury from air is zero. This is based on assumptions
made regarding speciation and fate and transport of mercury from stack emissions.  Therefore, the Bv value
for (1) elemental mercury was assumed to be zero, and (2) methyl mercury was assumed not to be
applicable. Bv values for mercuric chloride (dry weight basis) were obtained from U.S. EPA (1997).

It should be noted that uptake of mercury from air into the aboveground plant tissue is primarily in the
divalent form.  A part of the divalent form of mercury is assumed to be converted to the methyl mercury
form once in the plant tissue.
U.S. EPA Region 6                                                                U.S. EPA
Multimedia Planning and Permitting Division                                            Office of Solid Waste
Center for Combustion Science and Engineering                                                        C-8

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Bacci E., D. Calamari, C. Gaggi, and M. Vighi.  1990.  "Bioconcentration of Organic Chemical Vapors
       in Plant Leaves:  Experimental Measurements and Correlation." Environmental Science and
       Technology.  Volume 24.  Number 6.  Pages 885-889.

Bacci E., M. Cerejeira, C. Gaggi, G. Chemello, D. Calamari, and M. Vighi.  1992.  "Chlorinated Dioxins:
       Volatilization from Soils and Bioconcentration in Plant Leaves." Bulletin of Environmental
       Contamination and Toxicology. Volume 48. Pages 401-408.

Baes, C.F., R.D. Sharp, A.L. Sjoreen, and R.W. Shor. 1984.  "Review and Analysis of Parameters and
       Assessing Transport of Environmentally Released Radionuclides through Agriculture." Oak Ridge
       National Laboratory. Oak Ridge, Tennessee.

Belcher, G.D., and C.C. Travis. 1989.  "Modeling Support for the RURA and Municipal Waste
       Combustion Projects: Final Report on Sensitivity and Uncertainty Analysis for the Terrestrial
       Food Chain Model." Interagency Agreement No. 1824-A020-A1.  Office of Risk Analysis, Health
       and Safety Research Division. Oak Ridge National Laboratory. Oak Ridge, Tennessee. October.

Bintein, S., J. Devillers, and W. Karcher. 1993.  "Nonlinear Dependence of Fish Bioconcentrations on n-
       Octanol/Water Partition Coefficients." SAR and QSAR in Environmental Research.  Vol.  1.
       Pages 29-39.

Holcombe, G.W., D.A. Benoit, E.N. Leonard, and J.M. McKim,  1976. "Long-term Effects of Lead
       Exposure on Three Generations of Brook Trout (Salvenius fontinalis)."  Journal, Fisheries
       Research Board of Canada. Volume 33.  Pages 1731-1741.

Isensee, A.R., P.C. Kearney, E.A. Woolson, G.E. Jones, and V.P. Williams.  1973.  "Distribution of
       Alkyl Arsenicals in Model Ecosystems."  Environmental Science and Technology.  Volume 7,
       Number 9. Pages 841-845.

Lorber, M.  1995. "Development of an Air-to-plant Vapor Phase Transfer for Dioxins and Furans.
       Presented at the 15th International Symposium on Chlorinated Dioxins and Related Compounds".
       August 21-25, 1995 in Edmonton, Canada. Abstract in Organohalogen Compounds.
       24:179-186.

Lorber, M., and P. Pinsky. 1999.  "An Evaluation of Three Empirical Air-to-Leaf Models for
       Polychlorinated Dibenzo-p-Dioxins and Dibenzofurans." National Center for Environmental
       Assessment (NCEA). U. S. EPA, 401 M St. SW, Washington, DC. Accepted for Publication in
       Chemosphere.
U.S. EPA Region 6                                                               U.S. EPA
Multimedia Planning and Permitting Division                                           Office of Solid Waste
Center for Combustion Science and Engineering                                                        C-9

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McCrady, J.K., S.P. Maggard.  1993.  "Uptake and Photodegradation of
       2,3,7,8-Tetrachlorodibenzo-p-dioxin Sorbed to Grass Foliage." Environmental Science and
       Technology.  27:343-350.

Pietz, R.I., J.R. Peterson, J.E. Prater, and D.R. Zenz.  1984.  "Metal Concentrations in Earthworms From
       Sewage Sludge-Amended Soils at a Strip Mine Reclamation Site." J. Environmental Qual.
       Vol. 13, No. 4. Pp 651-654.

Southworth, G.R., J.J. Beauchamp, and P.K. Schmieder.  1978. "Bioaccumulation Potential of Polycyclic
       Aromatic Hydrocarbons in Daphnia Pulex."  Water Research. Volume 12. Pages 973-977.

Travis, C.C., and A.D. Arms.  1988. "Bioconcentration of Organics in Beef, Milk, and Vegetation."
       Environmental Science and Technology. 22:271-274.

U.S. EPA.  1993. Review Draft Addendum to the Methodology for Assessing Health Risks Associated
       with Indirect Exposure to Combustor Emissions.  Office of Health and Environmental
       Assessment. Office of Research and Development. EPA-600-AP-93-003. November 10.

U.S. Environmental Protection Agency (U.S. EPA). 1994a. Draft Report Chemical Properties for Soil
       Screening Levels. Prepared for the Office of Emergency and Remedial Response. Washington,
       D.C. July 26.

U.S. EPA.  1994b. Estimating Exposure to Dioxin-Like Compounds. Draft Report. Office of Research
       and Development. Washington, D.C.  EPA/600/6-88/005Ca,b,c.  June.

U.S. EPA.  1995a. Review Draft Development of Human Health-Based and Ecologically-Based Exit
       Criteria for the Hazardous Waste Identification Project. Volumes I and JJ.  Office of Solid
       Waste. March 3.

U.S. EPA.  1995b. Great Lakes Water Quality Initiative Technical Support Document for the Procedure
       to Determine Bioaccumulation Factors. EPA-820-B-95-005.  Office of Water, Washington, D.C.
       March.

U.S. EPA.  1997. Mercury Study Report to Congress, Volumes I through VIII. Office of Air Quality
       Planning and Standards and ORD.  EPA/452/R-97-001.  December.

U.S. EPA.  1998. Human Health Risk Assessment Protocol for Hazardous Waste Combustion Facilitites.
       External Peer Review Draft.  U.S. EPA Region 6 and U.S. EPA OSW. Volumes 1-3.
       EPA530-D-98-001A.  July.

Veith, G.D., K.J. Macek, S.R. Petrocelli, and J. Carroll. 1980.  "An Evaluation of Using Partition
       Coefficients and Water Solubility to Estimate Bioconcentration Factors for Organic Chemicals in
       Fish."  Pages 116-129. In J. G. Eaton, P. R. Parrish, and A.  C. Hendricks (eds.), Aquatic
       Toxicology.  ASTM STP 707. American Society for Testing and Materials, Philadelphia.
U.S. EPA Region 6                                                               U.S. EPA
Multimedia Planning and Permitting Division                                            Office of Solid Waste
Center for Combustion Science and Engineering                                                      C-10

-------
Screening Level Ecological Risk Assessment Protocol
Appendix C; Media-To-Receptor BCF Values	August 1999
Welsch-Pausch, K.M. McLachlan, and G. Umlauf. 1995.  "Determination of the Principal Pathways of
Polychlorinated Dibenzo-p-dioxins and Dibenzofurans to Lolium Multiflorum (Welsh Ray Grass)".
Environmental Science and Technology. 29: 1090-1098.

Weast, R.C. 1986. Handbook of Chemistry and Physics.  66th Edition. Cleveland, Ohio. CRC Press.
U.S. EPA Region 6                                                                U.S. EPA
Multimedia Planning and Permitting Division                                            Office of Solid Waste
Center for Combustion Science and Engineering                                                       C-l 1

-------
Screening Level Ecological Risk Assessment Protocol
Appendix C: Media-To-Receptor BCF Values	August 1999
                      MEDIA-TO-RECEPTOR BCF VALUES


                  Screening Level Ecological Risk Assessment Protocol

                                August 1999
C-l   SOIL-TO-SOIL INVERTEBRATE BIOCONCENTRATION FACTORS   	C-15

C-2   SOIL-TO-PLANT AND SEDIMENT-TO- PLANT BIOCONCENTRATION
      FACTORS               	C-29

C-3   WATER-TO-AQUATIC INVERTEBRATE BIOCONCENTRATION FACTORS ... C-36

C-4   WATER-TO-ALGAE BIOCONCENTRATION FACTORS	C-54

C-5   WATER-TO-FISH BIOCONCENTRATION FACTORS	C-66

C-6   SEDEMENT-TO-BENTfflC INVERTEBRATE BIOCONCENTRATION
      FACTORS	C-85

C-7   AIR-TO-PLANT BIOTRANSFER FACTORS	C-96

REFERENCES 	C-99
U.S. EPA Region 6                                                  U.S. EPA
Multimedia Planning and Permitting Division                                   Office of Solid Waste
Center for Combustion Science and Engineering                                          C-13

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0
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-day exposi
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PCB congeners.
factor of 5.99°.
11
h* en
3 =3
x >
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cd
i§ 00

ll
> op
f!
;an of 7 lab
'eight over

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oo










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CC
O
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^£
TABLE C-1
JRATE BIOCONCENTRATION F
et tissue) / (mg COPC/kg dry soil)
(Page 6 of 14)
NH i
w ^
a ^
w w
i|
^ DJD

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cc




















on
V
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Experimental Parameters







References









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a
^
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e



















Nitroaromatics


























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1
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N

o
1
•s
5
rA
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•o
3
O
d.
1






.2
'cd
1
O
«
£*
80
.S
_o
S
1
op
B
*55
3
irrogate compound. The BCF was calculated
here log K^, = 1.491 (U.S. EPA 1994b).

fcl •
ll
"efl *^
ll
o S

nzene or for a stn
eauchamp, and Si
ti CQ
"O rf
.fi "§
S o
^1
?1

U TT
J-
'3 's
a icf
g on
u o
9 ~~
a £

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•c "
f&
g EQ
O oo
Z -2

o
m
u
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edBCF
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B
U
E
o
o
o
05



















1
_3
"S
g
'S
5
4
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C
S
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C-
1






B
_O
3
ty
u
c
_o

o
00
ti
80
_B
|
"o
O
•s
80

3
rrogate compound. The BCF was calculated
here log K,,w = 1.996 (U.S. EPA 1994b).
3 S
« *
|f
"S *" '
fl
3 _a
O 0
uene or for a stru
eauchamp, and Si
2 «
O r^
5 t5

4 •§

0 TT
•8^
1 '*
M i*j°
i>
l-i 80


ca "*
ri i
— °°
~a o
'C "
fB
u CQ
0 80
Z 2.

"1
, _g
S u
or for a structura
eauchamp, and Si
B m
U ^J
C &

11
S o

JO -
edBCF
-o
g
S
1
u
05


















o
i
1

•a
|
o
5
c
p (




•o
c
3
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1


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.2
ed
CT*
o
CA
S
80
0
tH
80
B
|
2
u
fi°
*60
3
•o
J3
3
lilar surrogate compound. The BCF was calc
here log K,,,, = 4.640 (U.S. EPA 1994b).
C S
«5 ^^

S T^
1-1
cd ^
Wi U
itrobenzene or fo
eauchamp, and Si
§ H
tH yj*
J C

| 1
ll
1H CO
O ^
* vo

^2 Z:
'3 's
18 ^
1^ 80
o c

ca **
ca o
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"a d
•c "
§ CQ
o oo
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g
CO
^^
cJ
^
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>
edBCF
"O
1
E
1
u


















S

1
•a
>^\
x
1

ts
fN
23
CQ




•o
c
3
O
O.
1

e
o
C8
3
§•
8
g
w
"co
1

80
B
*>
_o
1
u
80
'S3
^
s
•3
^
imilar surrogate compound. The BCF was ca
'here log K,,w = 5.205 (U.S. EPA 1994b).
53 ?

= oo~
ISj
^ k4
3 o
CO 4>
cd 'a
t-i _g

:xyl)phthalate or i
eauchamp, and S
S w
>, j-"
* 1
o o
il
s|

a> ^-
1 ^
> :

S 80
U o

ca *
n 2
"3 d
O j.
o CQ
O oo
Z 5
00
cs
f— *
c*^
u
3
"3
>
ed BCF
•a
B
U
E
|
Ct5



















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JM
•g.

ti
^
^
Q




•a
c
3
O
Q
1





s
_o
1
1

Cfl
00
22
.s

_o
2
u

fiO
c
"CQ
•»4
iurrogate compound. The BCF was calculatec
'here log K^ = 9.330 (U.S. EPA 1994b).

c3
^ *"
.§&
ce ;2

fj


thalate or for a st
eauchamp, and S
n,
f"


'•3 0
8 ^

jo ^3-
Jl ^
'a '
> *
a ^
£ 80
U Q

ca *
a 2
"3 d
- 11
£
!i

-------











l-H
U
s
ea
iS














c«
OS
O
H
O
^






























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d

S
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>
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U
pa
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o
c
2
u
u
<




-H
c
3
O
E
d

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00
*^
Ov
00


&
CQ

,2
r"
ion equatioi
8
U
00
2
00
£
1
:ompound.The BCF was calculated using the :
arickoff and Long 1995).
o X


o* <»
§ o
£ "
•i *
fl
co 00
ca C-
t-l
<£ ^
°l
° .s
° §
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,2 c
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13 £
ca -5
y 3
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u
•fi
1


<




•a
c
1
E
o
U










c
Q
'S
3
rr
regression ei
00
_c

_o
"S
&
o
H>c§
5ate compound. The BCF was calculated usii
where log K^ = 0.250 (Karickoff and Long 1
•"* X^
tj OO

3 ^
-2 S3
E.1
r for a structurally-si
auchamp, and Schm
0 V
u, «
"S o
">>•£
0 3
CB O
n 00
o •—*

JO rT

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ca ^f

1.H 00
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CJ u
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00
fN

U
13
^
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S
cS
o
S

2
U




-o
c
1
E
o
U











c
_o
SB
;ression equ
S

oo
•S
^o
1
£
ite compound. The BCF was calculated using
where log K,,,, = 1.949 (U.S. EPA 1994b).
ob /-^
o oo

W3 ^^

C >*H
for a structurally-sir
auchamp, and Schm
to u
O pQ
-,
/^
5 1
*cc ^
rrogate compound. The BCF was calculated u
where log K^, = 0.55 (Based on equations de
3 X.
X 00

— 2
il

e or for a structurall;
auchamp, and Schm
•o o
_c ®
2€
«J O
S|
S 3
S 0
s^
^ VO
_o ^
_ca ^
> s
CB i^f

If

1 2
2 S
ca o
CJ |.
"C
'^ u
§ CQ
O 00



s
o

u
la
^
[L.
U
pa
1

Recomme























u
c
CB
X
0
5

~




•a

3
o
a.
3










c
_o
3
jgression eq
*-
OO
c
"%.
.2
u
£
&o
;ate compound. The BCF was calculated usin:
where log K^ = -0.268 (U.S. EPA 1995a).
DU ^i
2 °°

CQ i— t
3 QJ
Eu
.— 1
• for a structurally-si
auchamp, and Schm
o ^
o ®
gf
II
^- 3
— O


JU Tj-

1 '*
CS k^P

i_ dc
OJ o
cd *^
"cd ON
"° oo
"e3 O
cj u
"C
§ pa
O 00



s
o

'i
13
^
0-
o
pa
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e
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o
•a
•§
3
cd


c
u.




"O
J2
3
O
S
d
00
x
2
00
d
II
p.
u
m
oo
_o
c
.2
3
CT
ol
; regression <
00
c

i
_0
£
u
.2
ogate compound. The BCF was calculated us
, (U.S. EPA 1995a).
c 2:
§ 2;

S3 ^
r« "
"cfl *
or for a structurally-
ler 1978), where log
«> 0
"O .2s
1 ~°
O TO
* m
^ D«

U J=
"§ 1
'f «
CB J

o o
ca •£
^ o

"3 ^
0 VO
' C ^-
I""'
u '
l«§



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VO
C5

U
3
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^
&
pa
1

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u
•o
1
u
•5,
3





•y
c
3
O
a.
1
00
JO
X
Ov
oo
O

&
pa
r?
,2
§

ed
9
?
g regression
c
"S
5

(u
•S
s°
ogate compound. The BCF was calculated u:
i (U.S. EPA 1994b).
c S

cfl ^
s -

-a *f
or for a structurally-
ler 1978), where log
(O g
r2 '^
*6 w
>> c
.£ 3
^ "
hN M*

U JO
II

<« -

<3 o
$ *
i~|
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I
H
U
ta
TABLE C-1
KTEBRATE BIOCONCENTRATION
:/kg wet tissue) / (mg COPC/kg dry soil
(Page 8 of 14)
uJ LJ
p*^ ^r
||
T!» ^^^
6
H
Q
BC




















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1











S8
Experimental Parametel




.eferences
cc


IB

C
.•
0
p>
^
a
^
S
i
c
D























Other Chlorinated Organics





















o


o
3

>
&
n
•o
1

g
8
^













3on Tetrachloride

ra
u




•B
p
o
Q,
1









c
o
•a
CS
3
O*
U
_o
'53
eh
££
00
_n
23
o
u
g
'1
1
similar surrogate compound. The BCF was calcul
978), where log K^ = 2.717 (U.S. EPA 1994b).

structurally
Schmieder
es -a
£8
S §•
o c3
•"g -S
s 1
11
available for carbon tetri
<„„ - 1.146 (Southworth,

tH OO
0 0
s —
=a **
ra ^
- »
"3 d
•c "

o CC
0 00
Z. .2



VD
O\


i5

"3
U
n
•g
T3
g
a
g
o













achlorobenzene
X

K




•y
3
O
C
1









C
o
1
u
c
_o
CO
OO
2
1?
j

i2
U
.S
•3
1
imilar surrogate compound. The BCF was calcul
978), where log K^, = 5.503 (U.S. EPA 1994b).
CO »— <
structurally-
Schmieder
T3
S |
§1
i §
c u
^ CQ
available for hexachloro
K,,,, - 1.146 (Southworth,

^ oo

& -^

"ca ^
— °°
"3 d
•n ii

1 pa
o oo
Z 2





*o
en

u
3
"3
tt,
O
09

•o
§
g
g
0













achlorobutadiene
X
u
EC




•a
c
3
g
O
U








c
_o
!
£
.2
*co
en
O
60
c
1
Ig

u
J3
00
'S
3
1
JS
^
-similar surrogate compound. The BCF was calci
978) where log K^, = 4.731 (U.S. EPA 1994b).

i structural!;
Schmieder
~ -o
a §
g $
u 5
ll
•3 i
3 «
J CQ
available for hexachloro
KDW- 1.1 46 (Southworth,

1- Ol

^ "**
« !x:
*- ON
"° OC
"« o
:^i

§ cc





J*

U

"3
B
CQ
•a
u
1

C
8













:achlorocyclopentadiene
K
(U
p~*




•y
c
3
0
Q.
1
U





g
3
3
cy
u
'«
CA
K
00
00
'1
JD
1
1
00

*co
3
T3
3
•3
o
•3
u
Cfl
turally-similar surrogate compound. The BCF wa
1978), where log K^ = 4.907 (U.S. EPA 1994b).
CJ ^^
or for a strui
Schmieder

X
*S3
«
*2
ni
r *.
0
t-^
Q

tig the geometric mean of 13 laboratory values for
ight using a conversion factor of 5.99a.
.»* u
alculated us
over dry wi
0 V
BCF was
wet weigl
J3 -2
P "8
DDE were not available.
3ish (1980) were conver

^ . "Q
~- C
"^r rt
O flj
.,
« u
-a TJ
5 ca
:s i?
a, t-~
g 2
W C-










1
c2
fc
1
.S
'C
1






Chronic exposure







Davis (1971)







o\ —
d d

oo o\
O C-.
d d

-------






cc

PS
B
U
<
fe
^ s^
ll
H -^
3 ^
^1 >H
TABLE C-1
ATE BIOCONCENTR
tissue) / (mg COPC/kg <
Page 9 of 14)
& ~ -
M V
w s
w *
H Sf
OS <£
(3 U
z" o
HH r *i
iJ ec
^•4 M
8^
6
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j
0
t»
















w
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v.







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a
Experimental P,







eferences
A



"«
u
9
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>•

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w
I*
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p;
s
W
S





Aporrectodea trapezoides
Aparrectodea turgida
Allolobophora chlorotica
Lumbricus terrestris











hronic exposure
U







ON
f— <
'Xrf'
•9
5
1
8
>-.
o
n








f>
00
d





Not specified











hronic exposure
U






/— N
OO
vo
CN
la
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§
£
to
0>
£





o o o
(N VO >O
— Tt — '

in O O
oo •*<• 
£








Svo
^r
O rfj


o
•*
— ;
u
Recommended BCF Valu























eptachlor
E




-o
c
D
O
o,
o
O
to wet
•o
u
S
^
c
o
o
in Beyer and Gish (1980) was

*o
c
I
1M
u
3
"3
>
u
o
•o

.tory value for heptachlor epo>
ra
|
•O
J2
—
00
C
"oo
S
1
JS
3
BCF was calc
99".
liable. The
factor of 5.'
5 e
£ .2
ll
M
> C3
g g>
l!
ex -^
u oo
-= •«
^ >•
^5 ?
<*" >,
s £
M ^
•o S
S °
13 £
£X M
S w
a &





Aporrectodea trapezoides
Aparrectodea turgida
Allolobophora chlorotica
Lumbricus terrestris











hronic exposure
U






y^S
8
2
tn
5
T3
i
u
n








o
•*
o
t--
<*„
8

u
Recommended BCF Valu





















S
1
1
2
u
03
S
ac




-b
c
3
O
tx
1
U





wing regression equation:
0

2
1
00 ^
.g vi
3 2
1 «
•2 R
g J
— -a
3 ^
U CB
ate compound. The BCF was
re log K™ = 7.540 (Karickoff
bo o
s •§
5
H gf
— 0\
1?
i*^
ll
or for a struct
:hamp, and Sc
II
f™
H
J3 O
s I
x -S
U 3
-C 0
£ S£
« yo
jj -q-
X) *~i
_« -^
03 J^
O
1— CD
> .2
« x
P3
*-t {•*.
C3 2
•° x
It
C "
"5, Q-i
g U
u CQ
O OC
2 ^
















Inorganics























S
d
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minum \v
copper, I
-i E
u. 3
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ta j:
T3 0
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tl
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fM
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o!
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copper, I
1 E
>-, 3
o "5
<" C
5 8
a x>
"O o
"3 p"
rj C
1 1
11


,— *
,— i
d
i>
Recommended BCF Valu























_0
"H
u
tn
-5




T3
C
D
a
i

-------














x
o
H
u
^j
ta
51
M !*>
< •«
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fig
- H sr
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Reference:







eft
1
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^-
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00
1

Si
?
o
"u
0
1
00
00
ON
J
•o
h«
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g
53

u
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1
elow. The values repoi
i
•-H
e«
o3
O
"5
<§

u
_p3
C3

C*
I
V!
O
g
u
E •
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fi ON
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8»

| 1
ulated using
conversion !
u &
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u c
s 3
0. •§)
iC b1
P -8












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exposure
"V
00












id Lee (1988
§
•>
u.
55
•f
u
s


o r^
d d
2 2 o
d d d






"3
n
Recommended
































Barium


•o
c
3
O
O,
1
U

g"

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u
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u
cn
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1
'3
empirical data <
C1
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oo
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C
U
cn
1
Ui
£
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f the recommended val
o
Sea

o
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H
1
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5
cn
B-
U
03
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recommends
and zinc).
o 73
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o 1
is
> o
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i i
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Beryllium


•y
c
1
o
rj





o
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c3
u
3
ca
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th empirical dai
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Cadmium


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c
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u

>
/— V
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u
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ca
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id Simmers, Rhi
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ed
w
E
E
5i
'alues reported in Rhett
i*-
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B
3
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T3
ca
u
l-t
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3 ON
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exposure
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d

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Chromium


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-------














I
H
fa
Z S
TABLE C-l
IRATE BIOCONCENTRATIO
et tissue) / (mg COPC/kg dry so
(Page 11 of 14)
3 *
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W U
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1
1
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T3
Compoun
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E
T3
ia
u
o"
'£
u
CO
5-

U
3
BJ

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cd
:h empirical data
.a
S
c
'i
o
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1
M
"e3
1
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c
tic mean of the recomme
u
«
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&(2
ra
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ai
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if
l|
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.,- s
were not available
lorganic mercury, i
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rt rt
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rt Cli

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chromiuin





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d
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2
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e
o
u
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u
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^^
1
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00
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5
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g
1
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te values reported in Rhe
S
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5
CQ
>>
1
II
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2
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wet weigh













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oo
00
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§
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E








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CN O r-
O O O
odd













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Ma (1987)








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d













Not specified






















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o\
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d













Alabophera sp.
Lumbricus sp.
Octolasium sp.










Chronic exposure









^
ON
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1
1








en
O
d





s
d
o
3
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tt.

Recommended






















ric chloride
3
I




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1-
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i,
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*-
(U
?
2
T3

1988) were conv
and Lee (
2"

e
V)
i
g
t>
Q
O.
; chloride. The values re
1
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1
JM
CQ
^3
1
o
I
3
V)
•s
u
E
sing the geometric
factor of 5.99*.
3 S
"S -I
"3 g
^— o
CO (J

KJ OJ)
^ C
IThe BCF
weight us:













Eiseniafoetida
8 |
1^1 "s
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111
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28-day exposure; tissue
reported for the first thi
concentration of 0.05 w
conservative BCF valui






00
00
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u
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I
1






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00
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1 mercury
f
1




•y
Compoun
S3
§
t .

00
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1
^
—
g
o
f
1
snt (1985) were e
and Momi
o"

!*
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11
CQ S
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1J K

1 below. The values repo
'eight to result in the vah
! b
8 *
2 2
8 I
•i °
CO
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0 £
§!,
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fla j^
O cc
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£
sing the geometric
rcent soil moisture
3 O
0) O
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2
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u
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1
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fat
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References




a
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o
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>
a.
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o
2
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1
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CN
d
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1
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1 Compound:

g"
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03
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2
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empirical dat
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mic mercury, i
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S T3
1 Empirical data for
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04
d
o

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ra
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03
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t)
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ca
n
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ith empirical
>
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u
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u
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09
; recommended BCF
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~ o
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re not availabl
inic mercury,
II
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Empirical data for
1 chromium, copper,
                                                                                                                                               55
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tt,
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lation equivalenc;
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.
lation equivalenc
3


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3
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d
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8
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en
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d

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^
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73

u
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A















Pteronarcys dorsata











\
X
u
1
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g
&
1
^
O
Mayer et al. (
(1980b)






o
TJ-
t~-
















Corydalus cornutus











2
3
a
X
u
1
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r-
1
c
1
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GO
cd
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Mayer et al. (
(1980b)






8

















Orconectes nais











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Nereis diversicolor











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1
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(1980b)






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Penaeus duorarum











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Crassostrea virginica











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Courtney and
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13
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fli
e
g
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14 to 28-day exposure duration





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30-day exposure duration
14-day exposure duration; The reported \
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factor of 5.99".

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27-day exposure duration








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nded BCF Value:
u
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T3
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1
5



Compound:




























CO*
ues as folk
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c
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nded BCF Value:
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Acetone



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d,
i
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5
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1
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VO
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j
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2
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ated using
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tu
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inyl chloride
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a.


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CO
1
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6
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d Organics
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cs


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3
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arbon tetrachloride
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ex
C
ra
JC
u
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0
2
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gp
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en
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S
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31.2

lf>
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exachlorobenzene
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as follows:
en
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ed
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cd
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o
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3
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g
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xposure duratior
u
S
i
o
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adic(1996)
3
1
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cs
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duration
2
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Cfl
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43 C^
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duration
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ing the geometric mea
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C
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s calculated using the
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u
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8
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I
1



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CA
a
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CA
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0
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CA
Oi
s
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CA
ca
CA
U
3
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ic mean of 5 labor
§

1
u
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OO
c
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1
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8
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28-day exposure duration


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14-day exposure duration; the re
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TABLE C-3
WATER-TO-AQUATIC INVERTEBRATE BIOCONCENTRA
(mg COPC / kg wet tissue) / (mg dissolved COPC / L
(Page 18 of 18)



















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Experimental Parameters
Reference




GR
u
5
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presented as the amount of COPC in invertebrate tissue divided by the amount of CO
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ss an invertebrate's total weight is 83.3 percent moisture, which is based on the moisl
is calculated as follows:
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(total) /fw)-l
1) = BCF based on dissolved concentration of COPC in water
JCF based on the field derived data for total concentration of COPC in water
f COPC that is freely dissolved in the water
1 / [1 + ((DOC x K,,w) / 10) + (POC x K™)]
= Dissolved organic carbon, kilograms of organic carbon / liter of water (2.0 x Ifr06
= Octanol-water partition coefficient of the COPC, as reported in U.S. EPA (1994b)
= Paniculate organic carbon, kilograms of organic carbon / liter of water (1.5 x 10 w
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af

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18
TABLE C-5
FISH BIOCONCENTRAT
wet tissue) / (mg dissolved
(Page 7 of 19)
3?


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Not reported






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Pimephales promela
Cyprinodon variegai

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U.S. EPA (1987)





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Freshwater fish
Recommended BCF






i

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; ' en
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U.S. EPA (1980h)
Oliver and Niimi (1988)
llorobutadiene
lue was calculated using the geome
1 >
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0 «n "c
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1





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Laska, Bartell, Laseter (1976)
llorocyclopentadiene
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follows:
laboratory values as
8
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Gates and Tjeerdema (1993
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28-day exposure duration
Id values.
Field samples. The field values reported in Saiki,
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converted to wet weight using a conversion factor of
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calculated for each of the 4 fish species.
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mean of the
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en
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K
S
5
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.and Bush (1997)
J2
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CO
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12-day exposi
Nitroaromatic!









, and Bush (1997)
U
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b
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C-l ^J"
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i



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1 d2
s
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: 'S£
§ w
STco
' 'S3 _t
VI _
following regre
5 logK,,,, = 1.49
|l
00 *
i S ^
*GO 00

• -a t>
I O "
3 53
U gj

The BCF was cal
:hamp, and Schmi
M
4> ed
! IB
'H
<8 5
II
i ^
fl> fll -5
C lM O
™ (t\ >~
1,3-Dinitrobenze
this compound w«
log K,,w- 1.146(5
1 2

"O «_ ||
3 g EL.
I !|
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oo

S
1
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PQ
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2,4-Dinitrotoluet


Compound:




































j follows:
S
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3
OQ
BCF value was b;
"8
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c
The recommf




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1
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5

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s

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1

4-day exposur









1 Pearson (1983)
s
§

'3
n
3

oo
Tl

1

V>
ci
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O
PQ
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u
1
8

S oo
II Empirical da
log BCF = 0.

r^
ci
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3
1
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PQ
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i
8

«



























Nitrobenzene


Compound:



















21
•^
S
jfg:

"*d
"eg C?
Following regre!
elogK^l.8
« J
a-g
00 -

"S ^
^ r**
"S "*
*j «3
"3 "5
o ••?*
The BCF was cal
champ, and Schm
3
•o S

r this compc
Southworth,
«2
U Tj-
S °
S ^
S oo
.1 g
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J
in

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I
J
Pentachloronitrol


Compound:
















i


2~
^^
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|B|
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K 2 S^
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e log K..-4.6.
•hthalate Estei
-II


co oo
5 t^*
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^3 c3
3 T3
— O

The BCF was ca
champ, and Schm


«B j
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this compound w<
log^-i.neo
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Reference







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xachlorobenzEne
o


Compound:




















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B -
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; log Kow = 5.503 (U.
u S3
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'ai oo

"8 -
U
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1.1
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d 1


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11
compound wen:
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1 11
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compound were
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tC 2 J1
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=* 53
Compound:
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log BCF = 0.

t**l
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3
1
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ntachlorobenzene
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13 Is;
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sis
§ t3 g
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111
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79-day exposure di
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dry weight using a















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^
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0


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o
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3
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n
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73
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I
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ntachlorophenol
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|| Compound:




















£"
C "*
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following regression
e log KOW = 5.080 (U
o S3
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OJO *
c ™
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3 r~ ,
•o 2

13 S3
1 "8
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o S
; BCF was
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£ J
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11
11
compound were
K,,w- 1.146 (Son
c'' CJi
& 2
J2 oo
1 ^
ilS

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-------
Screening Level Ecological Risk Assessment Protocol
Appendix C; Media-To-Receptor BCF Values	August 1999
Adams, W.C.  1976. The Toxicity and Residue Dynamics of Selenium in Fish and Aquatic Invertebrates.
        Ph.D. Thesis. Michigan State University. East Lansing, Michigan.

Adams, W.J., G.M. DeGraeve, T.D. Sabourin, J.D. Cooney, and G.M. Mosher. 1986. "Toxicity and
        Bioconcentration of 2,3,7,8-TCDD to Fathead Minnows (Pimephales promelas)." Chemosphere.
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Anderson, A.C., et al. 1979. "Fate of the Herbicide MSMA in Microcosms." In D.D. Hemphill (ed.).
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Anderson, D.R., and E.B. Lusty.  1980.  "Acute Toxicity and Bioaccumulation of Chloroform to Four
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Andryushchenko, V. V., and G.G. Polikarpov. 1973.  "An Experimental Study of Uptake of Zn65 and DDT
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Baes, C.F., m, R.D. Sharp, A.L. Sjoreen, and R.W. Shor. 1984. "A Review and Analysis of Parameters
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Banerjee, S., R.H. Suggatt, and D.P. O'Grady. 1984.  "A Simple Method for Determining
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U.S. EPA Region 6                                                         U.S. EPA
Multimedia Planning and Permitting Division                                             Office of Solid Waste
Center for Combustion Science and Engineering                                                       C-99

-------
Screening Level Ecological Risk Assessment Protocol
Appendix C; Media-To-Receptor BCF Values	August 1999

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Baudin, J. P.  1974.  "Premieres Donnees sur 1'Etude Experimentale du Cycle du Zinc dans 1'Etang de
       1'Olivier." JieMillieu. Volume 24. Series B. Page 59.

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       Three Generations of Brook Trout (Salvelinus fontinalis)." Transactions, American Fisheries
       Society. Volume 105, Number 2.  Pages 550-358.

Besser, J.M., T.J. Canfield, and T.W.  LaPoint. 1993. "Bioaccumulation of Organic and Inorganic
       Selenium in a Laboratory Food Chain." Environmental Toxicology and Chemistry. Volume 12.
       Pages 57-72.

Beyer, W.N. and C.D. Gish.  1980. "Persistence in Earthworms and Potential Hazards to Birds of Soil
       Applied l,r-(4,4-Dichlorodiphenyltrichloroethane (DDT), Dieldrin, and Heptachlor".  /. Appl.
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Bills, T.D., and L.L. Marking.  1977.  "Effects of Residues of the Polychlorinated Biphenyl Arpclor 1254
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       Production of Lymnnaea palustris During Chronic Exposure to Lead." Journal of Fisheries
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Boudou, A.,  and F. Ribeyre.  1984. "Influence of Exposure Length on the Direct Bioaccumulation of Two
       Mercury Compounds by Salmo gairdneri (Fry) and the Relationship Between Organism Weight
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Branson, D.R., I.T. Takahashi, W. M. Parker, and G.E. Blau. 1985. "Bioconcentration Kinetics of
       2,3,7,8-Tetrachlorodibenzo-p-dioxin in Rainbow Trout." Environmental Toxicology and
       Chemistry. Volume 4. Pages 779-788.
U.S. EPA Region 6                                                          U.S. EPA
Multimedia Planning and Permitting Division                                              Office of Solid Waste
Center for Combustion Science and Engineering                                                      C-100

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Brown, D., and R.S. Thompson.  1982.  "Phthalates and the Aquatic Environment: Part EL The
       Bioconcentration and Depuration of Di-2-ethylhexyl Phthalate (DEHP) and Di-isodecyl Phthalate
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Bruggeman, W.A., A. Oppenhuizen, A. Wijbenga, and O. Hutzinger. 1984.  "Bioaccumulation of Super-
       Lipophilic Chemicals in Fish." Toxicological and Environmental Chemistry.  Volume 7.
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Calabrese, A., J.R. Maclnnes, D.A. Nelson, R.A. Greig, and P.P. Yevich. 1984. "Effects of Long-Term
       Exposure to Silver and Copper on Growth, Bioaccumulation and Histopathology in the Blue
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Cappon, C.J.  1981. "Mercury and Selenium Content and Chemical Form in Vegetable Crops Grown in
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       Activity of Mytilus edulis L. and Mya arenaria L." In FJ. Vernberg, A. Calabrese, F.P.
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Cleveland, L., E.E. Little, SJ. Hamilton, D.R. Buckler, and J.B. Hunn. 1986. "Interactive Toxicity of
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Deneer, J.W., T.L. Sinnige, W. Seinen, and J.L.M. Hermens.  1987. "Quantitative Structure-Activity

U.S. EPA Region 6                                                         U.S. EPA
Multimedia Planning and Permitting Division                                              Office of Solid Waste
Center for Combustion Science and Engineering                                                      C-101

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       Relationships for the Toxicity and Bioconcentration Factor of Nitrobenzene Derivatives towards
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       Marine Biology.  Volume 43. Pages 265-276.

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       Four Marine Phytoplankters." Marine  Ecology - Progress Series. Volume 18.  Pages 210-213.

Frekag, D., H. Geyer, A. Kraus, R. Viswanathan, D. Kotzias, A. Attar, W. Klein, and F. Korte. 1982.
       "Ecotoxicologjcal Profile Analysis.  Vn. Screening Chemicals for Their Environmental Behavior
       by Comparative Evaluation."  Ecotoxicology and Environmental Safety.  Volume 6. Pages 60-81.

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       of Water Pollution Control Federation. Volume 34. Pages 1151-1155.

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       Behavior of Xenobiotics." Environmental Science and Technology.  Volume 17, Number 10.
       Pages 590-595.

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       Striped Bass (Morone saxatilis)." Pesticide Biochemistry and Physiology. Volume 46.
       Pages 161-170.
U.S. EPA Region 6                                                         U.S. EPA
Multimedia Planning and Permitting Division                                              Office of Solid Waste
Center for Combustion Science and Engineering                                                      C-102

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George, S.G., and T.L. Coombs.  1977. "The Effects of Chelating Agents on the Uptake and
        Accumulation of Cadmium by Mytilus edulis." Marine Biology. Volume 39.  Pages 261-268.

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        Relationship Between w-Octanol/Water Partition Coefficient and Bioaccumulation of Organic
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        Organic Chemicals and Their Bioaccumulation by the Alga Chlorella."  Chemosphere.
        Volume 10, Number 11/12.  Pages 1307-1313.

Giesy, J.P., Jr.,  HJ. Kanio, J.W. Boling, R.L. Knight, S. Mashburn, and S. Clarkin.  1977.  "Effects of
        Naturaly Occurring Aquatic Organic Fractions on CadmiumToxicity to Simocephalus serrulatus
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Gilek, M., M. Bjork, D. Broman, N. Kautsky, and C. Naf.  1996. "Enhanced Accumulation  of PCB
        Congeners by Baltic Sea Blue Mussels, Mytilus edulis, with Increased Algae Enrichment."
        Environmental Toxicology and Chemistry. Volume 15, Number 9.  Pages 1597-1605.

Gillespie, R., T. Reisine, and E.J. Massaro.  1977. "Cadmium Uptake by the Crayfish, Orconectes
        propinquus." Environmental Research. Volume 13. Pages 364-368.

Gish,C.D.  1970. "Organochlorine Insecticide Residues in  Soils and Soil Invertebrates from Agricultural
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        on Laboratory-Reared Embryos and Fry of the Sheepshead Minnow." In W.A. Rogers, R.
        Dimmick, andR. Summerfelt (eds.)  Proceedings, 30th Annual Conference Southeast Association
        of Game Fish Commissions.  October 24-27, 1976. Jackson,  Mississippi.

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        Clam (Corbiculafluminea) in Artificial Stream Systems." Hydrobiologia. Volume 102.
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Halter, M.T.  1974. "The Acute Toxicity Polychlorinated Biphenyl, Aroclor 1254, to the Early like Stages
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Hamelink, J.L.,  and R.C. Waybrant. 1976.  "DDE and Lindane in a Large-Scale Model Lentic
        Ecosystem." Transactions, American Fisheries Society.  Volume 105. Pages 124-134.

Hamelink, J.L.,  and R.C. Waybrant. 1977. "DDE and Lindane in a Large-Scale Model Lentic
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        In Substituent Constants for Correlation Analysis in Chemistry and Biology. Wiley-Interscience.
        New York. As cited in NRC (1981).
U.S. EPA Region 6                                                          U.S. EPA
Multimedia Planning and Permitting Division                                              Office of Solid Waste
Center for Combustion Science and Engineering                                                       C-103

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Hansen, D.J., et al.  1971. "Chronic Toxicity, uptake and Retention of Aroclor 1254 in Two Estuarine
       Fishes." Bull. Environ. Contain. Toxicol. 6: 113.

Hansen, D.J., et al.  1973. "Aroclor 1254 in Eggs of Sheepshead Minnows: Effect on Fertilization
       Success and Survival of Embryos and Fry."  Proceedings 27th Annual Conference South East
       Game Fish Comm.  Page 420.

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       7: 363.

Hansen, D.J., et al.  1975. "Effects of Aroclor 1016 on Embryos, Fry, Juveniles, and Adults of
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       Aqueous Cadmium by Rainbow Trout (Salmo gairdneri Richardson) and Lake Whitefish
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Hodson, P.V., DJ. Spry, and B.R. Blunt.  1980. "Effects on Rainbow Trout (Salmo gairdneri) of a
       Chronic Exposure to Waterborne Selenium." Canadian Journal of Fisheries and Aquatic
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Holcombe, G.W., D.A. Benoit, E.N. Leonard, and J.M. McKim. 1976.  "Long-term Effects of Lead
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       Michigan.

Hutchinson, T.C., and H. Czyrska. 1972. "Cadmium and Zinc  Toxicity and Synergism to Floating
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        Quality Parameters, ASTM STP 573, American Society for Testing and Materials, Philadelphia.

U.S. EPA Region 6                                                          U.S. EPA
Multimedia Planning and Permitting Division                                              Office of Solid Waste
Center for Combustion Science and Engineering                                                      C-104

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Ecemoto, Y., K. Motoba, T. Suzuki, and M. Uchida.  1992.  "Quantitative Structure-Activity Relationships
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        Bioaccumulation Potential of Hexachlorobenzene (HCB). Journal of Agriculture and Food
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Isensee, A.R., P.C. Kearney, E.A. Woolson, G.E. Jones, and V.P. Williams. 1973.  "Distribution of Alkyl
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        the Polychaete Nereis diversicolor." Estuarine Coastal Marine Science. Volume 4.
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Jouany, J.M., P. Vasseur, and J.F. Ferard. 1982. "Ecotoxicite Directe et Integree du Chrome Hexavalent
        sur Deux Niveaux Trophiques Associes: Chlorella vulgaris et Daphnia magna."  Environmental
        Pollution. Volume 27A. Pages 207-221.

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        Recommend Log KQW Values."  Environmental Research Laboratory.  Athens, GA. April 10.

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        Sediments."  Water Research.  Volume 13. Pages 241-248.

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        Pentachlorophenol in Goldfish." Bulletin, Japanese Society of Scientific Fisheries.  Volume 46,
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        Chlorobenzenes by Guppies." Chemosphere. Volume 9, Number 1. Pages 3-19.

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        Volume 11.  Page 275.

Korte, F., D. Freitag, H. Geyer. W.  Klein, A.G. Kraus, and E. Lahaniatis.  1978.  "Ecotoxicologic Profile

U.S. EPA Region 6                                          "               U.S. EPA
Multimedia Planning and Permitting Division                                              Office of Solid Waste
Center for Combustion Science and Engineering                                                      C-105

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       Analysis: A Concept for Establishing Ecotoxicologic Priority Lists for Chemicals."
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Laseter, J.L., C.K. Bartell, A.L. Laska, D.G. Holmquist, D.B. Condie, J.W. Brown, and R.L. Evans.
        1976. "An Ecological Study of Hexachlorobutadiene (HCBD)." U.S. Environmental Protection
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       Pages 235-252.
U.S. EPA Region 6                                                          U.S. EPA
Multimedia Planning and Permitting Division                                              Office of Solid Waste
Center for Combustion Science and Engineering                                                       C-106

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       Hexachlorobenzene and Hexachlorobiphenyl by Sheepshead Minnows in Static Sediment/Water
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       and Fate of Hexachlorocyclopentadiene, Chlorodane, Heptachlor, Heptachlor Epoxide in a
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       Dioxins, and Dibenzofurans.  Volume HI—Volatile Organic Chemicals. Lewis Publishers.
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U.S. EPA Region 6                                                          U.S. EPA
Multimedia Planning and Permitting Division                                              Office of Solid Waste
Center for Combustion Science and Engineering                                                      C-107

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       Freshwater Mussel, Anodonta anatina L." Ecotoxicology and Environmental Safety. Volume 20.
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       (2,3,7,8-Tetrachlorodibenzo-p-dioxin) in Sevesco." Pp 275-283. In Satchell 1983 . As cited in
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Mauck, W.L., et al.  1978.  "Effects of the Polychlorinated Biphenyl Aroclor 1254 on Growth, Survival,
       and Bone Development in Brook Trout (Salvelinus fontinalis)." Journal of Fisheries Research
       Board of Canada. Volume 35. Page 1084.

Mayer, F.L., Jr. 1976.  "Residue Dynamics of Di-2-ethylhexyl Phthalate in Fathead Minnows
       (Pimephales promelas)." Journal of Fisheries Research Board of Canada.  Volume 33.  Pages
       2610-2613.

Mayer, F.L, Jr., P.M. Mehrle, and H.O. Sanders. 1977. "Residue Dynamics and Biological Effects of
       Polychlorinated Biphenyls in Aquatic Organisms." Archives, Environmental Contamination and
       Toxicology. Volume 5. Pages 501-511.

McKim, J.M., G.F. Olson, G.W. Holcombe, and E.P. Hunt.  1976.  "Long-term Effects of Methylrnercuric
       Chloride on Three Generations of Brook Trout (Salvelinus fontinalis): Toxicity, Accumulation,
       Distribution, and Elimination." Journal of Fisheries Research Board of Canada. Volume 33.
       Pages 2726-2739.

McLusky, D.S., and C.N.K. Phillips.  1975. "Some Effects of Copper on the Polychaete Phyllodoce
       maculata." Estuarine and Coastal Marine Science. Volume 3. Pages 103-108.

Mehrle, P. M., D. R. Buckler, E.E. Little, L.M.  Smith, J.D. Petty, P.H. Peterman, D.L. Stalling, G.M.
       DeGraeve,  J.T. Coyle, and WJ. Adams. 1988. "Toxicity and Bioconcentrations of 2,3,7,8-
       Tetrachlorodibenzodioxin and 2,3,7,8-Tetrachlorodibenzofuran in Rainbow Trout."
       Environmental Toxicology and Chemistry. Volume 7. Pages 47-62.

Mehrle, P.M., and F.L. Mayer.  1976.  "Di-2-Ethylhexyl Phthalate: Residue Dynamics and Biological
       Effects in Rainbow Trout and Fathead Minnows." Trace Substances in  Environmental Health-X,
       Proceedings, University of Missouri's 10th Annual Conference on Trace Substances in
       Environmental Health, June 8-10, 1976. University of Missouri Press, Columbia.
U.S. EPA Region 6                                                         U.S. EPA
Multimedia Planning and Permitting Division                                              Office of Solid Waste
Center for Combustion Science and Engineering                                                      C-108

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Metayer, C., C. Amiard-Triquet, and J.P. Baud.  1990. "Variations Inter-Specificques de la
       Bioaccumulation et de la Toxicite de L'Argent A L'Egard de Trois Mollusques Bivalves Marins."
       Water Research. Vol 24, Number 8. Pages 995-1001.

Metcalf, R.L., I.P. Kapoor, P.U. Lu, C.K. Schuth, and P. Sherman.  1973.  "Model Ecosystem Studies of
       the Environmental Fate of Six Organochlorine Pesticides." Environmental Health Perspectives.
       Volume 4.  Pages 35-44.

Metcalf, R.L., J.R. Sanborn, P.-Y. Lu, and D. Nye.  1975.  "Laboratory Model Ecosystem Studies of the
       Degradation and fate of Radio-labeled Tri-, Tetra-, and Pentachlorobiphenyl Compared with
       DDE."  Archives, Environmental Contamination and Toxicology. Volume 3, Number 2.
       Pages 151-165.

Metcalf, R.L., O.K. Sangha, and IP. Kapoor. 1971. "Model Ecosystem for the Evaluation of Pesticide
       Biodegradability and Ecological Magnification." Environmental Science and Technology.
       Volume 5, Number 8. Pages 709-713.

Muir, D.C.G., W.K. Marshall, and G.R.B. Webster.  1985.  "Bioconcentration of PCDDs by Fish: Effects
       of Molecular Structure and Water Chemistry." Chemosphere. Volume 14.  Pages 829-833.

Munda, I.M.  1979. "Temperature Dependence of Zinc Uptake in Fucus virsoides (Don.) J. Ag. and
       Enteromorpha prolifera (O.F. Mull.) J. Ag. from the Adriatic Sea." Botanica Marina.
       Volume 22. Pages 149-152.

Namminga, H.,  and J. Wilhm. 1977.  "Heavy Metals in Water, Sediments, and Chironomids." Journal of
       Water Pollution Control Federation.  Volume 49, Number 7.  Pages 1725-1731.

National Academy of Sciences. (NAS). 1974. Chromium.  Pages 86-89. U.S. Government Printing
       Office.  Washington, D.C.

National Research Council (NRC).  1979. Polychlorinated Biphenyls.  National Academy of Sciences.
       Washington, D.C.

National Research Council (NRC).  1981. Formaldehyde an Other Aldehydes. National Academy Press.
       Washington, D.C.

Nebeker, A.V., F.A. Puglisi, and D.L. DeFoe. 1974. "Effect of Polychlorinated Biphenyl Compounds on
       Survival and Reproduction of the Fathead Minnow and Flagfish." Transactions, American
       Fisheries Society. Volume 103. Pages 562-568.

Nebeker, A.V., W.L. Griffis, C.M. Wise, E. Hopkins, and J.A. Barbitta.  1989. "Survival, Reproduction,
       and Bioconcentration in Invertebrates and Fish Exposed to Hexachlorobenzene."  Environmental
       Toxicology and Chemistry. Volume 8, Number 601-611.

Nehring, R.B.  1976.  "Aquatic Insects as Biological Monitors of Heavy Metal Pollution." Bulletin,
       Environmental Contamination and  Toxicology. Volume 15, Number 2.  Pages 147-154.

Nehring, R.B., R. Nisson, and G. Minasian.  1979. "Reliability of Aquatic Insects Versus Water Samples
       as Measures of Aquatic Lead Pollution." Bulletin, Environmental Contamination and

U.S. EPA Region 6                                                        U.S. EPA
Multimedia Planning and Permitting Division                                             Office of Solid Waste
Center for Combustion Science and Engineering                                                      C-109

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       Toxicology. Volume 22, Number l/2.  Pages 103-108.

Newsted, J.L., and J.P. Giesy.  1987.  "Predictive Models for Photoinduced Acute Toxicity of Polycyclic
       Aromatic Hydrocarbons to Daphnia magna, Strauss (Cladocera, Crustacea)." Environmental
       Toxicology and Chemistry. Volume 6.  Pages 445-461.

Niimi, A.J., H.B. Lee, and G.P. Kissoon. 1989. "Octanol/Water Partition Coefficients and
       Bioconcentration Factors of Chloronitrobenzenes in Rainbow Trout (Salmo gairdneri)."
       Environmental Toxicology and Chemistry. Volume 8. Pages 817-823.

Nimmo, D.R., et al.  1975.  "Toxicity of Aroclor 1254 and its Physiological Activity in Several Estuarine
       Organisms." Arch. Environ. Contain. Toxicol. Volume 3. Page 22.

Nimmo, D.W.R., D.V. Lightner and L.H. Banner.  1977. "Effects of Cadmium on the Shrimps, Penaeus
       duorarum, Palaemonetes pugio, and Palaemonetes vulgaris." Pages 131-183. In F.J. Vernberg,
       A. Calabrese, P.P. Thurberg, and W.B. Vernberg (eds). Physiological Responses of Marine Biota
       to Pollutants. Academic Press, Inc. New York, New York.

Oliver, B.G.  1987. "Biouptake of Chlorinated Hydrocarbons from Laboratory-Spiked and Field
       Sediments by Oligochaete Worms." Environmental Science and Technology.  Volume 21. Pages
       785-790.

Oliver, B.G., and A.J. Niimi. 1983.  "Bioconcentration of Chlorobenzenes from Water by Rainbow Trout:
       Correlations with Partition Coefficients and Environmental Residues." Environmental Science
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Oliver, E.G., and A.J. Niimi. 1985.  "Bioconcentration Factors of Some Halogenated Organics for
       Rainbow Trout: Limitations on Their  Use for Prediction of Environmental Residues."
       Environmental Science and Technology. Volume 19.  Pages 842-849.

Oliver, E.G., and A.J. Niimi. 1988.  "Trophodynamic Analysis of Polychlorinated Biphenyl Congeners
       and Other Chlorinated Hydrocarbons in the Lake Ontario Ecosystem." Environmental Science
       and Technology. Volume 22.  Pages 388-397.

Opperhuizen, A., E.W.v.d Velde, F.A.P.C. Gobas, D.A.K. Liem, and J.M.D.v.d. Steen.  1995.
       "Relationship Between Bioconcentration in Fish and Steric Factors of Hydro-phobic Chemicals."
       Chemosphere. Volume 14.  Pages  1871-1896.

Parrish, P.R., et al. 1974. "Effects of Polychlorinated Biphenyl, Aroclor 1016, on Estuarine Animals."
       Association South East Biol. Bull.  Volume 21. Page 74.

Parrish, P.R., E.E. Dyar, J.M. Enos, and W.G. Wilson. 1978. "Chronic Toxicity of Chlordane,
       Trifluralin, and Pentachlorophenol to  Sheepshead Minnows (Cyprinodon variegatus)."  U.S.
       Environmental Protection Agency, EPA 600/3-78-010. Gulf Breeze, Florida.  January.

Patrick, R., T. Bott, and R. Larsen.  1975.  "The Role of Trace Elements in Management of Nuisance
       Growths."  U.S. Environmental Protection Agency, EPA 660/2-75-008. Corvallis, Oregon.

Pentreath, J.R.  1973. "The Accumulation and Retention of 65Zn and 54Mn by the Plaice, Pleuronectes

U.S. EPA Region 6                                                         U.S. EPA
Multimedia Planning and Permitting Division                                               Office of Solid Waste
Center for Combustion Science and Engineering                                                      C-l 10

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       platessaL. Journal of Experimental Marine Biology and Ecology. Vol 12. Pages 1-18. As
       cited in U.S. EPA (1980g).

Perez, K.T., E.W.  Davey, N.F. Lackie, G.E. Morrison, P.O. Murphy, A.E. Soper, and D.L. Winslow.
       1983.  "Environmental Assessment of a Phthalate Ester, Di(2-Ethylhexyl) Phthalate (DEHP),
       Derived from a Marine Microcosm." Pages 180-191. In: Bishop W.E., R. D. Cardwell and B. B.
       Heidolph (Eds.) Aquatic Toxicology and Hazard Assessment: Sixth Symposium. ASTM STP 802.
       American  Society for Testing and Materials, Philadelphia.

Pesch, C.E., and D. Morgan. 1978.  "Influence of Sediment in Copper Toxicity Tests with Polychaete
       Neanthes arenaceodentata." Water Research. Volume 12. Pages 747-751.

Pesch, G.G., and N.E. Stewart. 1980.  "Cadmium Toxicity to Three Species of Estuarine Invertebrates."
       Marine Environmental Research. Volume 3. Pages 145-156.

Phillips, D.J.H. 1976.  'The Common Mussel Mytilus edulis as an Indicator of Pollution by Zinc,
       Cadmium, Lead, and Copper. I. Effects of Environmental Variables on Uptake of Metals."
       Marine Biology.  Volume 38. Pages 59-69.

Pietz, R.I., J.R. Peterson, I.E. Prater, and D.R. Zenz. 1984.  "Metal Concentrations in Earthworms From
       Sewage Sludge-Amended Soils at a Strip Mine Reclamation Site." J. Environmental Qual. Vol.
       13, No. 4.  Pp 651-654.

Podowski, A.A., and M.A.Q. Khan.  1984. "Fate of Hexachlorocyclopentadiene in Water and Goldfish."
       Archives, Environmental Contamination and Toxicology. Volume 13. Pages 471-481.

Pringle, B.H., D.E. Hissong, E.L. Katz, and S.T. Mulawka. 1968. "Trace Metal Accumulation by
       Estuarine Mollusks." Journal of Sanitary Engineers Division.  Volume 94. Pages 455-475.

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       Sediments  from the Fraser River." Environmental Toxicology and Chemistry. Volume 15,
       Number 9. Pages 1555-1563.

Reich, A.R., J.L. Peerkins, and G. Cutter.  1986. "DDT Contamination of a North Alabama Aquatic
       Ecosystem." Environmental Toxicology and Chemistry.  Volume 5. Pages 725-736.

Rice, C.P., and D.S. White. 1987. "PCB Availability Assessment of River Dredging Using Caged Clams
       and Fish." Environmental Toxicology and Chemistry.  Volume 6.  Pages 259-274.
Reinecke, A.J., and G. Nash. 1984. "Toxicity of 2, 3, 7, 8-TCDD and Short Term Bioaccumulation by
       Earthworms (Oligochaeta)" Soil Biol. Biochem. 1:39-44. In Beyer 1990.

Rhett, R.G., J.W. Simmers, and C.R. Lee.  1988. "Eisenia Foetida Used as a Biomonitoring Tool to
       Predict the Potential Bioaccumulation of Contaminants from Contaminated Dredged Material." in
       Edwards and Neuhauser 1988.

Roesijadi, G., J.W. Anderson, and J.W. Blaylock.  1978. "Uptake of Hydrocarbons from Marine
       Sediments Contaminated with Prudhoe Bay Crude Oil: Influence of Feeding Type of Test Species

U.S. EPA Region 6                                                          U.S. EPA
Multimedia Planning and Permitting Division                                              Office of Solid Waste
Center for Combustion Science and Engineering                                                      C-l 11

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       and Availability of Polycyclic Aromatic Hydrocarbons." Journal of Fisheries Research Board of
       Canada. Volume 35.  Pages 608-614.

Saiki, M.K., D.T. Castleberry, T.W. May, B.A. Martin, and F.N. Bullard.  1995. "Copper, Cadmium,
       and Zinc Concentrations in Aquatic Food Chains from the Upper Sacramento River (California)
       and Selected Tributaries." Archives in Environmental Contamination and Toxicology.  Volume
       29. pages 484-491.

Sanborn, J.R. 1974. "The Fate of Select Pesticides in the Aquatic Environment." U.S. Environmental
       Protection Agency, EPA-660/3-74-025.  Corvallis, Oregon.

Sanborn, J.R., R.L. Metcalf, C.C. Yu, and P.Y. Lu.  1975. "Plasticizers in the Environment: The Fate of
       Di-AT-Octyl Phthalate (DOP) in Two Model Ecosystems and Uptake and Metabolism of DOP by
       Aquatic Organisms."  Archives, Environmental Contamination and Toxicology.  Volume 3,
       Number 2. Pages 244-255.

Sanders, H.O., F.L. Mayer, Jr., and D.F. Walsh. 1973. "Toxicity Residue Dynamics, and Reproductive
       Effects of Phthalate Esters in Aquatic Invertebrates." Environmental Research. Volume 6,
       Number 1. Pages 84-90.

Saouter, E., L. Hare, P.G.C. Campbell, A. Boudou, and F. Ribeyre.  1993.  "Mercury Accumulation in the
       Burrowing Mayfly, Hexagenia rigida (Ephemeroptera) Exposed to CH3HgCL or HgCl^ in Water
       and Sediment."  Water Research.  Volume 27, Number 6. Pages 1041-1048.

Schauerte, W., J.P. Lay, W. Klein, and F. Korte. 1982. "Long-Term Fate of Organochlorine Xenobiotics
       in Aquatic Ecosystems."  Ecotoxicology and Environmental Safety. Volume 6.  Pages 560-569.

Schimmel, S.C., J.M. Patrick, Jr. and J. Forester. 1976. "Heptachlor: Toxicity to and Uptake by Several
       Estuarine Organisms." Journal of Toxicology and Environmental Health. Volume 1.  Pages 955-
       965.

Schimmel, S.C., J.M. Patrick, Jr., and L.F. Faas. 1978. "Effects of Sodium Pentachlorophenate on
       Several Estuarine Animals: Toxicity Uptake and Depuration." Pages 147-155. In K.R.  Rao. (Ed).
       Penachlorophenol: Chemistry, Pharmacology, and Environmental Toxicology. Plenum Press.
       New York, New York.

Schrap, S.M., and A. Opperhuizen. 1990. "Relationship Between Bioavailability and Hydrophobicity:
       Reduction of the Uptake of Organic Chemicals by Fish Due  to the Sorption of Particles."
       Environmental Toxicology and Chemistry. Volume 9.  Pages 715-724.

Schroeder, H.A. 1970.  "Barium Air Quality Monograph." American Petroleum Institute, Air Quality
       Monograph Number 70-12.

Scura, E.D. and G.H. Theilacker.  1977.  "Transfer of the Chlorinated Hydrocarbon PCB in a Laboratory
       Marine Food Chain." Marine Biology.  Volume 40. Pages  317-325.
U.S. EPA Region 6                                                         U.S. EPA
Multimedia Planning and Permitting Division                                             Office of Solid Waste
Center for Combustion Science and Engineering                                                      C-l 12

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Shuster, C.N., Jr., and B.H. Pringle. 1968. "Effects of Trace Metals on Estuarine Mollusks."
       Proceedings, First Mid-Atlantic Industrial Waste Conference, November 13-15, 1967.
       Pages 285-304.

Simmers, J.W., R.G. Rhett, and C.R. Lee. 1983. Application of a Terrestrial Animal Bioassay for
       Determining Toxic Metal Uptake from Dredged Materila. International Congress Heavy Metals on
       the Environment, Heidelberg. 1284 pp. In Rhett 1988.  Cited in Edwards and Neuhauser 1988.

Snarski, V.M., and G. F. Olson.  1982.  "Chronic Toxicity and Bioaccumulation of Mercuric Chloride in
       the Fathead Minnow (Pimephales promelas)." Aquatic Toxicology.  Volume 2. Pages 143-156.

Snarski, V.M., and F. A. Puglisi.  1976. Effects ofAroclor 1254 on Brook Trout (Salvelinus fontinalis).
       U.S. Environmental Protection Agency, EPA-600/3-76-112. Environmental Research Laboratory-
       Duluth. Duluth, Minnesota.

Sodergren, A. 1982.  "Significance of Interfaces in the Distribution and Metabolism of Di-2-ethylhexyl
       Phthalate in an Aquatic Laboratory Model Ecosystem."  Environmental Pollution (Series A).
       Volume 27.  Pages 263-274.

Southworth, G.R., JJ. Beauchamp, and P.K. Schmieder.  1978.  "Bioaccumulation Potential of Polycyclic
       Aromatic Hydrocarbons in Daphnia Pulex."  Water Research. Volume 12. Pages 973-977. As
       cited in Lyman, Reehl, and Rosenblatt (1982). As cited in Lyman, Reehl, and Rosenblatt (1982).

Spehar, R.L.  1976.  "Cadmium and Zinc Toxicity to Jordanellafloridae." U.S. Environmental Protection
       Agency, EPA-600/3-76-096. Environmental Research Laboratory-Duluth. Office of Research
       and Development.  Duluth, Minnesota. November.

Spehar, R.L., J.T. Fiandt, R.L. Anderson, and D.L. DeFoe.  1980.  "Comparative Toxicity of Arsenic
       Compounds and Their Accumulation in Invertebrates and Fish." Archives, Environmental
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Spehar, R.L., H.P. Nelson, M.J. Swanson, and J.W. Renoos. 1985. "Pentachlorophenol Toxicity to
       Amphipods and Fathead Minnows at Different Test pH Values." Environmental Toxicology and
       Chemistry. Volume 4. Pages 389-397.

Spehar, R.L., G.D. Veith, D.L. DeFoe, and B.V. Bergstedt.  1979.  "Toxicity and Bioaccumulation of
       Hexachlorocyclopentadiene, Hexachloronorbornadiene and Heptachloronorbornene in Larval and
       Early Juvenile Fathead Minnows, (Pimephales promelas)." Bulletin, Environmental
       Contamination and Toxicology.  Volume 21.  Pages 576-583.

Stehly, G.R., and W.L. Hayton. 1990. "Effect of pH of the Accumulation Kinetics of Pentachlorophenol
       in Goldfish."  Archives of the Environmental Contamination and Toxicology. Volume 19.
       Pages 464-470.

Stephan, C.E. 1993.  "Derivation of Proposed Human Health and Wildlife Bioaccumulation Factors for
       the Great Lakes Initiative." U.S. Environmental Protection Agency, Office of Research and
       Development. U.S. Environmental Research Laboratory. NTIS PB93-154672.

Stokes, P.M., T.C. Hutchinson, and K. Krauter. 1973. "Heavy  Metal Tolerance in Algae Isolated From

U.S. EPA Region 6                                                          U.S. EPA
Multimedia Planning and Permitting Division                                              Office of Solid Waste
Center for Combustion Science and Engineering                                                       C-l 13

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       Polluted Lakes Near the Sudbury, Ontario Smelters." Water Pollution Research Journal of
       Canada.  Volume 8. Pages 178-201. (Abstract only).

Sundelin, B.  1983. "Effects of Cadmium on Pontoporeia affinis (Crustacea: Amphipoda) in Laboratory
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       Bioconcentration of Di-2-ethylhexyl Phthalate in Rainbow Trout." Environmental Toxicology and
       Chemistry. Volume 9.  Pages 989-995.

Theede, H., N. Scholz, and H. Fischer.  1979.  "Temperature and Salinity Effects on the Acute Toxicity of
       Cadmium to Laomedea loveni (Hydrozoa)." Marine Ecology - Progress Series. Volume 1.
       Pages 13-19.

Thompson, S.E., C.A. Burton, D.L. Quinn, and Y.C. Ng.  1972.  Concentration Factors of Chemical
       Elements in Edible Aquatic Organisms.  UCRL-50564 Rev. 1. Lawrence Livermore Laboratory.
       University of California.

Thurberg, P.P., A. Calabrese, E. Gould, R.A. Greig, M.A. Dawson, and R.K. Tucker.  1977.  "Response
       of the Lobster, Homarus americanus, to Sublethal Levels of Cadmium and Mercury."  In:
       Vernberg, F.J., A. Calabrese, P.P. Thurberg, and W.B. Verberg (eds.). Physiological Responses
       of Marine Biota to Pollutants.  Academic Press. New York, NY.

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       Environmental Science and Technology. 22(3): 271-274.

U.S. EPA. 1976. "An Ecological Study of Hexachlorobutadiene (HCBD)." Office of Toxic Substances.
       Washington, D.C.  EPA 560/6-76/010.

U.S. EPA. 1978.  "In-depth Studies on Health and Environmental Impacts of Selected Water Pollutants."
       Washington, D.C.

U.S. EPA. 1979.  "Water Related Environmental Fate of 129 Priority Pollutants." EPA Monitoring and
       Data Support Division. Washington, D.C. Volume I and H. EPA 440/4-79-029a.

U.S. EPA. 1980a.  "Ambient Water Quality Criteria for Heptachlor."  Office of Water Regulations and
       Standards.  Criteria and Standards Division. Washington, D.C.  EPA 440/5-80-052. October.

U.S. EPA. 1980b.  "Ambient Water Quality Criteria for Polychlorinated Biphenyls."  EPA 400/5-80/068.
       Office of Water Regulations and Standards Division. Washington, D.C.

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U.S. EPA. 1985.  "Health Assessment Document for Polychlorinated Dibenzo-p-dioxins."  Office of
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       D.C.

U.S. EPA Region 6                                                          U.S. EPA
Multimedia Planning and Permitting Division                                             Office of Solid Waste
Center for Combustion Science and Engineering                                                      C-114

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U.S. EPA.  1992a. "National Study of Chemical Residues in Fish." Office of Science and Technology.
       EPA 823/R-92/008b. September.

U.S. EPA.  1992b. "Criteria and Related Information for Toxic Pollutants." Water Management Division,
       EPA Region VI.

U.S. EPA.  1992c. Technical Support Document for Land Application of Sewage Sludge. Office of
       Water. EPA822/R-93/001a. November.

U.S. EPA.  1992d. Estimating Exposure to Dioxin-Like Compounds. Draft Report.  Office of Research
       and Development. Washington, D.C. EPA/600/6-88/005B.  August.

U.S. EPA.  1994a. Estimating Exposure to Dioxin-Like Compounds. Draft Report.  Office of Research
       and Development. Washington, D.C. EPA/600/6-88/005a,b,c. June.

U.S. EPA.  1994b. Draft Report Chemical Properties for Soil Screening Levels. Prepared for the Office
       of Emergency and Remedial Response. Washington, D.C. July 26.

U.S. EPA.  1994c. Review Draft Technical Background Document for Soil Screening Guidance. Office
       of Solid Waste Emergency Response. EPA/540/R-94/106. December.

U.S. EPA.  1994d. CHEMS-Compound Properties Estimation and Data. Version 1.00. CHEMDAT8
       Air Emissions Program. Prepared for Chemical and Petroleum Branch, OAQPS. Research
       Triangle Park, North Carolina. November 18.

U.S. EPA.  1994e. Revised Draft Guidance for Performing Screening Level Risk Analyses at
       Combustion Facilities Burning Hazardous Wastes: Attachment C, Draft Exposure Assessment
       Guidance for RCRA Hazardous Waste Combustion Facilities. Office of Emergency and
       Remedial Response. Office of Solid Waste. December 14.

U.S. EPA.  1995a. Review Draft Development of Human Health Based and Ecologically Based Exit
       Criteria for the Hazardous Wastes Identification Project. Volumes I and II.  Office of Solid
       Waste. March 3.

U.S. EPA.  1995b. "Great Lakes Water Quality Initiative Technical Support Document for the Procedure
       to Determine Bioaccumulation Factors." EPA 820/B-95/005. March.

U.S. EPA. 1996. Ecological Data Quality Levels Reference Database, Version 3.0.  EPA Region 5,
       Wastes, Pesticides, and Toxics Division.

U.S. EPA.  1998. Human Health Risk Assessment Protocol for Hazardous Waste Combustion Facilitites.
       External Peer Review Draft. U.S. EPA Region 6 and U.S. EPA OSW.  Volumes 1-3.
       EPA530-D-98-001A. July.

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       Toxicology and Chemistry. Volume 7. Pages 213-219.

Van Hook, R.I. 1974. "Cadmium, Lead, and Zinc Distributions Between Earthworms and Soils:
       Potentials for Biological Accumulation." Bull. Contam. Toxicol.  12:509-512.

U.S. EPA Region 6                                                         U.S. EPA
Multimedia Planning and Permitting Division                                             Office of Solid Waste
Center for Combustion Science and Engineering                                                     C-l 15

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Veith, G.D., D.L. DeFoe and B.V. Bergstedt. 1979. "Measuring and Estimating the Bioconcentration
       Factor of Chemicals in Fish." Journal of Fisheries Research Board of Canada. Volume 36.
       Pages 1040-1048.

Veith, G.D., D.W. Kuehl, F.A. Puglisis, G.E. Glass, and J.G. Eaton.  1977. "Residues of PCBs and DDT
       in the Western Lake Superior Ecosystem." Archives of Environmental Contamination and
       Toxicology.  Volume 5. Pages 487-499.

Veith, G.D., KJ. Macek, S.R. Petrocelli, and J. Carroll.  1980. "An Evaluation of Using Partition
       Coefficients and Water Solubility to Estimate Bioconcentration Factors for Organic Chemicals in
       Fish." Pages 116-129. In J. G. Eaton, P. R. Parrish, and A. C. Hendricks (eds.), Aquatic
       Toxicology.  ASTM STP 707.  American Society for Testing and Materials, Philadelphia.

Vighi, M.  1981.  "Lead Uptake and Release in an Experimental Trophic Chain." Ecotoxicology and
       Environmental Safety. Volume 5. Pages 177-193.

Wang, X., S. Harada, M. Watanabe, H. Koshikawa, and H.J. Geyer.  1996. "Modelling the
       Bioconcentration of Hydrophobic Organic Chemicals in Aquatic Organisms."  Chemosphere. Vol
       32, Number 9. Pages 1783-1793.

Watras, C.J., and N.S. Bloom.  1992. "Mercury and Methylmercury in Individual Zooplankton:
       Implications for Bioaccumulation." Limnology and Oceanography. Volume 37, Number 6.
       Pages 1313-1318.

Watras, C.J., J. MacFarlane, and F.M.M. Morel.  1985.  "Nickel Accumulation by Scenedesmus and
       Daphnia: Food Chain Transport and Geochemical Implications." Canadian Journal of Fisheries
       and Aquatic Science.  Volume 42. Pages 724-730.

Williams, D.R., and J.P.Giesy, Jr. 1979.  "Relative Importance of Food and Water Sources to Cadmium
       Uptake by Gambusia affinis (Poecilidae)." Environmental Research. Volume 16.
       Pages 326-332.

Wofford, H.W., C.D. Wilsey, G.S. Neff, C.S. Giam, and J.M. Neff.  1981.  "Bioaccumulation and
       Metabolism of Phthalate Esters by Oysters, Brown Shrimp, and Sheepshead Minnows."
       Ecotoxicology and Environmental Safely.  Volume 5. Pages 202-210.

Wood, L.W., P. O'Keefe, and B. Bush. 1997. "Similarity Analysis of PAH and PCB Bioaccumulation
       Patterns in Sediment-Exposed Chironomus teutons Larvae."  Environmental Toxicology and
       Chemistry. Volume 16, Number 2. Pages 283-292.

Yockim, R.S., A.R. Isensee, and G.E. Jones. 1978. "Distribution and Toxicity of TCDD and 2,4,5-T in
       an Aquatic Model Ecosystem." Chemosphere. Volume 7, Number  3. Pages 215-220.0

Zaroogian, G.E., and S. Cheer.  1976. "Accumulation of Cadmium by the American Oyster, Crassostrea
       virginica." Nature. Volume 261. Pages 408-410.

Zaroogian, G.E., G. Morrison, and J.F. Heltshe. 1979. "Crassostrea virginica as an Indicator of Lead
       Pollution." Marine Biology.  Volume 52.  Pages 189-196.
U.S. EPA Region 6                                                         U.S. EPA
Multimedia Planning and Permitting Division                                             Office of Solid Waste
Center for Combustion Science and Engineering                                                      C-l 16

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             APPENDIX D

  BIOCONCENTRATION FACTORS (BCFs)
FOR WILDLIFE MEASUREMENT RECEPTORS
 Screening Level Ecological Risk Assessment Protocol

               August 1999

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Screening Level Ecological Risk Assessment Protocol
Appendix D; Wildlife Measurement Receptor BCF Values	August 1999

                                  APPENDIX D

                              TABLE OF CONTENTS

Section                                                                       Page

D-1.0 GENERAL GUIDANCE	D-l

D-l.l BIOTRANSFER FACTORS FOR MAMMALS (Bamamma^	D-3

D-1.2 BIOTRANSFER FACTORS FORBIRDS (Babird) 	D-5

REFERENCES: APPENDIX D TEXT	D-9

TABLES OF WILDLIFE MEASUREMENT RECEPTOR BCF VALUES	D-ll
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Appendix D; Wildlife Measurement Receptor BCF Values	August 1999

                                        APPENDIX D

                       WILDLIFE MEASUREMENT RECEPTOR BCFs

Appendix D provides recommended guidance for determining values for compound-specific, media to
receptor, bioconcentration factors (BCFs) for wildlife measurement receptors.  Wildlife measurement
receptor BCFs should be based on values reported in the scientific literature, or estimated using physical
and chemical properties of the compound.  Guidance on use of BCF values in the screening level
ecological risk assessment is provided in Chapter 5.

Section D-1.0 provides the general guidance recommended to select or estimate compound BCF values for
wildlife measurement receptors. Sections D-1.0 through D-1.3 further discuss determination of BCFs for
specific media and receptors.  References cited in Sections D-l.l through D-1.3 are located following
Section D-1.3.

For the compounds commonly identified in risk assessments for combustion facilities (identified in Chapter
2) and the mammal and bird example measurement receptors listed in Chapter 4, BCF values have been
determined following the guidance in Sections D-1.0 through D-1.3. BCF values for these limited number
of compounds and pathways are included in this appendix (see Tables D-l through D-3) to facilitate the
completion of screening ecological risk assessments. However, it is expected that BCF values for
additional compounds and receptors may be required for evaluation on a site specific basis. In such cases,
BCF values for these additional compounds could be determined following the same guidance
(Sections D-1.0 through D-1.3) used in determination of the BCF values reported hi this appendix. For the
calculation of BCF values for measurement receptors not represented in Sections D-l.l through Dl-3 (e.g.,
amphibians and reptiles), an approach consistent to that presented in this appendix could be utilized by
applying data applicable to those measurement receptors being evaluated.

For additional discussion on some of the references and equations cited in Sections D-1.0 through D-1.3,
the reader is recommended to review the Human Health Risk Assessment Protocol (HHRAP) (U.S. FJPA
1998) (see Appendix A-3), and the source documents cited in the reference section of this appendix.

D-1.0  GENERAL GUIDANCE

This section describes general procedures for developing compound-specific BCFs from biotransfer
factors (Ba) for assessing exposure of measurement receptors. A biotransfer factor is the ratio of the
compound concentration in fresh (wet) weight animal tissue to the daily intake of compound by the
animal through ingestion of food items and media (soil, sediment, surface water). Therefore, as
discussed in Chapter 5, biotransfer factors and receptor-specific ingestion rates can be used to calculate
food item- and media-to-animal BCFs.  This approach provides an estimate of biotransfer of compounds
from applicable food items and media to measurement receptors ingesting these items.

Biotransfer factors could also be used directly in equations to calculate dose to measurement receptors.
However, in order to promote consistency in evaluating exposure across all trophic levels within complex
food webs, BCFs calculated from Ba values are recommended in this guidance for evaluating
measurement receptors. The use of Ba values to determine BCF values, and the use of BCF values in
general, for the estimation of compound concentrations in measurement receptors may introduce
U.S. EPA Region 6                                                                U.S. EPA
Multimedia Planning and Permitting Division                                            Office of Solid Waste
Center for Combustion Science and Engineering                                                        D-l

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Appendix D; Wildlife Measurement Receptor BCF Values	August 1999

uncertainty.  Major factors that influence the uptake of a compound by an animal, and therefore
uncertainty, include bioavailability, metabolic rate, type of digestive system, and feeding behavior.
Uncertainties also should be considered regarding the development of biotransfer values in comparison to
how they are being applied for estimating exposure. For example, biotransfer values may be used to
estimate contaminant uptake to species from items ingested that differ from the species and intakes used
to empirically develop the values. Also, biotransfer data reported in literature may be specific to tissue or
organ analysis versus whole body.  As a result, BCFs may be under- or over-estimated to an unknown
degree.

BCFs for Measurement Receptors Ingesting Food Items BCF values for measurement receptors
ingesting food items (plants  or prey) can be calculated using the compound specific Ba value applicable
to the animal (e.g., mammal, bird, etc.) and the measurement receptor-specific ingestion rate as follows:
                             BCFF_A  = BaA •  IRF                           Equation D-1-1
       where
               BCFF.A =      Bioconcentration factor for food item (plant or prey)-to-animal
                             (measurement receptor) [(mg COPC/kg FW tissue)/(mg COPC/kg FW
                             food item)]
               BaA    =      COPC-specific biotransfer factor applicable for the animal
                             (day/kg FW tissue)
               IRF    =      Measurement receptor food item ingestion rate (kg FW/day)

As an example of applying the above equation, BCF values for plants-to-wildlife measurement receptors
listed in Chapter 4 are provided in Table D-l at the end of this appendix. Measurement-receptor specific
ingestion rates used to calculate BCFs are presented in Table 5-1. Ba values applicable to the mammal
and bird measurement receptors in Table D-l are discussed in Sections D-l.l and D-l.2, respectively.

BCFs for Measurement Receptors Ingesting Media  BCF values for measurement receptors in trophic
levels 2, 3, and 4 ingesting media (i.e., soil, surface water, and sediment) can be calculated using the
compound specific Ba value applicable to the animal (e.g., mammal, bird, etc.) and the measurement
receptor-specific ingestion rate as follows:
                            BCFM A  = BaA ' IRu                           Equation D-l-2
        where
               BCFM.A =      Bioconcentration factor for media-to-animal (measurement receptor)
                             [(mg COPC/kg FW tissue)/(mg COPC/kg WW or DW media)]
               BaA    =      COPC-specific biotransfer factor applicable for the animal
                             (day/kg FW tissue)
U.S. EPA Region 6                                                               U.S. EPA
Multimedia Planning and Permitting Division                                            Office of Solid Waste
Center for Combustion Science and Engineering                                                       D-2

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Appendix D; Wildlife Measurement Receptor BCF Values	August 1999

              IRU    =      Measurement receptor media ingestion rate (WW or DW kg/day)

Equation D-l-2 assumes that BaA provides a reasonable estimate of the uptake of a compound from
incidental ingestion of abiotic media during foraging.

As an example of applying the above equation, BCF values for various wildlife measurement receptors
listed in Chapter 4 are provided in Table D-2 (water) and Table D-3 (soil and sediment).
Measurement-receptor specific ingestion rates used to calculate BCFs are presented in Table 5-1. Ba
values applicable to the mammal and bird measurement receptors for which values were calculated are
discussed in Sections D-l.l and D-1.2, respectively.

BCFs for Dioxins and Furans As discussed in Chapter 2, the BCF values for PCDDs and PCDFs are
calculated using bioaccumulation equivalency factors (BEFs). Consistent with U.S. EPA (1995b), BEFs
are expressed relative to the BCF for 2,3,7,8-TCDD as follows:
                       BCFj = BCF2^TCDD • BEFj                      Equation D-l-3
       where
              BCFj         =      Food item-to-animal or media-to-animal BCF foryth PCDD or
                                   PCDF congener for food item-to-animal pathway [(mg
                                   COPC/kg FW tissue)/(mg COPC/kg FW plant)]or media-to-
                                   animal pathway [(mg COPC/kg FW tissue)/(mg COPC/kg WW
                                   media)]
              BCF2,3j,8-TCDD =      Food item-to-animal or media-to-animal BCF for 2,3,7,8-TCDD
              BEFj         =      Bioaccumulation equivalency factor for/th PCDD or PCDF
                                   congener (unidess)

The use of BEFs for dioxin and furan congeners is further discussed in Chapter 2.

D-l.l  BIOTRANSFER FACTORS FOR MAMMALS (Bamammal)

As discussed in Section D-1.0, calculation of BCF values to be used in pathways for mammals ingesting
food items and media requires the determination of COPC-specific biotransfer factors for mammal
measurement receptors (Bamammc^. This section discusses selection of the fiOn^m^ values used to
calculate the COPC and measurement receptor specific BCF values presented in Tables D-l through D-3.

Organics For organics (except PCDDs and PCDFs), the following correlation equation from Travis and
Arms  (1988) was used to derrive Bammmal values on a FW basis:
                        l°SBamammal =-7.6  + \ogKow                       Equation D-l-4
U.S. EPA Region 6                                                             U.S. EPA
Multimedia Planning and Permitting Division                                          Office of Solid Waste
Center for Combustion Science and Engineering                                                      D-3

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Appendix D; Wildlife Measurement Receptor BCF Values	August 1999
       where
              Bamammai      =     Biotransfer factor for mammals (day/kg FW tissue)
              Kow           =     Octanol-water partition coefficient (unitless)

To calculate the values presented in Tables D-l through D-3, COPC-specific Km values were obtained
from Appendix A-2.

Biotransfer factors obtained from Travis and Arms (1988) were derived from correlation equations
developed from data on experiments conducted with beef cattle ingesting food items and media
containing compound classes such as DDT, pesticides, PCDDs, PCDFs, and PCBs. As further literature
is developed for other species and compounds, the Travis and Arms (1988) correlation equation should
be compared for applicability to species and compound, and best fit correlation for estimation of uptake.

PCDDs and PCDFs Bamammal values for PCDD and PCDFs were derrived from Ba values for cattle as
presented in:

       •     U.S. EPA 1995a. "Further Studies for Modeling the Indirect Exposure Impacts from
              Combustor Emissions." Memorandum from Matthew Lorber, Exposure Assessment
              Group, and Glenn Rice, Environmental Criteria and Assessment Office, Washington,
              D.C. January 20.

U.S. EPA (1995a) determined Ba values for cattle from McLachlan, Thoma, Reissinger, and Hutzinger
(1990). These empirically determined Ba values were recommended by U.S. EPA (1995a) over the
Travis and Arms (1988) correlation equation for dioxins and furans.

Inorganics For metals (except cadmium, mercury, selenium, and zinc), Ba values on a fresh weight
basis were obtained from Baes, Sharp, Sjoreen, and Shor (1984). For cadmium, selenium, and zinc, U.S.
EPA (1995a) indicated that Ba values were derived by dividing uptake slopes [(g compound/kg DW
tissue)/(g compound/kg DW feed)], obtained from U.S. EPA (1992), by a daily consumption rate of
20 kilograms DW per day by cows.

For use in calculating BCF values presented in Tables D-l through D-3 of this appendix, dry weight Ba
values were converted to fresh weight basis by assuming a tissue moisture content (by mass) of
70 percent for cows. Moisture content information was obtained from the following:

       •      U.S. EPA. 1997a.  Exposure Factors Handbook. "Food Ingestion Factors".  Volume H
              EPA/600/P-95/002Fb. August.

       •      Pennington, J.A.T. 1994. Food Value of Portions Commonly Used. Sixteenth Edition.
              J.B. Lippincott Company, Philadelphia.

Mercuric Compounds  Based on assumptions made regarding speciation and fate and transport of
mercury from stack emissions (as discussed in Chapter 2), elemental mercury is assumed not to deposit
onto soils, water, or plants.  Therefore, it is also not available in food items or media for ingestion and
subsequent uptake by measurement receptors. As a result, no BCF values for elemental mercury are
U.S. EPA Region 6                                                              U.S. EPA
Multimedia Planning and Permitting Division                                           Office of Solid Waste
Center for Combustion Science and Engineering                                                       DA

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Appendix D; Wildlife Measurement Receptor BCF Values	August 1999

presented in Tables D-l through D-3 of this appendix.  If site-specific field data suggest otherwise, Ba
values for elemental mercury can be derived from uptake slope factors provided in U.S. EPA (1992) and
U.S. EPA  (1995a), using the same consumption rates as were discussed earlier for the metals like
cadmium,  selenium, and zinc.

Bammmat values for mercuric chloride and methyl mercury were derived from data in U.S. EPA (1997b).
U.S. EPA  (1997b) provides Ba values for mercury in cows, but does not specify the form of mercury.  To
obtain the  Ba values for mercuric chloride and methyl mercury presented in Tables D-l through D-3 of
this guidance, consistent with U.S. EPA (1997b) total mercury was assumed to be composed of
87 percent divalent mercury (as mercuric chloride) and 13 percent methyl mercury in herbivore animal
tissue. Also, assuming that the Ba value provided in U.S. EPA (1997b) is for the total mercury in the
animal tissue, then biotransfer factors in U.S. EPA (1997b) can be determined for mercuric chloride and
methyl mercury, as follows:

       •       The default Ba value of 0.02 day/kg DW for total mercury obtained from U.S. EPA
               (1997b) was converted to a fresh weight basis assuming a 70 percent moisture content in
               cow tissue (U.S.  EPA 1997a; Pennington 1994). The fresh weight Ba value for total
               mercury was multiplied by 0.13 to obtain a Bamammal value for methyl mercury, and
               by 0.87 to obtain a Bamammal value for mercuric chloride.

D-1.2  BIOTRANSFER FACTORS FOR BIRDS

As discussed in Section D-1.0, calculation of BCF values to be used in pathways for birds ingesting food
items and media requires the determination of COPC-specific biotransfer factors for bird measurement
receptors (Bahini). This section discusses selection of the Babird values used to calculate the COPC and
measurement receptor specific BCF values presented in Tables D-1 through D-3.

Oreanics  Babird values for organic compounds (except PCDDs and PCDFs) were derived from Bamamtal
values by assuming that the lipid content (by mass) of birds and mammals is 15 and 19 percent,
respectively. Therefore, Babird values presented in Tables D-l through D-3 were determined by
multiplying Bamammal values by the bird and mammal fat. content ratio of 0.8 (15/19).

Notable uncertainties associated with this approach include (1) extent to which specific organic
compounds bioconcentrate in fatty tissues, and (2) differences in lipid content, metabolism, and feeding
characteristics between species.

PCDDs and PCDFs Babird values presented in Tables D-l through D-3 for PCDD and PCDF congeners
were derrived from data provided in the following:

       •       Stephens, R.D., M. Petreas, and G.H. Hayward. 1995. "Biotransfer and
               Bioaccumulation of Dioxins and Furans from Soil: Chickens as a Model for Foraging
               Animals."  The Science  of the Total Environment.  Volume 175.  Pages 253-273.

Stephens, Petreas, and Hayward (1995) conducted experiments to determine the bioavailability and the
rate of PCDDs and PCDFs uptake from soil by foraging chickens.  Three groups  of White Leghorn
U.S. EPA Region 6                                                               U.S. EPA
Multimedia Planning and Permitting Division                                            Office of Solid Waste
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Screening Level Ecological Risk Assessment Protocol
Appendix D: Wildlife Measurement Receptor BCF Values	August 1999

chickens were studied—control group, low exposure group, and high exposure group. Eggs, tissues
(liver, adipose, and thigh), feed, and feces were analyzed.

Congener specific BaUrd values were derrived from the  Stephens, Petreas, and Hayward (1995) study by
dividing estimated whole body bioconcentration values for the high exposure group by a daily
consumption rate of soil. If congener specific BCF values were not reported for the high exposure group,
then estimated whole body values were determined using reported data for the low exposure group, if
available.  A default consumption rate of soil by chicken of 0.02 kg DW/day was determined as follows:

        (1)     Consumption rate of feed by chicken was obtained from U.S. EPA (1995a), which cites a
               value of 0.2 kg (DW) feed/day obtained from various literature sources.

        (2)     The fraction of feed that is soil (0.1) was obtained from Stephens, Petreas, and
               Hayward (1995).

        (3)     Feed consumption rate of 0.2 kg/day was multiplied by fraction of feed that is soil (0.1),
               to obtain the soil consumption rate by chicken of 0.2 x 0.1 = 0.02 kg DW soil/day.

Inorganics For metals (except cadmium, selenium, and zinc), Babird values were not available in the
literature.  For cadmium, selenium, and zinc, U.S. EPA (1995a) cites Ba values that were derived by
dividing uptake slopes [(g compound/kg dry DW tissue)/(g compound/kg DW feed)], obtained from U.S.
EPA (1992), by a daily ingestion rate of 0.2 kilograms DW per day by poultry. To determine BCF
values presented in Tables D-l through D-3 in this appendix, reported dry weight Ba values were
converted to fresh weight basis by assuming a tissue moisture content (by mass) of 75 percent for
poultry  (U.S. EPA 1997a; Pennington 1994).

Mercuric Compounds Based on assumptions made regarding speciation and fate and transport of
mercury from stack emissions (as discussed in Chapter 2), elemental mercury is assumed not to deposit
onto soils, water, or plants. Therefore, it is also not available in food items or media for ingestion and
subsequent uptake by measurement receptors. As a result, no BCF values for elemental mercury are
presented in Tables D-l through D-3 of this appendix.  If site-specific field data suggest otherwise, Ba
values for elemental mercury can be derived from uptake slope factors provided in U.S. EPA (1992) and
U.S. EPA  (1995a), using the same consumption rates as were discussed earlier for the metals like
cadmium,  selenium, and zinc.

Babird values for mercuric chloride and methyl mercury were derived from data in U.S. EPA (1997b).
U.S. EPA  (1997b) provides Ba values for mercury in poultry, but does not specify the form of mercury.
To obtain the Ba values for mercuric chloride and methyl mercury presented in Tables D-l through D-3
of this guidance, consistent with U.S. EPA (1997b) total mercury was assumed to be composed of
87 percent divalent mercury (as mercuric chloride) and 13 percent methyl mercury in herbivore animal
tissue.  Also, assuming that the Ba value provided in U.S. EPA (1997b) is for the total mercury in the
animal tissue, then biotransfer factors in U.S. EPA (1997b) can be determined for mercuric chloride and
methyl mercury, as follows:
U.S. EPA Region 6                                                                U.S. EPA
Multimedia Planning and Permitting Division                                            Office of Solid Waste
Center for Combustion Science and Engineering                                                        D-6

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Screening Level Ecological Risk Assessment Protocol
Appendix D;  Wildlife Measurement Receptor BCF Values	August 1999

        •       The default Ba value of 0.02 day/kg DW for total mercury obtained from U.S. EPA
               (1997b) was converted to a fresh weight basis assuming a 75 percent moisture content in
               poultry tissue (U.S. EPA 1997a; Pennington 1994).  The fresh weight Ba value for total
               mercury was multiplied by 0.13 to obtain a Babird value for methyl mercury, and by 0.87
               to obtain a Babird value for mercuric chloride.
U.S. EPA Region 6                                                                  U.S. EPA
Multimedia Planning and Permitting Division                                             Office of Solid Waste
Center for Combustion Science and Engineering                                                         D-7

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Appendix D; Wildlife Measurement Receptor BCF Values	August 1999
Baes, C.F., R.D. Sharp, A.L. Sjoreen, and R.W. Shor.  1984. "Review and Analysis of Parameters and
       Assessing Transport of Environmentally Released Radionuclides through Agriculture."
       Oak Ridge National Laboratory. Oak Ridge, Tennessee.

McLachlan, M.S., H. Thoma, M. Reissinger, and O. Hutzinger. 1990. "PCDD/F in an Agricultural
       Food Chain. Parti: PCDD/F Mass Balance of a Lactating Cow." Chemosphere.  Volume 20.
       Pages 1013-1020.

Pennington, J.A.T.  1994.  Food Value of Portions Commonly Used. Sixteenth Edition. J.B. Lippincott
       Company, Philadelphia.

Stephens, R.D., M. Petreas, and G.H. Hayward.  1995. "Biotransfer and Bioaccumulation of Dioxins and
       Furans from Soil:  Chickens as a Model for Foraging Animals." The Science of the Total
       Environment. Volume 175. Pages 253-273.

Travis, C.C., and A.D. Arms.  1988.  "Bioconcentration of Organics in Beef, Milk, and Vegetation."
       Environmental Science and Technology. 22:271-274.

U.S. EPA. 1992. Health Reassessment of Dioxin-Like Compounds, Chapters 1 to 8. Workshop Review
       Draft.  OHEA. Washington, D.C.  EPA/600/AP-92/001a through OOlh. August.

U.S. EPA. 1994. "Draft Guidance for Performing Screening Level Risk Analyses at Combustion
       Facilities Burning Hazardous Wastes. Attachment C, Draft Exposure Assessment Guidance for
       RCRA Hazardous Waste Combustion Facilities." April 15.

U.S. EPA 1995a. "Further Studies for Modeling the Indirect Exposure Impacts from Combustor
       Emissions." Memorandum from Matthew Lorber, Exposure Assessment Group, and Glenn Rice,
       Indirect Exposure Team, Environmental Criteria and Assessment Office, Washington, D.C.
       January 20.

U.S. EPA. 1995b. Great Lakes Water Quality Initiative Technical Support Document for the Procedure
       to Determine Bioaccumulation Factors. EPA-820-B-95-005.  Office of Water, Washington, D.C.
       March.

U.S. EPA. 1997a. Exposure Factors Handbook. "Food Ingestion Factors". Volume H
       EPA/600/P-95/002Fb. August.

U.S. EPA. 1997b. Mercury Study Report to Congress, Volumes I through VIII.  Office of Air Quality
       Planning and Standards and ORD.  EPA/452/R-97-001.  December.

U.S. EPA Region 6                                                             U.S. EPA
Multimedia Planning and Permitting Division                                          Office of Solid Waste
Center for Combustion Science and Engineering                                                       D-9

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Screening Level Ecological Risk Assessment Protocol
Appendix D; Wildlife Measurement Receptor BCF Values	   August 1999
               TABLES OF MEASUREMENT RECEPTOR BCF VALUES


                   Screening Level Ecological Risk Assessment Protocol

                                  August 1999
D-l   PLANTS TO WILDLIFE MEASUREMENT RECEPTORS	D-13

D-2   WATER TO WILDLIFE MEASUREMENT RECEPTORS	D-16

TABLE D-3  SOIL/SEDIMENT TO WILDLIFE MEASUREMENT RECEPTORS 	D-22
U.S. EPA Region 6                                                     U.S. EPA
Multimedia Planning and Permitting Division                                     Office of Solid Waste
Center for Combustion Science and Engineering                                             D-l 1

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            APPENDIX E




    TOXICITY REFERENCE VALUES




Screening Level Ecological Risk Assessment Protocol



              August 1999

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Screening Level Ecological Risk Assessment Protocol
Appendix E; Toxicity Reference Values	August 1999

                                  APPENDIX E

                              TABLE OF CONTENTS

Section                                                                     Page

E-1.0  TRVs FOR COMMUNITY MEASUREMENT RECEPTORS IN SURFACE WATER,
      SEDIMENT, AND SOIL 	E-l

E-2.0  TRVs FOR WILDLIFE MEASUREMENT RECEPTORS	E-5

REFERENCES: APPENDIX E TEXT 	E-7

TABLES OF TOXICITY REFERENCE VALUES	E-9
U.S. EPA Region 6                                                     U.S. EPA
Multimedia Planning and Penmitting Division                                     Office of Solid Waste
Center for Combustion Science and Engineering                                               E-i

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Screening Level Ecological Risk Assessment Protocol
Appendix E:  Toxicity Reference Values	August 1999

                                          APPENDIX E

                               TOXICITY REFERENCE VALUES
Appendix E presents implementation of the recommended approach (described in Chapter 5) for identifying
toxicity reference values (TRVs) for measurement receptors. Discussion is provided for determining
compound-specific TRY values for community and wildlife measurement receptors.

Following the guidance in Sections E-1.0 through E-1.2, U.S. EPA OSW has identified default TRY values
for the measurement receptors of the seven example food webs (listed in Chapter 4) and the compounds
commonly identified in ecological risk assessments for combustion facilities (identified in Chapter 2).
Section E-1.0 describes the determination of TRY values for surface water, sediment, and soil community
measurement receptors in the example food webs. Section E-2.0 describes determination of TRY values fen-
wildlife measurement receptors in the example food webs. Tables E-l through E-8 present the default TRY
values selected, the basis for selection of each value, and the references evaluated in determination of each
value.

TRY values for a limited number of compounds are included in this appendix (see Tables E-l through E-3)
to facilitate the completion of screening ecological risk assessments. However, it is expected that TRV
values for additional compounds and receptors may be required for evaluation on a site specific basis. In
such cases, TRV values for these additional compounds could be determined following the same guidance
used in determination of the 77?V values reported in this appendix. For the determination of TRV values for
measurement receptors not specifically represented in Sections E-1.0 through E-2.0 (e.g., amphibians and
reptiles), an approach consistent to that presented in this appendix could be utilized by applying data
applicable to those measurement receptors being evaluated.

The default TRVs provided in Tables E-l through E-8 are based on values reported in available scientific
literature. Toxicity  values identified in secondary reference sources were verified, where possible, by
reviewing the primary reference source. As noted in Chapter 5, TRV values may change as additional
toxicity research is conducted and the availability of toxicity data in the scientific literature increases.  As a
result, U.S. EPA OSW recommends evaluating the latest toxicity data before completing a risk assessment
to ensure that the toxicity data used in the risk assessment is the most current.  If more appropriate TRV
values can be documented, they should be used presented to the respective permitting authority for
approval.

TR Vs were not identified for amphibians and reptiles because of the paucity of lexicological information on
these receptors. Additional guidance on determination and use of TRV values in the screening level
ecological risk assessment is provided in Chapter 5.

E-1.0  TRVs FOR COMMUNITY MEASUREMENT RECEPTORS IN SURFACE WATER,
        SEDIMENT, AND SOIL

TRV values provided in this appendix for community measurement receptors in surface water, sediment,
and soil were identified from screening toxicity values developed and/or adopted by federal and/or state
regulator^' agencies.  As discussed in Chapter 5, these screening toxicity values are generally provided in
the form of standards, criteria, guidance, or benchmarks. For compounds  with no available screening
toxicity value,  TRVs were determined using toxicity values from available scientific literature. The

U.S. EPA Region 6                                                                 U.S. EPA
Multimedia Planning and Permitting Division                                             Office of Solid Waste
Center for Combustion Science and Engineering                                                        E-l

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Screening Level Ecological Risk Assessment Protocol
Appendix E; Toxicity Reference Values	August 1999

equilibrium partitioning (EqP) approach was used to compute several sediment TR Vs. Uncertainty factors
(UFs) were applied to toxicity values, as necessary, to meet the TRY criteria discussed in Chapter 5.  The
following sections discuss determination of 77?V values for community receptors in surface water,
sediment, and soil.

Freshwater TRVs Freshwater TRVs should be used for freshwater and estuarine ecosystems with a
salinity less than 5 parts per thousand. Freshwater 77? Vs, based on the dissolved concentration of the
compound in surface water, are listed in Table E-l. 77?Vs were identified using the following hierarchy:

        1.     Federal chronic ambient water quality criteria (AWQC) calculated for with no final
               residue value (U.S. EPA 1999; 1996b).  Federal AWQC for cadmium, copper, lead,
               nickel, and zinc were multiplied by a chemical-specific conversion factor to determine a
               TWbased on dissolved concentration (U.S. EPA 1999; 1996b).

        2.     Final chronic values (FCV) for COPCs for which their AWQC included a final residue
               value (U.S. EPA 1996b).

        3.     If inadequate data (insufficient number of families of aquatic life with toxicity data) were
               available to compute an AWQC or FCV, U.S. EPA (1999; 1996b) also reported
               secondary chronic values (SCV) calculated using the Tier II method in the Great Lakes
               Water Quality Initiative (GLWQI) (reported in 40 CFR Part 122).  This method is similar
               to the procedures for calculating an FCV. It uses statistically-derived "adjustment factors"
               to address deficiencies in available data. The adjustment factor decreases as the number of
               representative families increases.

        4.     If an AWQC, FCV, or GLWQI Tier n SCV value were not available, toxicity values cited
               by U.S. EPA (1987) were identified. These toxicity values represent the lowest available
               values. Further, additional toxicity values available from the AQUIRE database in U.S.
               EPA's ECOTOXicology Database System (U.S. EPA 1996a) were identified. If collected
               from a secondary source (such as AQUIRE), original studies were obtained and reviewed
               for accuracy. The toxicity values reported in Table E-l represent the lowest (most
               conservative), ecologically relevant, available value.

        5.     If toxicity data were unavailable, a surrogate TRY from a COPC with a similar structure
               was  identified.

        6.     If no surrogate was available, a TRV was not listed. The potential toxicity of a COPC
               with no 77? V should be addressed as an uncertainty (see Chapter 6)

Standard AQUIRE report summaries on tests were screened for duration, endpoint, effect, and
concentration. Studies were also screened for ecologically relevant effects by focusing on studies that
evaluated effects on survival, reproduction, and growth.  Aspects of endpoint, duration, and test organism
in each toxicity study were evaluated to identify the most appropriate study.  Several compounds, most
notably metals, had a large number of toxicity values based on various endpoints, organisms, and exposure
durations. In these instances, best scientific judgment was used to identify the most appropriate toxicity
value (see Chapter 5).
U.S. EPA Region 6                                                                 U.S. EPA
Multimedia Planning and Permitting Division                                             Office of Solid Waste
Center for Combustion Science and Engineering                                                         E-2

-------
Screening Level Ecological Risk Assessment Protocol
Appendix E;  Toxicity Reference Values _ August 1999

Chronic NOAEL-based values were not adjusted, but rather were carried through unchanged to become the
TRY. Toxicity values identified as "less than" a particular concentration were divided by 2 to represent an
average value because the true value is unknown, and it occurs between 0 and the noted concentration.
UFs discussed in Chapter 5 were applied to toxicity values not meeting TRY criteria.

Saltwater TRVs Saltwater TRVs are applicable to marine water bodies and estuarine systems with a
salinity greater than 5 ppt.  Saltwater TRVs are listed in Table E-2. Saltwater water 77? V development
followed the same procedure as described above for freshwater receptors, except no GLWQI Tier n SCVs
were available. In addition, if no saltwater 37? V for a surrogate compound was available, the
corresponding freshwater TRY was adopted.

Freshwater Sediment TRVs Freshwater sediment TRVs are listed in Table E-3. They are applicable to
water bodies with a salinity less than 5 ppt. Freshwater sediment TRVs were identified from various sets of
screening values and ecotoxicity review documents. The lowest available screening values among the
following sources were identified:

        1.      No effect level (NEL) and lowest effect level (LEL) values from "Ontario's Approach to
               Sediment Assessment and Remediation" (Persaud et al. 1993)

        2.      Apparent effects threshold (AET) values for the amphipod, Hyallela azteca, reported in
               "Creation of Freshwater Sediment Quality Database and Preliminary Analysis of
               Freshwater Apparent Effects Thresholds" (Washington State Department of Ecology
               1994)

        3.      Sediment effect concentrations jointly published by the National Biological Service and the
               U.S. EPA (Ingersoll et al. 1996).

If a screening value was not available in the sources listed above, toxicity studies and other values compiled
and reported by Jones, Hull, and Suter (1997) were reviewed to identify possible 77?Vs.   Relevant studies
were prioritized based on the criteria listed in Chapter 5, and uncertainty factors were applied, as
applicable, based on criteria presented (see Chapter 5).

If a screening or sediment toxicity value was not available for an organic COPC, a freshwater sediment
77? V was computed, using the EqP approach (see Chapter 5), from the compounds corresponding
freshwater 77? V and KK value.  The U.S. EPA Office of Water utilizes the EqP approach to develop
sediment quality criteria for nonionic (neutral) organic chemicals (U.S. EPA 1993). The EqP approach
assumes that the toxicity of a compound in sediment is a function of the concentration in  pore water and
that to be nontoxic, the pore water must meet the surface water final chronic value.  The EqP approach also
assumes that the concentration of a compound in sediment pore water depends on the carbon content of the
sediment and the compound's organic carbon partitioning coefficient (U.S. EPA 1993).  A 77? V may be
calculated using the following equation (U.S. EPA 1993):
                             TRVsed  = Koc ' foe  • rav«,                            Equation E-l
        where
               TRVsed =       Sediment TRV (|ag/kg)
U.S. EPA Region 6                                                                 U.S. EPA
Multimedia Planning and Permitting Division                                             Office of Solid Waste
Center for Combustion Science and Engineering                                                         E-3

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Screening Level Ecological Risk Assessment Protocol
Appendix E; Toxicity Reference Values	August 1999

               Koc    =       Organic carbon partition coefficient (L/kg)
              foc     =       Fraction of organic carbon in sediment (unitless)—default value = 4%
                              (0.04)
               TRVm  =       Corresponding surface water TRY (ug/L)

Marine Sediment TRVs Marine sediment TRVs are listed in Table E-4.  They are applicable to sediments
of marine water bodies and estuarine systems with a salinity greater than 5 ppt.  Marine sediment TRVs
were developed following the procedures used to identify the freshwater sediment TRVs.  Screening values
were compiled from the following sources:

       1.      No observed effect level (NOEL) sediment quality assessment guidelines for State of
               Florida coastal waters (MacDonald 1993).

       2.      Marine and estuarine effects range low (ERL) values from "Incidence of Adverse
               Biological Effects  Within Ranges of Chemical Concentrations in Marine and Estuarine
               Sediments" (Long et al. 1995)

       3.      ERL values from "The Potential for Biological Effects of Sediment-Sorbed Contaminants
               Tested in the National Status and Trends Program" (Long and Morgan 1991)

       4.      Marine sediment quality criteria from "Sediment Management Standards" (Washington
               State Department of Ecology 1991)

Screening values were adopted directly as 77? Vs. If a screening value was not available in the sources
listed above, toxicity values from a search of the scientific literature and those compiled and reported by
Hull and Suter (1994) were reviewed to identify possible TRVs. Original studies were obtained, where
possible, and toxicity values were verified.  Relevant studies were prioritized based on the criteria listed in
Chapter 5, and uncertainty factors  were applied, as appropriate, based on criteria (see Chapter 5).  If a
screening or ecologically relevant sediment toxicity value from the scientific literature were not available
for an organic COPC, a marine sediment 77?V was computed, using the EqP approach, from the COPC's
corresponding saltwater TRVand Koc value (see Equation E-l).

Terrestrial Plant TRVs  The terrestrial plant TRVs listed in Table E-5 are based on bulk soil exposures.
Available terrestrial plant toxicity values from the  scientific literature were used to develop presented TR V
values. Toxicity values were first identified from the following secondary sources:

        1.      Studies cited in Toxicological Benchmarks for Screening Potential Contaminants of
               Concern for Effects on Terrestrial Plants: 1997 Revision (Efrovmson, Will, Suter, and
               Wooten 1997).  Available studies  were obtained and reviewed for accuracy of toxicity
               values. UFs were applied depending on study endpoint and available information.

       2.      Toxicity values in the Phytotox database in U.S. EPA's  ECOTOXicology Database
               System. Available studies were obtained and toxicity values were verified. UFs were
               applied depending on study endpoint and available information.

        3.      Toxicity values in U.S. EPA Region 5 Ecological Data Quality Levels (EDQL) Database
               (PRC 1995).  The database contains media-specific EDQLs for the RCRA Appendix IX
               constituents (40 CFR Part 264). The EDQLs represent conservative media concentrations

U.S. EPA Region 6                                                                 U.S. EPA
Multimedia Planning and Permitting Division                                             Office of Solid Waste
Center for Combustion Science and Engineering                                                         E-4

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Screening Level Ecological Risk Assessment Protocol
Appendix E: Toxicity Reference Values	August 1999

               protective of media receptors and wildlife that might be exposed through food chains based
               in these media.  Available studies were obtained and toxicity values were verified.  UFs
               were applied depending on study endpoint and available information.

Original studies were obtained, where possible, and prioritized based on criteria listed in Chapter 5.
Uncertainty factors were applied, as appropriate, based on criteria (discussed in Chapter 5) to develop TRY
values. For COPCs without toxicity data, the TRY for a surrogate COPC was adopted.  If an appropriate
surrogate TRY was not available, no TRY value was identified.  Generally, review of toxicity data available
in the scientific literature indicates that limited TRVs are available for organic compounds; while TRVs for
metals are available.

Soil Invertebrate TRVs  The soil invertebrate TRVs listed in Table E-6 are based on bulk soil exposures.
Available soil invertebrate toxicity values from the scientific literature were used to develop TRVs for these
receptors.  Soil invertebrate toxicity values were first identified from the following secondary sources:

       1.      Studies cited in Toxicological Benchmarks for Potential Contaminants of Concern for
               Effects on Soil and Litter Invertebrates and Heterotrophic Process (Will and Suter n
               1995a).  Available studies were obtained and toxicity values were verified. UFs were
               applied depending on study endpoint and available information.

       2.      Scientific literature was searched for toxicity values for outstanding compounds. Relevant
               studies were obtained,  toxicity values were verified, and UFs were applied as described

Original studies were obtained, where possible, and prioritized based on criteria listed in Chapter 5.
Uncertainty factors were applied, as appropriate, based on criteria to develop TRVs. If no toxicity value
was available for a COPC, the TRY for a surrogate COPC was adopted.

E-2.0  TRVs FOR WILDLIFE MEASUREMENT RECEPTORS

TRY values for wildlife measurement receptors are listed in Tables E-7 (mammals) and E-8 (birds).  TRVs
were not developed for each avian and mammalian measurement receptor in the seven example food webs
because of the paucity of species-specific data. Rather, U.S. EPA OSW focused on identifying a set of
avian TRVs and a set of mammalian TRVs for the classes of compounds listed in Section 2.3.  U.S. EPA
OSW assumed that, among the literature reviewed for a particular guild, the lowest available toxicity value
across orders in class Aves and across orders in class Mammalia would provide a conservative estimate of
toxicity. Available mammalian and avian toxicity values from the scientific literature were used to develop
TRVs for these receptors.  Also, as previously noted, TRY values were not identified for amphibians and
reptiles because of the paucity of lexicological information on these receptors. Wildlife measurement
receptors TRV values were first identified from the following secondary sources:

       1.       Toxicity values compiled in  Toxicological Benchmarks for Wildlife: 1996 Revision
               (Sample, Opresko, and Suter 1996).

       2.       Toxicity values listed in the Terretox database of U.S. EPA's ECOTOXicology Database
               System (U.S. EPA 1996b) were screened to identify studies potentially meeting the criteria
               listed in Chapter 5.
U.S. EPA Region 6                                                                  U.S. EPA
Multimedia Planning and Permitting Division                                             Office of Solid Waste
Center for Combustion Science and Engineering                                                          E-5

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Screening Level Ecological Risk Assessment Protocol
Appendix E; Toxicity Reference Values	August 1999

Original studies were compiled, where possible, and reviewed to verify their accuracy based on criteria
listed in Chapter 5. In many cases, best scientific judgement was used to screen out studies with poor
experimental design (see Chapter 5). Uncertainty factors were applied, as appropriate, to develop TRVs
based on criteria presented in Chapter 5.

Conversions  Some avian and mammalian toxicity data are expressed in terms of compound concentration
in the food of the test organism. To convert to daily dose, it is necessary to determine the exposure
duration and organism body weight. If the study does not report this information, the results should not be
used to compute a 77? V. If information on exposure duration and organism body weight is available,
dietary concentration can be computed to dose using the following generic equation:
                                          C  ' IR
                                           DTI/                                   Equation E-2
                                           BW
       where
               DD    =       COPCdose(mgCOPC/kgBW/day)
               C      =       Concentration of COPC in diet (mg COPC/kg food)
               IR     -       Food ingestion rate (kg/day)
               BW    =       Test organism body weight (kg)
U.S. EPA Region 6                                                                U.S. EPA
Multimedia Planning and Permitting Division                                            Office of Solid Waste
Center for Combustion Science and Engineering                                                        E-6

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Screening Level Ecological Risk Assessment Protocol
Appendix E: Toxicity Reference Values	
     August 1999
Efroymson, R.A., M.E. Will, G.W. Suter H, and A.C. Wooten. 1997. Toxicological Benchmarks for
       Screening Contaminants of Potential Concern for Effects on Terrestrial Plants: 1997 Revision.
       Oak Ridge National Laboratory, Oak Ridge, TN. 128 pp. ES/ER/TM-85/R3. November.

Ingersoll, C.G., P.S. Haverland, E.L. Brunson, TJ. Canfield, F.J. Dwyer, C.E. Henke, N.E. Kemble, D.R.
       Mount, and R.G. Fox.  1996. "Calculation and Evaluation of Sediment Effect Concentrations for
       the Amphipod Hyallela azteca and the Midge Chironomous riparius." International Association
       of Great Lakes Research. Volume 22.  Pages 602-623.

Jones, D.S., G.W.  Suter n, and R.N.  Hull. 7997. Toxicological Benchmarks for Screening Contaminants
       of Potential Concern for Effects on Sediment-Associated Biota: 1997 Revision.  Oak Ridge
       National Laboratory, Oak Ridge TN. 34 pp. ES/ER/TM-95/R4. November.

Long, E.R., and L.G. Morgan.  1991. The Potential for Biological Effects of Sediment-Sorbed
       Contaminants Tested in the National Status and Trends Program.  National Oceanic and
       Atmospheric Administration (NOAA) Technical Memorandum No. 5, OMA52, NOAA National
       Ocean Service. August.

Long, E.R., D.D. MacDonald, S.L. Smith, and F.D. Calder.  1995. "Incidence of Adverse Biological
       Effects Within Ranges of Chemical Concentrations in Marine and Estuarine Sediments."
       Environmental Management. Volume 19. Pages 81-97.

MacDonald, D.D.  1993. Development of an Approach to the Assessment of Sediment Quality in Florida
       Coastal Waters.  Florida Department of Environmental Regulation.  Tallahassee, Florida.
       January.

Persaud, D., R. Jaaguagi, and A. Hayton. 1993. Guidelines for the Protection and Management of
       Aquatic Sediment Quality in  Ontario. Ontario Ministry of the Environment.  Queen's  Printer of
       Ontario. March.

Sample, B.E., D.M. Opresko, and G.W Suter H. 1996. Toxicological Benchmarks for Wildlife: 1996
       Revision. Oak Ridge National Laboratory, Oak Ridge, TN. 227 pp. ES/ER/TM-86YR3. June.

U.S. EPA. 1987. Quality Criteria for Water—Update #2. EPA 440/5-86-001.  Office of Water
       Regulations and Standards. Washington, D.C. May.

U.S. EPA. 1996a. ECOTOX.  ECOTOXicology Database System. A User's Guide. Version 1.0. Office
       of Research and Development.  National Health and Environmental Effects  Research Laboratory.
       Mid-Continent Ecology Division. Duluth, MN.  March.
U.S. EPA Region 6
Multimedia Planning and Permitting Division
Center for Combustion Science and Engineering
U.S. EPA
Office of Solid Waste
             E-7

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Screening Level Ecological Risk Assessment Protocol
Appendix E; Toxicity Reference Values	August 1999

U.S. EPA.  1996b.  "Ecotox Thresholds." ECO Update. EPA 540/F-95/038.  Office of Emergency and
       Remedial Response. January.

U.S. EPA.  1999. National Recommended Water Quality Criteria-Correction. EPA 822-Z-99-001.
       Office of Water.  April.

Washington State Department of Ecology.  1991. Sediment Management Standards. Washington
       Administrative Code 173-204.

Washington State Department of Ecology.  1994. Creation and Analysis of Freshwater Sediment Quality
       Values in Washington State. Publication No. 97-32-a. July.
U.S. EPA Region 6                                                                U.S. EPA
Multimedia Planning and Permitting Division                                            Office of Solid Waste
Center for Combustion Science and Engineering                                                        E-8

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Screening Level Ecological Risk Assessment Protocol
Appendix E; Toxicity Reference Values	August 1999
                TABLES OF TOXICITY REFERENCE (TRV) VALUES


                  Screening Level Ecological Risk Assessment Protocol

                                 August 1999
E-l   FRESHWATER TOXICITY REFERENCE VALUES 	E-ll

E-2   MARINE/ESTUARINE SURFACE WATER TOXICITY REFERENCE VALUES .. E-19

E-3   FRESHWATER SEDIMENT TOXICITY REFERENCE VALUES	E-27

E-4   MARINE/ESTUARINE SEDIMENT TOXICITY REFERENCE VALUES  	E-34

E-S   TERRESTRIAL PLANT TOXICITY REFERENCE VALUES	E-42

E-6   SOIL INVERTEBRATE TOXICITY REFERENCE VALUES 	E-57

E-7   MAMMAL TOXICITY REFERENCE VALUES	E-69

E-8   BIRD TOXICITY REFERENCE VALUES	E-84
U.S. EPA Region 6                                                  U.S. EPA
Multimedia Planning and Permitting Division                                   Office of Solid Waste
Center for Combustion Science and Engineering                                            E-9

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and calculated as follows: TRV = exp(mc[ln(hardness)]+bc) where
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Suter and Tsao (1996). Calculated using Great Lakes Water
Quality Initiative Tier n methodology.
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and calculated as follows: TRV = exp(mc[ln(hardness)]+bc) where
m,. = 0.8460 and bc = 0.0584. Criterion was converted to dissolved
concentration using a conversion factor of 0.997. A assumed
hardness of 100 mg/L and a conversion from mg/L to /^g/L were
used to calculate the displayed value.



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TABLE E-1












CE VALUES
Z
1x3
TER TOXICITY REFER
(Page 7 of 8)
FRESHWA









dized Procedure." Z. Wasser Abwasser Forsch. 15.
1
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CA
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REFERENCES
utants on Daphnia magna Straus
Toxic Action of Water Poll
"8
£
g
j.
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c 2
CO
1
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03
Fish." Annals NewYork Academy of Sciences.
_c
in Relation to Disea!
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UH CA GO
^ £ £
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Q

13
u
ihes." Journal of Hazardous Materials. Volume
VJ
iE
S
i to Fresh and Saltwa
13
_CJ
te Toxicity of 47 Industrial Chem
u
£
K
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ai
izdowski, and
Q
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g'oo
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for the Evaluation of Acute Toxi<
iment of Bioassay Methods
h abstract).
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;, with Englis
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Reproduction Test." Water Research. Volume 23.
>>
Q
phnia magna in the 2
Q
^s
^s
nful Effects of Water Pollutants tt
1989. "Results of the Harr
tj
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43
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ow." Environmental Toxicology and Chemistry.
c
c
§
i
u
TS
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a
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00
1
c
id Di-n-octyl Phthalate to Daphni
lie Toxicity of Di-n-butyl ai
U
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i£ vo
$ CA
•^ co
*£
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988. "Toxicity and Bioconcentration of
'. Volume 7. Pages 47-62.
- C
il
Coyle, and W.J. Adai
I Toxicology and Che
-.- s
^ s
i, D.L. Stalling, G.M. DeGraeve,
in in Rainbow Trout." Environnu
ll, J.D. Petty, P.H. Petermai
7,8-Tetrachlorodibenzofura
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Potential Contaminants of Conce
me.
Benchmarks for Screening
Oak Ridge, Tennessee. Jv
Toxicological
il Laboratory.
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LC50 of each HMW PAH exceeded 50 vgfL. This TRY she
assessing the risk of total HMW PAHs.




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                                                                                                                                 s

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t or more of the test animals lifetime expectancy. Acute exposures represent single exposures or multiple
e following general guidelines were used. For invertebrates and other lower trophic level aquatic biota:
rom 3 to 6 days, and (3) acute duration lasted 2 days or less. For fish: (1) chronic duration lasted for more
duration lasted less than 2 weeks.
L TRV. See Chapter 5 (Section 5.4) of the SLERAP for a discussion of the use of uncertainty factors.
:or.
tations are provided at the end of this appendix.
;ction 5.4. 1 .2) for a discussion of the use of best scientific judgement. Factors evaluated include test
:ty of toxicity data.







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1!
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Lethal concentration for 100 percent of the test organisms.
Lowest Observed Effect Concentration




n n n
s§ki
^3
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Lowest Observed Effect Level
Lethal threshold concentration for 50 percent of the test organ




n n
W 8
35

No Observed Adverse Effect Level
No Observed Effect Level




n II
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W J
< w
ii

Secondary Chronic Value
Toxicity Reference Value




n n
> >
0 g
vi H
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-------






TABLE E-2















ENCE VALUES
K
W
&
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U
RINE/ESTUARINE SURFACE WATER TOXI
(Page 7 of 8)
<
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REFERENCES













uatic Organisms." Environmental
O"
rs to Representative A
5
t Phthalate Esl
ti_.
d J. W. Gorsuch. 1995. "A Summary of the Acute Toxicity oi
. Pages 1569-1574.
§ 2
U
rS *o
•§>
"ft
11
S •«
oo U
11
03 ^
7; §>
Oi -S
d 8
-f i
R
c/r
1
'O
<


Diseases in Fish."
o
ts in Relation
I
13
1
"a
_o
JS
y
f^
s;
l-M
i
f
3
d
•a
bj*
"8
>'
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M^
^^
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D
«
cu
£
'S
M
J
t-T
"c5
o
£
<£
H
*.
ed
W
c
I
ii
«
the First 50 Multicentre Evaluation of I
78.
C4M ^1
ative Acute Toxicity o
Volume 26. Pages 65
£3
i1!
£ i
i|
ON g
.- s
98. Pages 535-546. Calleja, M.C., G. Persoone, and P. Gelad
: Non- Vertebrates." Archives of Environmental Contaminatio
CN .a
2 M
II
> 0
Y of Sciences. '
ity Chemicals t
s "
1 0
C n
" 1,
t°
o £
« 5
r
^
"S
g
•«;
ma/ of Hazardous Materials. Volume
a
Saltwater Fishes." Jo.
•a
As to Fresh an
3
id E. Rider. 1977. "The Acute Toxicity of 47 Industrial Chen
g
'%
o
•a
fi
Q
vi
.f
C
C 00
0> ^H
*""* f^l
J S
< s
•• «
»^' D
^ oe
- O3
0 a-
c£
o
Crt
S
03
Q
\ates)". Aquatic Toxicology and Risk
so
>ws (Cyprinodon varit
c
eepshead Min
w ^
atory Comparison of the Early Life-Stage Toxicity Test Using
Philadelphia, PA. Pages 354-375. As cited in AQUIRE 1991
s *•
.0 ts
(B T-I
IE
f5 00
a|
2^
i~
G -^
U>
^ W
d §
•o 5
C 
!<§
w 5
'5
shiuchi. 1981.
54. (Japanese, \
2^
. t-~
> S
OI
T3 „
g 0
CS OB
- S3
> C1-
2 ^
"o

15
CA
rt
K
Ironmental Toxicology and Chemistry.
^
'athead Minnow." Ew
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3,7,8-Tetrachlorodibenzofuran in Rainbow Trout." Environm
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REFERENCES













lala
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1-8 8
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C X CA (V
1 § !&
a.-5 S g>
& *^ CA S
o, S^ o "5
the three sets of freshwater toxicity value;
aes were not used because of the compexi
xicity to benthic invertebrates. Among th
torn the corresponding freshwater TRV u
ivater habitats were identified from
ific literature, available toxicity vali
e, and organic carbon content) in to
tses, a default TRV was calculated 1
^ -r~; Q. TO
1 §££
l~ •« .« r;
* ^ -5 «
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o .§
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C8 "
, C.E. Henke, N.E. Kemble, D.R. Mount,
ge Chironomous riparius." International
Brunson, T.J. Canfield, F.J. Dwyer
ihipod Hyallela azteca and the Mid,
H|
flj <
- 0)
•§5
CO LH
— S
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ection and Management of Aquatic Sedim
ton. 1993. Guidelines for the Prat
>,
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assuming a fractional organic content of 0.04. d
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5
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^ VI
Recommended NOEL for Florida Department of
Environmental Regulation (DER) (MacDonald 1993
This TRV may be used in risk of total HMW PAHs i
assessed.
^
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O O
*!


2
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1
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42
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Recommended NOEL for Florida DER (MacDonald
o
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—
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1
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u
c
u
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S



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s
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s
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1
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assuming a fractional organic content of 0.04.
I
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^



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d
















s
r"
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2
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e
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TRV is a LEL value from Persaud et al. (1993).
0
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3
3 S
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o
3
S
1
0
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0
c

•£
c
I
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Recommended NOEL for Florida DER (MacDonald

C*J

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JO
« s
^ 12
1


*2
2
1
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c
a
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^
1

Recommended NOEL for Florida DER (MacDonald

CO


2
3 S
2|

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3
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1
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nil
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assuming

p

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ted using EqP appro
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assuming

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ted using EqP appro
onal organic content
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assuming

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assuming

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onal organic content
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TRY was
assuming

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TRY was calculated using OC-based marine sediment
quality criterion from Washington State Department of
Ecology (1991) and fractional organic carbon content of
0.04, as follows:
TRY = 47 mg/kg * 0.04 * 1000 /^g/mg.
o

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TRY was calculated using OC-based marine sediment
quality criterion from Washington State Department of
Ecology (1991) and fractional organic carbon content of
0.04, as follows:
TRY = 58 mg/kg * 0.04 * 1000 //g/mg.
o
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00
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TRY was calculated using EqP approach (EPA 1993),
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No TRY was calculated because no Koc or Kow value was
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assuming a fractional organic content of 0.04. d
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a
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TRY was calculated using OC-based marine sediment
quality criterion from Washington State Department of
Ecology (1991) and a fractional OC content of 0.04, as
follows: TRY = 0.38 mg/kg * 0.04 * 1000 Mg/mg.

vi
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TRY was calculated using OC-based marine sediment
quality criterion from Washington State Department of
Ecology (1991) and a fractional OC content of 0.04, as
follows: TRY = 3.9 mg/kg * 0.04 * 1000 A>g/mg.

VO
in


u
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3
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u
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assuming a fractional organic content of 0.04. d


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Reference and Notes c
'S £? <— *
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q
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2
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15
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5*
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03 g
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TRY is a U.S. EPA Region V guideline val
classification of sediments for determining
of dredged material for open water disposa
Hull and Sutern (1994).

o

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p

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1
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CO
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No toxicity data available for divalent in
Total mercury is used as surrogate. Rec<
for Florida DER (MacDonald 1993).



d
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No toxicity data available for methyl me
mercury is used as surrogate. Recomme
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was calculated from the corresponding










REFERENCES









1
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U
XI
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"O
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diments in marine and estuarine habitats were identified from several sets of toxicity
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weren
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"o le of naturally-occurring sediment features (such as grain size, ammonia, sulfide, soil
0 K
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O. c
y: ."
"c il
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«
he lowest available toxicity value for a particular compound was adopted as the TRY,
ng EPA's equilibrium partitioning approach, assuming a 4 percent organic carbon con
" C/3
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(rt i>
> Ctf
^r i—
w u.
c/; CJ
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it-Associated Biota: 1994 Revision.
1
(jfectt on i
June.
Elf o
k. <*
<£ «
£l
Si g
V) £
§ rf
^ J>
. Suter n. 1994. Toxicological Benchmarks for Screening Contaminants of Potential
1-95/Rl. Environmental Sciences Division, Oak Ridge National Laboratory. Oak Ric
£ *
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w a«rf Trends Program. National Oceanic and
S
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CA
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acDonald, S.L. Smith, and F.D. Calder. 1995. "Incidence of Adverse Biological Effe
2

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. " Environmental Management. Volume 19. Pages 81-97.
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tment of Environmental Regulation.
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. Florida
2
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993. Development of an Approach to the Assessment of Sediment Quality in Florida
e, Florida. January.
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Ontario Ministry of the Environment.
6
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%
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uagi, and A. Hayton. 1993. Guidelines for the Protection and Management ofAquat
rinter of Ontario. March,
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<£,
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:>r hnical Basis for Deriving Sediment Quality Criteria for Nonionic Organic Contami
IK Office of Water. EPA-822-R-93-011. September.
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Reference and Notes d



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a)pyrene toxicity used as
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terize risk of total HMW
istrial plants.
O ca K ^ ul
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AL TOXICITY REFERENCE
(Page 6 of 15)
MAMM









ation. This source was reviewed to identify studies to develop TRVs for
id-specific toxicity values. For some compounds, the available
ch reference was obtained and reviewed to identify a single toxicity value
sed on a secondary source. As noted below, additional compendia were
ic scientific literature was searched, and relevant studies were obtained

REFERENCES










e § S .2
73

jlogically-relevant mammal toxicity infoi
obtained and reviewed to identify compc
discussed in Section 5.4. In most cases,
;ould not be obtained, a toxicity value is
in Sample, Opresko, and Suter 0 (1996)
for the TRV is highlighted in bold.
er n (1996) provides a comprehensive review of ecc
iformation presented, one or more references were <
tigle study meeting the requirements for a TRV, as <
compound. In a few cases where a primary study c
*-* --5 •-- ,?~!
3 r? « o
1/2 ^ « S
"2 " •» "
c c t> S
M O C «
r^ "O "S ^>.
^ « c C
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S
c
%>
-a
"S
•«
•Si
c
R
"S
5
•5
^>
eg
on Reproduction Study of Rats Given
neSO. Pages 241-252.
?i
nd B.A.Schwctz. 1979. "Three-Gener
wlogy and Applied Pharmacology. Vol
i, K.D. Nitschke, C.G. Humiston, R J. Kociba, a
orodibenzo-p-dloxin (TCDD) in the Diet." Toxit
* -^
•a w
g a
w i
. 01
<*:
ta ao,
r *~"
*? w"
b ri
f
g

(quatic Life and Associated Wildlife. EPA/600/R-93/055. Office of
•^
e>
,7,8-Tetrachlorodibenzop-dioxin Risks t>
identified the four studies listed below.
Report on Data and Methods for Assessment of 2,3,
velopment. Washington, D.C. March. This report
S £
-IS ^"^
v -n
S C
^1
cn M
£ 1
'™H OJ
. oi
<•
2
w
w
D
sh." Journal of Reproduction and Fertility. Volume 19. Pages 365-376.
£
d Mortality in Mink Fed on Great Lakes
c
es
1
1
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o
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trachlorodibenzo-p-dioxin on Developmental Parameters of Neonatal
f2
)f Epidermal Growth Factor and 2,3,7,8-
Volume 17. Pages 27-31.
i, and A.C. Napolitano. 1988. "Biological Effects c
of Environmental Contamination and Toxicology.
c tn
C3 ^J
•K -S
= "S
«|
 .5
ei S
1
<
,4',5'-, 2,3,6,2', 3', 6'-, and 3,4,5,3',4',5'-Hexachlorobiphenyl and Aroclor
r4
"Toxicological Manifestations of 2,4,5,
le 15. Pages 63-79.
, W.J. Breslin, B.A. Olson, and R.K. Ringer. 1985.
d of Toxicology and Environmental Health. Volum
c S
CB C
• -« I*
£ 5
3 £
« r
^'•i
42
tti .5
js
_o
J2
<
" Archives of Environmental Contamination and Toxicology. Volume 17.
•^
,7,8-Tetrachlorodibenzo-p-dioxin to Mir
ich, and S.J. Bursain. 1988. "Acute Toxicity of 2,3
JB
"3
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-------
                 APPENDIX F

EQUATIONS FOR COMPUTING COPC CONCENTRATIONS
        AND COPC DOSE INGESTED TERMS

      Screening Level Ecological Risk Assessment Protocol

                   August 1999

-------
Screening Level Ecological Risk Assessment Protocol
Appendix F: Equations for COPC Concentration and Dose Ingested	August 1999

                              APPENDIX F

                          TABLE OF CONTENTS
Table                                                                Page

EQUATIONS FOR COMPUTING COPC CONCENTRATIONS

F-l-1       COPC CONCENTRATIONS IN TERRESTRIAL PLANTS FOR TERRESTRIAL
           FOOD WEBS	F-l

F-l-2       COPC CONCENTRATIONS IN HERBIVOROUS MAMMALS IN FOREST,
           SHORTGRASS PRAIRIE, TALLGRASS PRAIRIE, AND SHRUB/SCRUB FOOD
           WEBS  	F-3

F-l-3       COPC CONCENTRATIONS IN INVERTEBRATES IN FOREST, SHORTGRASS
           PRAIRIE, TALLGRASS PRAIRIE, AND SHRUB/SCRUB FOOD WEBS	F-7

F-l-4       COPC CONCENTRATIONS IN HERBIVOROUS BIRDS IN FOREST,
           SHORTGRASS PRAIRIE, TALLGRASS PRAIRIE, AND SHRUB/SCRUB FOOD
           WEBS  	F-9

F-l-5       COPC CONCENTRATIONS IN OMNIVOROUS MAMMALS IN FOREST,
           TALLGRASS PRAIRIE, SHORTGRASS PRAIRIE, AND SHRUB/SCRUB FOOD
           WEBS  	F-13

F-l-6       COPC CONCENTRATIONS IN OMNIVOROUS BIRDS IN FOREST, TALLGRASS
           PRAIRIE, SHORTGRASS PRAIRIE, AND SHRUB/SCRUB FOOD WEBS  	F-22

F-l-7       COPC CONCENTRATIONS IN AQUATIC VEGETATION IN THE
           FRESHWATER/WETLAND, BRACKISH/INTERMEDIATE MARSH, AND
           SALTMARSH FOOD WEBS 	F-29

F-l-8       COPC CONCENTRATIONS IN ALGAE IN THE
           FRESHWATERAVETLAND BRACKISH/INTERMEDIATE MARSH,
           AND SALTMARSH FOOD WEBS	F-31

F-l-9       COPC CONCENTRATIONS IN HERBIVOROUS MAMMALS IN
           FRESHWATERAVETLAND, BRACKISH/INTERMEDIATE MARSH, AND
           SALTMARSH FOOD WEBS 	F-33

F-l-10       COPC CONCENTRATIONS IN HERBIVOROUS BIRDS IN
           FRESHWATERAVETLAND, BRACKISH/INTERMEDIATE MARSH, AND
           SALTMARSH FOOD WEBS 	F-38

F-l-11       COPC CONCENTRATIONS IN BENTHIC INVERTEBRATES IN
           FRESHWATERAVETLAND, BRACKISH/INTERMEDIATE MARSH, AND
           SALTMARSH FOOD WEBS	F-43
U.S. EPA Region 6                                                U.S. EPA
Multimedia Planning and Permitting Division                                  Office of Solid Waste
Center for Combustion Science and Engineering                                          F-i

-------
Screening Level Ecological Risk Assessment Protocol
Appendix F; Equations for COPC Concentration and Dose Ingested	August 1999

                               APPENDIX F

                           TABLE OF CONTENTS
Table

F-l-12      COPC CONCENTRATIONS IN WATER INVERTEBRATES IN
           FRESHWATER/WETLAND, BRACKISH/INTERMEDIATE MARSH, AND
           SALTMARSH FOOD WEBS                                     F-45

F-l-13      COPC CONCENTRATIONS IN HERBIVOROUS AND PLANKTIVOROUS FISH IN
           FRESHWATER/WETLAND, BRACKISH/INTERMEDIATE MARSH, AND
           SALTMARSH FOOD WEBS  	F-47

F-l-14      COPC CONCENTRATIONS IN OMNIVOROUS MAMMALS IN
           FRESHWATER/WETLAND, BRACKISH/INTERMEDIATE MARSH, AND
           SALTMARSH FOOD WEBS	F-50

F-l-15      COPC CONCENTRATIONS IN OMNIVOROUS BIRDS IN
           FRESHWATER/WETLAND, BRACKISH/INTERMEDIATE MARSH, AND
           SALTMARSH FOOD WEBS  	F-60

F-l-16      COPC CONCENTRATIONS IN OMNIVOROUS FISH IN
           FRESHWATER/WETLAND, BRACKISH/INTERMEDIATE MARSH, AND
           SALTMARSH FOOD WEBS  	F-69

F-l-17      COPC CONCENTRATIONS IN CARNIVOROUS FISH IN
           FRESHWATER/WETLAND, BRACKISH/INTERMEDIATE MARSH, AND
           SALTMARSH FOOD WEBS  	F-72
EQUATIONS FOR COMPUTING COPC DOSE INGESTED TERMS
F-2-1       COPC DOSE INGESTED TERMS IN HERBIVOROUS MAMMALS IN FOREST,
           SHORTGRASS PRAIRIE, TALLGRASS PRAIRIE, AND SHRUB/SCRUB FOOD
           WEBS  	F-75

F-2-2       COPC DOSE INGESTED TERMS IN HERBIVOROUS BIRDS IN FOREST,
           SHRUB/SCRUB, SHORTGRASS PRAIRIE, AND TALLGRASS PRAIRIE FOOD
           WEBS  	F-79

F-2-3       COPC DOSE INGESTED TERMS IN OMNIVOROUS MAMMALS IN FOREST,
           SHRUB/SCRUB, SHORTGRASS PRAIRIE, AND TALLGRASS PRAIRIE FOOD
           WEBS  	F-84

F-2-4       COPC DOSE INGESTED TERMS IN OMNIVOROUS BIRDS IN FOREST,
           SHRUB/SCRUB, TALLGRASS PRAIRIE, AND SHORTGRASS PRAIRIE FOOD
           WEBS  	F-92

U.S. EPA Region 6                                                U.S. EPA
Multimedia Planning and Permitting Division                                 Office of Solid Waste
Center for Combustion Science and Engineering                                          F-ii

-------
Screening Level Ecological Risk Assessment Protocol
Appendix F; Equations for COPC Concentration and Dose Ingested	August 1999

                               APPENDIX F

                           TABLE OF CONTENTS
Table                                                                Page

F-2-5       COPC DOSE INGESTED TERMS IN CARNIVOROUS MAMMALS IN FOREST,
           SHORTGRASS PRAIRIE, TALLGRASS PRAIRIE, AND SHRUB/SCRUB FOOD
           WEBS 	F-98

F-2-6       COPC DOSE INGESTED TERMS IN CARNIVOROUS BIRDS IN FOREST,
           SHORTGRASS PRAIRIE, TALLGRASS PRAIRIE, AND SHRUB/SCRUB FOOD
           WEBS 	F-106

F-2-7       COPC DOSE INGESTED TERMS IN HERBIVOROUS MAMMALS IN
           FRESHWATER/WETLAND, BRACKISH/INTERMEDIATE MARSH, AND
           SALTMARSH FOOD WEBS  	F-114

F-2-8       COPC DOSE INGESTED TERMS IN HERBIVOROUS BIRDS IN
           FRESHWATER/WETLAND, BRACKISH/INTERMEDIATE MARSH, AND
           SALTMARSH FOOD WEBS  	F-120

F-2-9       COPC DOSE INGESTED TERMS IN OMNIVOROUS MAMMALS IN
           FRESHWATER/WETLAND MARSH, BRACKISH/INTERMEDIATE MARSH, AND
           SALTMARSH FOOD WEBS  	F-126

F-2-10      COPC DOSE INGESTED TERMS IN OMNIVOROUS BIRDS IN
           BRACKISH/INTERMEDIATE MARSH, SALTMARSH, AND
           FRESHWATER/WETLAND FOOD WEBS 	F-136

F-2-11      EQUATIONS FOR COMPUTING COPC DOSE INGESTED TERMS IN
           CARNIVOROUS MAMMALS IN BRACKISH/INTERMEDIATE MARSH,
           SALTMARSH, AND FRESHWATER/WETLAND FOOD WEBS	 F-143

F-2-12      COPC DOSE INGESTED TERMS IN CARNIVOROUS BIRDS IN
           BRACKISH/INTERMEDIATE MARSH, SALTMARSH, AND
           FRESHWATERAVETLAND FOOD WEBS 	F-153

F-2-13      COPC DOSE INGESTED TERMS IN CARNIVOROUS SHORE BIRDS IN
           BRACKISH/INTERMEDIATE MARSH, SALTMARSH, AND
           FRESHWATERAVETLAND FOOD WEBS 	 F-164
U.S. EPA Region 6                                                U.S. EPA
Multimedia Planning and Permitting Division                                 Office of Solid Waste
Center for Combustion Science and Engineering                                          F-iii

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iable is calculated with the equation in Table B-3-1. This variable represents t
ue to wet and dry deposition of COPCs onto plant surfaces. The limitations ant
ing this variable include the following:
Variables Q, Dydp, and Dywp are COPC- and site-specific. Uncertainties ass
site-specific.
In calculating the variable Fw, values of r assumed for most organic compoun
insoluble polystyrene microspheres tagged with radionuclides — may accurate
organic compounds under site-specific conditions.
The empirical relationship used to calculate the variable Rp, and the empirica
relationship, may not accurately represent site-specific plant types.
The recommended procedure for calculating the variable kp does not consider
processes. This conservative approach contributes to the possible overestimal
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iable is calculated with the equation in Table B-3-2.
inties associated with the use of this equation include the following:
The algorithm used to calculate values for the variable F, assumes a default v
(Whitby's average surface area of particulates [aerosols]) of background plus
value for urban sources. If a specific site is located in an urban area, the use i
more appropriate. The ST value for urban sources is about one order of magni
background plus local sources and would result in a lower Fv value; however,
only a few percent lower.
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iable is calculated with the equation in Table B-3-3. Cs is the COPC concentra
iable is calculated using emissions data, ISCST3 air dispersion and deposition i
t equations (presented in Appendix B).
inties associated with the use of this equation include the following:
The availability of site-specific information, such as meteorological data, will
estimates.
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s variable is COPC-, site-, and receptor-specific, and is calculated using the following equation to com
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s variable is species- and site-specific, and depends on the percentage of the dietary food item that is
taminated. U.S. EPA OSW recommends that a default value of 1.0 be used for all food types when siti
>rmation is not available. The following uncertainty is associated with this variable:
The actual amount of contaminated food ingested by a species depends on food availability, diet
composition, and animal behavior. Therefore, the default value of 100 percent may not accurate
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greater mixing depth. This uncertainty may overestimate
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potential mixing with in situ materials) in comparison to
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information is not available. The following uncertainty is i
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. The default value for a screening level ecological risk assessment is 100 percent for computing
on an exclusive diet. For calculating an equal diet, Fdla is determined based on the number of di
inents in the total diet. The application of an equal diet is further discussed in Chapter 5.
tainties associated with this variable include:
The actual proportion of the diet that is comprised of a specific dietary item depends on sever
including: food availability, animal behavior, species composition, and seasonal influences. '
uncertainties may over- or under- estimate Fdla when applided to site-specific receptors.
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estimate exposure from ingestion of a single dietary item.
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variable is COPC- and site-specific and is calculated using Table B-2-17. Uncertainties as
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All of the variables in the equation in Table B-2-17 are COPC- and site-specific. Thei
default values rather than site-specific values, for any or all of these variables, will coi
or overestimation of C^,,.
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variable is species- and site-specific, and depends on the percentage of water ingested that
OSW recommends that a default value of 1 .0 be used when site specific information is not
ollowing uncertainty is associated with this variable:
The actual amount of contaminated water ingested by species depends on site-specific
homerange, and animal behavior; therefore, the default value of 100 percent may not a
specific conditions, and the proportion of ingested water that is contaminated will like
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'ariable is site-specific and COPC-specific; it is calculated using the eqi
ated with this variable include:
Modeled soil concentrations may not accurately represent site-speci
COPC concentration in soil used to calculate the COPC concentratil
overestimated to an unknown degree.
BCFS.INV values may not accurately represent site-specific soil condi
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ated with this variable:
FCMs do not account for metabolism, thus for COPCs with signific
over-estimated to an unknown degree.
The application of FCMs for computing concentration in terrestrial
uncertainty (see Chapter 5)
are obtained from the U.S. EPA (1995) "Great Lakes Water Quality In
ocedure to Determine Bioaccumulation Factors."
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Default: 1.0
ariable is species- and site-specific, and depends on the percentage of tl
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mtion is not available. The following uncertainty is associated with thi
The actual amount of contaminated food ingested by a species depei
composition, and animal behavior. Therefore, the default value of 1
site-specific conditions, and may overestimate the proportion of con
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iable is site- and COPC-specific; it is calculated using the equation in Table
inties introduced by this variable include the following:
Some of the variables in the equations in Tables B-3-1, B-3-2, and B-3-3 —
Dywp — are COPC- and site-specific.
hi the equation in Table B-3-1, uncertainties associated with other variable
(values for organic compounds estimated on the basis of the behavior of pol
(estimated on the basis of a generalized empirical relationship), kp (estimal
chemical degradation), and Yp (estimated on the basis of national harvest y
All of these uncertainties contribute to the overall uncertainty associated wi
In the equation in Table B-3-3, COPC-specific soil-to-plant bioconcentratio
reflect site-specific conditions.
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lated. U.S. EPA OSW recommends that a default value of 1.0 be used for all food types when si
on is not available. The following uncertainty is associated with this variable:
The actual amount of contaminated food ingested by a species depends on food availability, die
composition, and animal behavior. Therefore, the default value of 100 percent may not accurat
site-specific conditions, and may overestimate the proportion of contaminated food ingested.
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able is site-specific and COPC-specific; it is calculated using the equation in Table F-1-2. Unce
d with this variable include:
Variables: CTP, Cs, and €„.,„, are COPC- and site-specific.
Variables: BCFTF.HM, BCFS.HM, and BCFW.,,M are based on biotransfer factors for beef cattle (Ba,
receptor specific ingestion rates, and therefore may introduce uncertainty when used to comput
concentrations in site-specific mammals.
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variable is species- and site-specific, and depends on the percentage of th
minated. U.S. EPA OSW recommends that a default value of 1.0 be use(
nation is not available. The following uncertainty is associated with this
The actual amount of contaminated food ingested by a species depen
composition, and animal behavior. Therefore, the default value of H
site-specific conditions, and may overestimate the proportion of con
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variable is species- and site-specific, and depends on the percentage of th
nal. The default value for a screening level ecological risk assessment is
ntration based on an exclusive diet. For calculating an equal diet, Fditl i;
•y components in the total diet. The application of an equal diet is furthe
rtainties associated with this variable include:
The actual proportion of the diet that is comprised of a specific dieta
including: food availability, animal behavior, species composition, z
uncertainties may over- or under- estimate Fdle, when applied to site-
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estimate exposure from ingestion of a single dietary item.
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exposure when applied to site-specific receptors.
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variable is site-specific and COPC-specific; it is calculated using the equ
iated with this variable include:
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Variables: SCFTP.HS, BCFS.,,B, and BCFW.,,B are based on biotransfer
receptor specific ingestion rates, and therefore may introduce uncert
concentrations for site-specific herbivorous birds.
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include the following:
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default values rather than site-specific values, for any or all of these varii
or overestimation of C^.,,,,.
Uncertainty associated with/^ is largely the result of uncertainty associal
and may be significant in specific instances. Uncertainties associated wi1
be significant because of many variable-specific uncertainties.
eq of uncertainly associated with the variables d^ and dbs is expected to b(
ion for estimating a variable (d^) is generally available or because the pro
The uncertainty associated with the variables /„. and CMO, is associated wil
OC content values can vary widely for different locations in the same med
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incentration in herbivorous mammals through indirect water exposure (tot;
values are provided in Appendix D.
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able is species- and site-specific, and depends on the percentage of water :
iV recommends that a default value of 1.0 be used when site specific infon
wing uncertainty is associated with this variable:
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homerange, and animal behavior; therefore, the default value of 100 perc
specific conditions, and the proportion of ingested water that is contamin;
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and may overestimate the proportion of contamin
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iable is species- and site-specific, and depends on the percentage of the diet that is comprised of
rates. The default value for a screening level ecological risk assessment is 100 percent for computing
ation based on an exclusive diet. For calculating an equal diet, Fdltl is determined based on the numbe
omponents in the total diet. The application of an equal diet is further discussed in Chapter 5.
nties associated with this variable include:
The actual proportion of the diet that is comprised of a specific dietary item depends on several factor
including: food availability, animal behavior, species composition, and seasonal influences. These
uncertainties may over- or under- estimate Fdla when applied to site-specific receptors.
The default value of 100 percent for an exclusive diet introduces uncertainty and may over-estimate
exposure from ingestion of a single dietary item.
The default value for an equal diet introduces uncertainty and may over- or under- estimate exposure
applied to site-specific receptors.
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iable is site- and COPC-specific; it is calculated using the equation in Table F-1-1.
nties introduced by this variable include the following:
Some of the variables in the equations in Tables B-3-1, B-3-2, and B-3-3 — including Cs, Cyv, Q, Dyd
Dywp — are COPC- and site-specific.
In the equation in Table B-3-1, uncertainties associated with other variables include the following: F,
(values for organic compounds estimated on the basis of the behavior of polystyrene microspheres), %
(estimated on the basis of a generalized empirical relationship), kp (estimation process does not consi
chemical degradation). All of these uncertainties contribute to the overall uncertainty associated with
In the equation in Table B-3-3, COPC-specific soil-to-plant bioconcentration factors (BCFTP) may not
reflect site-specific conditions.
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iable is COPC-, site-, habitat- and receptor-specific, and is calculated using the following equation to
the COPC concentration in omnivorous birds through indirect dietary exposure. BCFTP.OB values are
1 in Appendix D.
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iable is COPC- and site-specific, and should be calculated using
weight basis.
nties associated with this variable include:
For soluble COPCs, leaching might lead to movement to belov
greater mixing depth. This uncertainty may overestimate Cs.
Deposition to hard surfaces may result in dust residues that ha1
mixing with in situ materials) in comparison to that of other re
Cs.
Modeled soil concentrations may not accurately represent site-:
COPC concentration in soil may be under- or overestimated to
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iable is COPC-, site-, habitat- and receptor-specific, and is calcu
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iable is species- and site-specific, and depends on the percentagi
W recommends that a default value of 1 .0 be used for a screenin
ion is not available. The following uncertainty is associated wit
The actual amount of contaminated soil ingested by species de]
home range, and animal behavior; therefore, the default value <
specific conditions, and the proportion of soil ingested that is c
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Varies (calculated - Table B-2-17)
PC- and site-specific and is calculated using Table B-2-17. Uncertainties asso
s following:
variables in the equation in Table B-2-17 are COPC- and site-specific. Therel
ilues rather than site-specific values, for any or all of these variables, will conn
imation of CMOI.
ity associated with/^. is largely the result of uncertainty associated with defaull
)e significant in specific instances. Uncertainties associated with the variable i
cant because of many variable-specific uncertainties.
rtainly associated with the variables d^ and dbs is expected to be minimal eithe
mating a variable (dm) is generally available or because the probable range for
:ainty associated with the variables /„ and CMot is associated with estimates of
t values can vary widely for different locations in the same media, the uncertai
dues may be significant in specific cases.
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cies- and site-specific, and depends on the percentage of water ingested that is
ends that a default value of 1.0 be used when site specific information is not a\
rtainty is associated with this variable:
1 amount of contaminated water ingested by species depends on site-specific ir
ge, and animal behavior; therefore, the default value of 100 percent may not ac
onditions, and the proportion of ingested water that is contaminated will likely
n. 1 8 a B °
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site-specific.
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hen applied to site-specific organisms.
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ihic level-specific and is provided in Chaptei
this variable:
letabolism, thus for COPCs with significant
wn degree.
)r computing concentration in terrestrial fooi
. EPA 1995 "Great Lakes Water Quality Inil
ccumulation Factors."
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-specific, and depends on the percentage of i
ecommends that a default value of 1 .0 be us<
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minated food ingested by a species depends
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variable is species- and site-specific, and depends on the percentage of the diet
tebrates. The default value for a screening level ecological risk assessment is 1
sntration based on an exclusive diet. For calculating an equal diet, Fdle, is deteri
ry components in the total diet. The application of an equal diet is further discu
irtainties associated with this variable include:
The actual proportion of the diet that is comprised of a specific dietary item de]
including: food availability, animal behavior, species composition, and seasoni
uncertainties may over- or under- estimate Fdla when applied to site-specific rei
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from ingestion of a single dietary item.
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applied to site-specific receptors.
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Default: 1.0
variable is species- and site-specific, and depends on the percentage of the diets
iminated. U.S. EPA OSW recommends that a default value of 1.0 be used for a]
mation is not available. The following uncertainty is associated with this varia
The actual amount of contaminated food ingested by a species depends on food
and animal behavior. Therefore, the default value of 100 percent may not accu
conditions, and may overestimate the proportion of contaminated food ingestec
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variable is species- and site-specific, and depends on the percentage of the diet that is comprised o
tebrates. The default value for a screening level ecological risk assessment is 100 percent for com
miration based on an exclusive diet. For calculating an equal diet, F^,, is determined based on th<
ry components in the total diet. The application of an equal diet is further discussed in Chapter 5.
rtainties associated with this variable include:
The actual proportion of the diet that is comprised of a specific dietary item depends on several fa
including: food availability, animal behavior, species composition, and seasonal influences. Thes
uncertainties may over- or under- estimate Fdia when applied to site-specific receptors.
The default value of 100 percent for an exclusive diet introduces uncertainty and may over-estima
from ingestion of a single dietary item.
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applied to site-specific receptors.
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Varies (calculated - Table F-1-9)
variable is site-specific and COPC-specific; it is calculated using the equation in Table F-1-9. Uni
dated with this variable include:
Variables: CAV, C/^C,^, and Cmlot are COPC- and site-specific.
Variables: BCFBS_HM and BCFW.HM are based on biotransfer factors for beef cattle (Babaf), and rec
ingestion rates, and therefore may introduce uncertainty when used to compute concentrations for
herbivorous mammals.
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Default: 1.0
variable is species- and site-specific, and depends on the percentage of the dietary food item that i
minated. U.S. EPA OSW recommends that a default value of 1.0 be used for all food types when
nation is not available. The following uncertainty is associated with this variable:
The actual amount of contaminated food ingested by a species depends on food availability, diet c
and animal behavior. Therefore, the default value of 100 percent may not accurately reflect site-s
conditions, and may overestimate the proportion of contaminated food ingested.
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s variable is site-specific and chemical-specific; it is calculated using the equation in Table F-1
ociated with Ihis variable include:
Variables: CAV, C^C,,^ and €„.,„, are COPC- and site-specific.
Variables: BCFBS.HB and BCFW.HB are based on biotransfer factors for chicken (Bachtcken ), and
ingestion rates, and therefore may introduce uncertainty when used to compute concentration
herbivorous birds.
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s variable is species- and site-specific, and depends on the percentage of the dietary food item t
[laminated. U.S. EPA OSW recommends lhat a defaull value of 1.0 be used for all food types w
jrmation is not available. The following uncertainty is associated with this variable:
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and animal behavior. Therefore, the default value of 100 percent may not accurately reflect s
conditions, and may overestimate the proportion of contaminated food ingested.
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is variable is species- and site-specific, and depends on the percentage of the diet that is comprised c
bivorous birds. The default value for a screening level ecological risk assessment is 100 percent for
icentration based on an exclusive diet. For calculating an equal diet, Fdie, is determined based on th
tary components in the total diet. The application of an equal diet is further discussed in Chapter 5.
certainties associated with this variable include:
The actual proportion of the diet that is comprised of a specific dietary item depends on several fi
including: food availability, animal behavior, species composition, and seasonal influences. The
uncertainties may over- or under- estimate Fdia when applied to site-specific receptors.
The default value of 100 percent for an exclusive diet introduces uncertainty and may over-estinu
from ingestion of a single dietary item.
The default value for an equal diet introduces uncertainty and may over- or under- estimate expos
applied to site-specific receptors.
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is variable is site-specific and COPC-specific; it is calculated using the equation in Table F-1-8. Un
ociated with this variable include:
CdYI values are COPC- and site-specific.
BCF\v-a. values are intended to represent "generic algae species", and therefore may over- or und<
exposure when applied to site-specific species.
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is variable is COPC-, site-, habitat- and receptor-specific, and is calculated using the following equa
npute the COPC concentration in aquatic omnivorous mammals through indirect dietary exposure. 1
ues are provided in Appendix D.
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This variable is species- and site-specific, and depends on the percentage of
contaminated. U.S. EPA OSW recommends that a default value of 1.0 be us
information is not available. The following uncertainty is associated with tl
(1) The actual amount of contaminated food ingested by a species depends
and animal behavior. Therefore, the default value of 100 percent may
conditions, and may overestimate the proportion of contaminated food
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default value for a screening level ecological risk assessment is 100 percent i
exclusive diet. For calculating an equal diet, Fdta is determined based on th
total diet. The application of an equal diet is further discussed in Chapter 5.
Uncertainties associated with this variable include:
(1) The actual proportion of the diet that is comprised of a specific dietary
including: food availability, animal behavior, species composition, anc
uncertainties may over- or under- estimate Fdlel when applied to site-spi
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from ingestion of a single dietary item.
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applied to site-specific receptors.

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with this variable include:
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should be summarized as part of each SLERA report.
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under-estimate exposure when applied to site-specific vegetation.
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values are provided in Appendix D.
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Default: 1.0
This variable is species- and site-specific, and depends on the perce
contaminated. U.S. EPA OSW recommends that a default value of
information is not available. The following uncertainty is associate
(1) The actual amount of contaminated food ingested by a species
and animal behavior. Therefore, the default value of 100 perc
conditions, and may overestimate the proportion of contamini

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This variable is species- and site-specific, and depends on the perce
vegetation. The default value for a screening level ecological risk a
concentration based on an exclusive diet. For calculating an equal
dietary components in the total diet. The application of an equal dii
Uncertainties associated with this variable include:
(1) The actual proportion of the diet that is comprised of a specifi
including: food availability, animal behavior, species compos
uncertainties may over- or under- estimate Fdla when applied 1
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from ingestion of a single dietary item.
(3) The default value for an equal diet introduces uncertainty and
applied to site-specific receptors.

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s equation calculates the concentration of contaminants sor
i equation include the following:
The default variable values recommended for use in the '
site-specific water body conditions. The degree of uncer
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allowing reasonable estimates is generally available.
Uncertainties associated with variables fbs, CMO, and Kdbs
content values in their calculation. The uncertainty may
is known to vary widely in different locations in the sam
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\ OS W recommends that a default value of 1 .0 be used for
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conditions, and the proportion of soil ingested that is cor
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COPC concentration in aquatic omnivorous mammals through indirect water exposure.
in Appendix D.
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The following uncertainty is associated with this variable:
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specific conditions, and the proportion of ingested water that is contaminated will

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This variable is COPC- and trophic level-specific and is provided in Chapter 5, Table 5-2.
uncertainties are associated with this variable:
(1) FCMs do not account for metabolism, thus for COPCs with significant metabolism, cc
estimated to an unknown degree.
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Chapter 5)
FCMs are obtained from the U.S. EPA 1995 "Great Lakes Water Quality Initiative Technic;
the Procedure to Determine Bioaccumulation Factors."
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information is not available. The following uncertainty is associated with this variable:
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concentration based on an exclusive diet. For calculating an equal diet, Fdll, is determined t
dietary components in the total diet. The application of an equal diet is further discussed ir
Uncertainties associated with this variable include:
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including: food availability, animal behavior, species composition, and seasonal influ
uncertainties may over- or under- estimate Fdlt, when applied to site-specific receptors
(2) The default value of 100 percent for an exclusive diet introduces uncertainty and may
from ingestion of a single dietary item.
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applied to site-specific receptors.
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1. U.S. EPA OSW recommends that a default value of 1.0 be used for all food types when
s not available. The following uncertainty is associated with this variable:
ual amount of contaminated food ingested by a species depends on food availability, diet c
mal behavior. Therefore, the default value of 100 percent may not accurately reflect site-s
>ns, and may overestimate the proportion of contaminated food ingested.
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onents in the total diet. The application of an equal diet is further discussed in Chapter 5.
. associated with this variable include:
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ig: food availability, animal behavior, species composition, and seasonal influences. The;
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gestion of a single dietary item.
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i this variable include:
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;le dietary item.
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include:
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equation calculates the concentration of contaminants sorbed to bed sediments. Uncertai
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site-specific water body conditions. The degree of uncertainty associated with default vz
expected to be limited either because the probable ranges for these variables are narrow
allowing reasonable estimates is generally available.
Uncertainties associated with variables f,,,, CMol and Kdbs are largely associated with the
content values in their calculation. The uncertainty may be significant in specific instani
is known to vary widely in different locations in the same medium. This variable is site-
maximum COPC concentration in sediment in the assessment area and is computed fron
concentrations using the ISCST3 air dispersion and deposition model, and fate and trans
in Chapter 3.
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range, and animal behavior; therefore, the default value of 100 percent may not accurate!
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This variable is COPC- and site-specific and is calculated using Table B-2-
equation include the following:
( 1 ) All of the variables in the equation in Table B-2-17 are COPC- and si
values rather than site-specific values, for any or all of these variable;
overestimation of C^.,,,,.
(2) Uncertainty associated with/^ is largely the result of uncertainty asst
may be significant in specific instances. Uncertainties associated wit
significant because of many variable-specific uncertainties.
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information for estimating a variable (dw) is generally available or because
narrow. The uncertainty associated with the variables f^. and CMo, is associ
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values rather than site-specific values, for any or all of these variables, will contribute to the under- or
overestimation of C^,,,.
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may be significant in specific instances. Uncertainties associated with the variable Lf and K^ may also be
significant because of many variable-specific uncertainties.
degree of uncertainly associated with the variables dw and dbs is expected to be minimal either because
mation for estimating a variable (d^.) is generally available or because the probable range for a variable (dbs) :
>w. The uncertainty associated with the variables /«, and CKrlol is associated with estimates of OC content.
use OC content values can vary widely for different locations in the same medium, the uncertainty associated
using default OC values may be significant in specific cases.
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following uncertainty is associated with this variable:
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Varies
variable is receptor-specific, and is discussed in Chapter 5. Inj
rovided in Chapter 5, Table 5-1. Uncertainties associated with
Food ingestion rates are influenced by several factors includin
and reproduction, and dietary composition. Ingestion rates are
activity level and body weight U.S. EPA (1993). These factor;
when used to estimate daily dose.
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uninated. U.S. EPA OSW recommend that a default value of 1
mation is not available. Uncertainties associated with this var:
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conditions, and may overestimate the proportion of contaminal
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stimate dietary exposure.
Otol
variable is species- and site-specific, and depends on the perce:
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entration based on an exclusive diet. The application of an equ
rtainties associated with this variable include:
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including: food availability, animal behavior, species composi
default value of 100 percent for the exclusive diet, may over-e
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    is variable is site-specific and COPC-specific; it is calculated using the equation in Table F-1-3. Uncertainties
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    ormation is not available. The following uncertainty is associated with this variable:
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    icentration based on an exclusive diet. For calculating an equal diet, Fdie, is determined based on the number of
    tary components in the total diet. The application of an equal diet is further discussed in Chapter 5.
    certainties associated with this variable include:
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    variable is site- and COPC-specific; it is calculated using the equation in Table F-1-1.
    rtainties introduced by this variable include the following:
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    Dywp — are COPC- and site-specific.
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    for organic compounds estimated on the basis of the behavior of polystyrene microspheres), Rp (estimated on
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    mation is not available. The following uncertainty is associated with this variable:
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    lonents in the total diet. The application of an equal diet is further discussed in Chapter 5.
    rtainties associated with this variable include:
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    (Page 1 of 8)
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    is variable is site-specific and COPC-specific; it is calculated using the equation in Table F-1-5. Un
    ociated with this variable include:
    Variables Cs and Cwlo, are COPC- and site-specific. Uncertainties associated with these variable
    site-specific.
    Variables BCFS.OM and BCFW.OM are based on biotransfer factors for beef (Bab,ef), and receptor sp
    rates, and therefore may introduce uncertainty when used to compute concentrations for site-speci
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    armation is not available. The following uncertainty is associated with this variable:
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    icentration based on an exclusive diet. For calculating an equal diet, Fiia is determined based on th
    tary components in the total diet. The application of an equal diet is further discussed in Chapter 5.
    certainties associated with this variable include:
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    including: food availability, animal behavior, species composition, and seasonal influences. The:
    uncertainties may over- or under- estimate Fila when applied to site-specific receptors.
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    ociated with this variable include:
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    site-specific.
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    herbivorous mammals.
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    ormation is not available. Uncertainties associated with this variable include:
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    and animal behavior. Therefore, the default value of 100 percent may not ace
    conditions, and may overestimate the proportion of contaminated food ingesti
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    certainties associated with this variable include:
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    including: food availability, animal behavior, species composition, and seasoi
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    sociated with this variable include:
    ) Variables Cs and Cmia are COPC- and site-specific. Uncertainties associated with these variable;
    site-specific.
    ) Variables BCFS.OB and BCFW_OB are based on biotransfer factors for chicken (BacMckm ), and recepti
    ingestion rates, and therefore may introduce uncertainty when used to compute concentrations for
    omnivorous birds.
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    formation is not available. The following uncertainty is associated with this variable:
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    conditions, and may overestimate the proportion of contaminated food ingested.
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    sed on an exclusive diet. For calculating an equal diet, Fdla is determined based on the number of di
    mponents in the total diet. The application of an equal diet is further discussed in Chapter 5.
    icertainties associated with this variable include:
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    including: food availability, animal behavior, species composition, and seasonal influences. The;
    uncertainties may over- or under- estimate Fdla when applied to site-specific receptors.
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    from ingestion of a single dietary item.
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    applied to site-specific receptors.
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    variable is COPC- and site-specific, and should be calculated u
    dry weight basis.
    :rtainties associated with this variable include:
    For soluble COPCs, leaching might lead to movement to belov
    mixing depth. This uncertainty may overestimate Cs.
    Deposition to hard surfaces may result in dust residues that ha
    mixing with in situ materials) in comparison to that of other re
    Modeled soil concentrations may not accurately represent site-
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    variable is site-, receptor-, and habitat-specific, and is discussei
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    wing:
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    s variable is COPC- and site-specific and is calculated using Table B-2-17. Uncertainties
    tion include the following:
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    values rather than site-specific values, for any or all of these variables, will contribute to
    overestimation of Cmlol.
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    degree of uncertainly associated with the variables d^ and dbs is expected to be minimal ei
    mation for estimating a variable (d^) is generally available or because the probable range
    >w. The uncertainty associated with the variables /,„, and €„.,„, is associated with estimates
    use OC content values can vary widely for different locations in the same medium, the un<
    using default OC values may be significant in specific cases.
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    variable is receptor- and habitat-specific, and is discussed in Chapter 5.. Ingestion rates f
    iurement receptors are presented in Chapter 5, Table 5-1. The following uncertainty is ass
    We:
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    under- estimate BCFW.CB to an unknown degree.
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    variable is receptor-specific, and is discussed in Chapter 5. Ingestion rates for example
    rovided in Chapter 5, Table 5-1. Uncertainties associated with this variable include:
    Food ingestion rates are influenced by several factors including: metabolic rate, energy
    and reproducdon, and dietary composition. Ingestion rates are also influenced by ambi
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    when used to estimate daily dose.
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    variable is species- and site-specific, and depends on the percentage of the dietary food
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    [nation is not available. The following uncertainty is associated with this variable:
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    rtainties associated with this variable include: •
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    variable is site-specific and COPC-specific; it is calculated using the equation in Table F-l-i
    iated with this variable include:
    Cdw values are COPC- and site-specific. Uncertainties associated with this variable will be
    BCFw-AL values are intended to represent "generic algae species", and therefore may over- o
    exposure when applied to site-specific species.
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    is variable is receptor-specific, and is discussed in Chapter 5. Ingestion rates for exam
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    iated with this variable include the following:
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    site-specific water body conditions. The degree of uncertainty associated with default variable valu
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    allowing reasonable estimates is generally available.
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    Uncertainties may also be associated with the variable Lj- and kM
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    This variable is site-specific and COPC-specific; it is calculated using the equation in
    associated with this variable include:
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    (2) BCFW.M values are intended to represent "generic water invertebrate species", e
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    information is not available. The following uncertainty is associated with this variab
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    equation calculates the concentration of COPCs in bed sediments. Uncertainties ai
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    uncertainties may over- or under- estimate Fdta when applied to site-specific receptors.
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    from ingestion of a single dietary item.
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    lonents in the total diet. The application of an equal diet is further discussed in Chapter 5.
    rtainties associated with this variable include:
    The actual proportion of the diet that is comprised of a specific dietary item depends on several factors
    including: food availability, animal behavior, species composition, and seasonal influences. These
    uncertainties may over- or under- estimate Fd(a when applied to site-specific receptors.
    The default value of 100 percent for an exclusive diet introduces uncertainty and may over-estimate exp
    from ingestion of a single dietary item.
    The default value for an equal diet introduces uncertainty and may over- or under- estimate exposure wl
    applied to site-specific receptors.
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    variable is site-specific and COPC-specific; it is calculated using the equation in F-l-
    ciated with this variable include:
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    The data set used to calculate BCF^,, is based on a limited number of test organisms
    under-estimate exposure when applied to site-specific organisms.
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    •mation is not available. The following uncertainty is associated with this variable:
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    variable is species- and site-specific, and depends on the percentage of the diet that is
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    d on an exclusive diet. For calculating an equal diet, Fdll, is determined based on the
    ponents in the total diet. The application of an equal diet is further discussed in Chapt
    srtainties associated with this variable include:
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    including: food availability, animal behavior, species composition, and seasonal infli
    uncertainties may over- or under- estimate Fdla when applied to site-specific receptor
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    lociated with this variable include:
    i Variables CSfd and CMO, are COPC- and site-specific.
    i Variables BCFS.OM and BCFW_OM are based on biotransfer factors for beef (Babeef), and receptor specific ingestion
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    variable is site-specific and COPC-specific; it is calculated using the equati
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    Variables BCFS.HM and BCFW.HM are based on biotransfer factors for beef c
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    minated. U.S. EPA OSW recommends that a default value of 1.0 be used f
    nation is not available. Uncertainties associated with this variable include
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    tary components in the total diet. The application of an equal diet is further discussed in Chapter 5.
    certainties associated with this variable include:
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    from ingestion of a single dietary item.
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    applied to site-specific receptors.
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    iated with this variable include:
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    Variables BCFS.HB and BCFW.HB are based on biotransfer factors for chicken (BaMcktn ), and n
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    ry components in the total diet. The application of an equal diet is further discussed in Chap
    rtainties associated with this variable include:
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    including: food availability, animal behavior, species composition, and seasonal influences.
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    TABLE F-:
    
    
    ED TERMS
    ALTMARS1
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    Varies (calculated - Table B-2-19)
    n calculates the concentration of COPCs in bed sediments. Uncertainties associal
    bllowing:
    fault variable values recommended for use in the equation in Table B-2-19 may n
    ecific water body conditions. The degree of uncertainty associated with default vt
    ed to be limited either because the probable ranges for these variables are narrow
    ig reasonable estimates is generally available.
    ainties associated with variables yj,,, C^^, and Kdh, are largely associated with the
    t values in their calculation. The uncertainty may be significant in specific instani
    vn to vary widely in different locations in the same medium. This variable is site-
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    : is species- and site-specific, and depends on the percentage of soil ingested that
    jcommends that a default value of 1.0 be used for a screening level risk assessmei
    is not available. The following uncertainty is associated with this variable:
    tual amount of contaminated soil ingested by species depends on site-specific info
    mge, and animal behavior; therefore, the default value of 100 percent may not ace
    c conditions, and the proportion of soil ingested that is contaminated will likely bi
    is ^ .2 S E '§
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    ^
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    | equation include the following:
    
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    (1) All of the variables in the equation in Table B-2-17 are COPC- and si
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    narrow. The uncertainty associated with the variables /„. and CMOI is associ
    
    
    
    
    
    
    
    
    
    
    
    
    
    
    
    
    
    
    
    
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    73
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    variable:
    
    
    
    
    
    
    
    
    
    
    
    
    
    
    
    
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    tion calculates the concentration of COPCs in bed sediments. Uncertainties asso
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    default variable values recommended for use in the equation in Table B-2-19 ma
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    variable is COPC- and site-specific and is calculated using Table B-2-]
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    All of the variables in the equation in Table B-2- 17 are COPC- and sit
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    Uncertainty associated with/TO is largely the result of uncertainty asso<
    Uncertainties may also be associated with the variable Lj. and kM.
    legree of uncertainly associated with the variables dx and dbs is expect*
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    use OC content values can vary widely for different locations in the san
    using default OC values may be significant in specific cases.
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    -------
                APPENDIX G
    
    
    
    
     STATE NATURAL HERITAGE PROGRAMS
    
    
    
    
    Screening Level Ecological Risk Assessment Protocol
    
    
    
    
                  August 1999
    

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    Screening level Ecological Risk Assessment Protocol
    Appendix G: State Natural Heritage Programs	August 1999
                                       APPENDIX G
    
                                   TABLE OF CONTENTS
    
    Table                                                                          Page
    
    G           STATE NATURAL HERITAGE PROGRAMS	G-l
    U.S. EPA Region 6                                                         U.S. EPA
    Multimedia Planning and Permitting Division                                      Office of Solid Waste
    Center for Combustion Science and Engineering                                                 G-i
    

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    Department of Conservatio
    (FedEx/UPS: 159 Hospital
    93 State House Station
    Augusta, ME 04333-0093
    207-287-8044
    207-287-8040 (Fax)
    E"S
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    ll §
    Louisiana Natural Heritage
    Department of Wildlife &
    P.O. Box 98000
    Baton Rouge, LA 70898-5
    504-765-2821
    504-765-2607 (Fax)
    
    
    
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    1
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    Kentucky Natural Heritage Pro,
    Kentucky State Nature Preservi
    801 Schenkel Lane
    Frankfort, KY 40601
    502-573-2886
    502-573-2355 (Fax)
    
    
    
    
    
    Kansas Natural Heritage Inventory
    Kansas Biological Survey
    2041 Constant Avenue
    Lawrence, KS 66047-2906
    913-864-3453
    913-864-5093 (Fax)
    as
    eo
    9 "
    
    08 1
    Minnesota Natural Heritagi
    Research
    Department of Natural Res
    500 Lafayette Road, Box 7
    St. Paul, MN 51555
    612-297-4964
    612-297-4961 (Fax)
    
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    Michigan Natural Features
    Mason Building, 5th Floor
    (FedEx/UPS: 530 W. Alle
    Lansing, MI 48909-7944
    517-373-1552
    517-373-6705 (Fax)
    
    
    
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    Massachusetts Natural Heritage
    Species Program
    Division of Fisheries & Wildlif
    Route 135
    Westborough, MA 01581
    508-792-7270
    508-792-7275 (Fax)
    
    §
    "3
    1
    U
    Maryland Heritage & Biodiversity
    Programs
    Department of Natural Resources
    Tawes State Office Building, E-1
    Annapolis, MD 21401
    410-974-2870
    410-974-5590 (Fax)
    
    c
    5
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    Nebraska Natural Heritage
    Game and Parks Commissi
    2200 North 33rd Street
    P.O. Box 30370
    Lincoln, NE 68503
    402-471-5421
    402-471-5528 (Fax)
    
    C
    I
    Montana Natural Heritage
    State Library Building
    15 15 E. 6th Avenue
    Helena, MT 59620
    406-444-3009
    406-444-0581 (Fax)
    
    
    
    
    
    
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    Missouri Natural Heritage Divi
    Missouri Department of Consei
    P.O. Box 180
    (FedEx: 2901 West Truman Bl'
    Jefferson City, MO 65102-018
    573-751-4115
    573-526-5582 (Fax)
    
    
    
    
    i
    Mississippi Natural Heritage Prog
    Museum of Natural Science
    1 1 1 North Jefferson Street
    Jackson, MS 39201
    601-354-7303
    601-354-7227 (Fax)
    
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    New Mexico Natural Herit:
    University of New Mexico
    2500 Yale Boulevard, SE, !
    Albuquerque, NM 87131-1
    505-277-1991
    505-277-7587 (Fax)
    1 §
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    New Jersey Natural Herita]
    Office of Natural Lands M
    22 South Clinton Ave., CM
    Trenton, NJ 08625-0404
    609-984-1339
    609-984-1427 (Fax)
    
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    172 Pembroke Street
    P.O. Box 1856
    Concord, NH 03302
    603-271-3623
    603-271-2629 (Fax)
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    Nevada Natural Heritage Program
    Department of Conservation & Ns
    1550 E. College Parkway, Suite 1'
    Carson City, NV 89710
    702-687-4245
    702-885-0868 (Fax)
    
    £ ~>
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    Ohio Natural Heritage Dati
    Division of Natural Areas ,
    North Dakota Natural Heri
    North Dakota Parks and R<
    1835 Bismarck Expresswa;
    Bismarck, ND 58504
    701-328-5357
    701-328-5363 (Fax)
    
    
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    NC Department of Environmen
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    P.O. Box 27687
    Raleigh, NC 2761 1-7687
    919-733-7701
    919-715-3085 (Fax)
    
    
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    Department of Environmental Cor
    700 Troy-Schenectady Road
    Latham, NY 121 10-2400
    518-783-3932
    518-783-3916 (Fax)
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    Pittsburgh, PA 15222
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    412-281-1792 (Fax)
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    Portland, OR 97214
    503-731-3070; 230-122
    503-230-9639 (Fax)
    
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    Pierre, SD 57501-3182
    605-773-4227
    605-773-6245 (Fax)
    
    
    
    
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    103 S. Main Street, 10 South
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    802-241-3700
    802-241-3295 (Fax)
    
    
    
    
    
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    1596 West North Tern
    Salt Lake City, UT 84
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    101 S. Webster Street, Box 7921
    Madison, WI 53707
    608-266-7012
    608-266-2925 (Fax)
    
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    (FedEx: 1111 Washing!
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    360-902-1340
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                APPENDIX H
    
    
    
    
          TOXICOLOGICAL PROFILES
    
    
    
    
    Screening Level Ecological Risk Assessment Protocol
    
    
    
                   August 1999
    

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    Protocol for Screening Level Ecological Risk Assessment
    Toxicological Profile: Contents	August 1999
    
                                     APPENDIX H
    
                              TOXICOLOGICAL PROFILES
    
    Profile                                                                    Page
    
    
    
    H-l   ACETONE	H-l
    
    H-2   ACRYLONTTRILE	H-4
    
    H-3   ALUMINUM	H-8
    
    H-4   ANTIMONY 	H-ll
    
    H-5   ARSENIC	H-14
    
    H-6   BERYLLIUM	H-19
    
    H-7   BIS(2-ETHYLHEXYL)PHTHALATE	H-21
    
    H-8   CADMIUM 	H-26
    
    H-9   CHROMIUM	H-29
    
    H-10  COPPER  	H-32
    
    H-ll  CROTONALDEHYDE	H-35
    
    H-12  CUMENE (ISOPROPYLBENZENE)	H-38
    
    H-13  DDE	H-41
    
    H-14  DICHLOROFLUOROMETHANE	H-45
    
    H-15  DICHLOROETHENE, 1-1-  	H-47
    
    H-16  DESHTROTOLUENES	H-51
    
    H-17  DI(N)OCTYLPHTHALATE	H-55
    
    H-18  DIOXAN, 1,4- 	H-58
    
    H-19  DffiENZO-p-DIOXINS  	H-61
    
    H-20  DIBENZOFURANS	H-67
    U.S. EPA Region 6                                                  U.S. EPA
    Multimedia Planning and Permitting Division                                  Office of Solid Waste
    Center for Combustion Science and Engineering                                              H-i
    

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    Protocol for Screening Level Ecological Risk Assessment
    Toxicological Profile; Contents	August 1999
    
                                    APPENDIX H
    
                             TOXICOLOGICAL PROFILES
    
    Profile                                                                   Page
    
    H-21   HEXACHLOROBENZENE	H-69
    
    H-22   HEXACHLOROBUTADffiNE	H-73
    
    H-23   HEXACHLOROCYCLOPENTADffiNE 	H-77
    
    H-24   HEXACHLOROPHENE 	H-80
    
    H-25   HYDRAZINE	H-82
    
    H-26   MERCURY	H-84
    
    H-27   METHANOL	H-88
    
    H-28   NTTROPROPANE, 2-	H-90
    
    H-29   POLYNUCLEAR AROMATIC HYDROCARBONS (PAHS) 	H-92
    
    H-30   POLYCHLORESfATED BIPHENYLS (PCBs) 	H-97
    
    H-31   PENTACHLOROPHENOL	H-101
    
    H-32   THALLIUM	H-105
    
    H-33   VINYL CHLORIDE	H-109
    U.S. EPA Region 6                                                 U.S. EPA
    Multimedia Planning and Permitting Division                                  Office of Solid Waste
    Center for Combustion Science and Engineering                                            H-ii
    

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    Protocol for Screening Level Ecological Risk Assessment
    Toxicological Profile H-l:  Acetone	August 1999
                                               ACETONE
    1.0     SUMMARY
    
    Acetone is a highly volatile organic compound. Volatilization and biodegradation are the major fate
    processes affecting acetone released to soil, surface water, and sediment.  Routes of exposure for wildlife
    include ingestion, inhalation, and dermal uptake.  Acetone is not bioconcentrated by aquatic organisms, and
    is not bioaccumulated by mammals and birds. Therefore, it does not bioaccumulate in aquatic or terrestrial
    food chains.
    
    The following is a profile of the fate of acetone in soil, surface water and sediment; and the fate after
    uptake by ecological receptors. Section 2 discusses the environmental fate and transport in soil, water and
    sediment. Section 3 discusses the fate in ecological receptors.
    
    2.0     FATE IN SOIL, SURFACE WATER AND SEDIMENT
    
    Volatilization and leaching are the two primary transport properties affecting the fate of acetone in soils
    (HSDB 1997).  Volatilization is more significant than leaching. The extent of leaching depends on soil
    characteristics.  Evidence also suggests that acetone rapidly degrades in soil (HSDB  1997).
    
    Volatilization and biodegradation are the major fate processes affecting the fate of acetone in surface water.
    The volatilization half-life for acetone from a model river is approximately 18 hours when estimated using
    1-meter depth, a current of 1 m/second, and wind velocity of 3 m/second (Thomas 1982).  In addition,
    acetone does not partition well to sediments because it is highly soluble in water.  Dispersion of acetone
    from the water column to sediment and suspended solids in water is likely to be insignificant, due to the
    complete miscibility of acetone in water.
    
    Biodegredation is the most significant degradation process of acetone in water (Rathbun et al. 1982).
    Studies on wastewater have shown that aquatic microbial communities quickly acclimate to acetone, and
    rapidly biodegrade it (Urano and Kato 1986a,b).  When tested in seawater, acetone was biodegraded much
    slower than when tested in freshwater (Takemoto et al. 1981).
    U.S. EPA Region 6                                                               U.S. EPA
    Multimedia Planning and Permitting Division                                           Office of Solid Waste
    Center for Combustion Science and Engineering                                                         H-l
    

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    Protocol for Screening Level Ecological Risk Assessment
    lexicological Profile H-l:  Acetone	August 1999
    Photolysis as a degradation process for acetone in water is insignificant.  Studies have shown that
    photodecomposition was not observed when acetone contaminated distilled or natural water was exposed to
    sunlight for 2-3 days (Rathbun et al. 1982).
    
    3.0    FATE IN ECOLOGICAL RECEPTORS
    
    For most aquatic systems, acetone will exist in water rather than sediment, due to acetone's high water
    solubility and low sediment adsorption coefficient.  Bioaccumulation does not occur in aquatic organisms
    as suggested by the low log K^ value for acetone (Rathbun et al. 1982). Adult haddock tested under static
    conditions at 7.9°C showed a bioconcentration factor of 1 for acetone (Rustung et al. 1931).
    Biomagnification along the aquatic food chain is also considered insignificant for acetone as suggested by
    the low KOW value.
    
    Acetone is a highly volatile compound and may be inhaled in large quantities. Acetone is very water
    soluble, so it is quickly absorbed following inhalation into the blood stream and dispersed throughout the
    body. A large portion of acetone is excreted primarily unchanged through the lungs and urine, with only a
    small portion reduced and excreted as carbon dioxide (Encyclopedia of Occupational Health and Safety
    1983). Because acetone is quickly eliminated, wildlife receptors will not accumulate it in tissues.
    
    No information was available on the fate of acetone after exposure by birds or plants.
    
    4.0    REFERENCES
    
    ATSDR.  1994. Toxicological Profile for Acetone. Agency for Toxic Substances and Disease Registry,
           Atlanta, GA.
    Encyclopedia of Occupational Health and Safety. 1983. p 38.  As cited in HSDB  1997.
    HSDB.  1997.  Hazardous Substances Data Bank.
    Rathbun R, Stephens D, Schultz D,Tai D. 1982. "Fate of Acetone in Water."  Chemosphere
            11:1097-1114.
    Rustung E, Frithjof K, Foyen A. 1931.  "The Uptake and Distribution of Acetone in the Coldblooded
            Organism." Biochem Z 242:366-376.
    U.S. EPA Region 6                                                              U.S. EPA
    Multimedia Planning and Permitting Division                                          Office of Solid Waste
    Center for Combustion Science and Engineering                                                        H-2
    

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    Protocol for Screening Level Ecological Risk Assessment
    Toxicological Profile H-l: Acetone	August 1999
    
    Takemoto S, Kuge Y, Nakamoto M. 1981. "The Measurement of BOD in Sea Water." Suishitsu Okaku
           Kenkyu 4:80-90.  As cited in ATSDR 1994.
    
    Thomas R.  1982.  "Volatilization from Water." In: Lyman W, Reehl W, Rosenblatt D, eds. Handbook of
           Chemical Property Estimation Methods.  McGraw-Hill Book Company, New York, pp 15-1 to
           15-34.
    
    Urano K, Kato Z.  1986a. "Evaluation of Biodegradation Rates of Priority Organic Compounds." J Haz
           Mate 13:147-159.
    
    Urano K, Kato Z.  1986b. "A Method to Classify Biodegradabilities of Organic Compounds."  J Haz Matr
           13:135-145.
    U.S. EPA Region 6                                                           U.S. EPA
    Multimedia Planning and Permitting Division                                         Office of Solid Waste
    Center for Combustion Science and Engineering                                                      H-3
    

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    Protocol for Screening Level Ecological Risk Assessment
    Toxicological Profile H-2;  Acrylonitrile	August 1999
                                          ACRYLONITRILE
    1.0    SUMMARY
    
    Acrylonitrile is a highly water soluble volatile organic compound. Volatilization and biodegradation are the
    major fate processes affecting acrylonitrile released to surface soil, surface water, and sediment. Routes of
    exposure for wildlife include ingestion, inhalation, and dermal uptake. Acrylonitrile is not bioconcentrated
    by aquatic organisms, and is not bioaccumulated by mammals and birds.  Therefore, it does not
    bioaccumulate in aquatic or terrestrial food chains.
    
    The following is a profile of the fate of acrylonitrile in soil, surface water, and sediment; and the fate after
    uptake by ecological receptors.  Section 2 discusses the environmental fate and transport in surface soil,
    surface water, and sediment. Section 3 discusses the fate in ecological receptors.
    
    2.0    FATE IN SOIL, SURFACE WATER, AND SEDIMENT
    
    Due to its high water solubility, acrylonitrile is highly mobile in moist soils (EPA 1987). Adsorption into
    the soil is considered insignificant (Kenaga 1980).  Evaporation of acrylonitrile from dry soils is expected
    to occur rapidly because of its high vapor pressure (Norris 1967; EPA 1987) and high Henry's Law
    constant (Meylan 1991).
    
    Acrylonitrile is readily soluble in water and does not strongly adsorb to soil or sediment (Klein et al. 1957;
    ATSDR  1990). Acrylonitrile biodegrades rapidly in water (Miller and Villaume 1978; EPA 1987).
    Aerobic microorganisms readily degrade acrylonitrile, particularly if acclimation time is allowed (Cherry et
    al. 1956; Stover and Kincannon 1983; Mills and Stack 1954, 1955).
    
    Acrylonitrile rapidly volatilizes from surface water. A volatilization half-life of 1-6 days in water has been
    estimated (Thomas 1982; HSDB 1997).
    
    3.0    FATE IN ECOLOGICAL RECEPTORS
    Based on experimental and estimated bioconcentration factors, the bioconcentration of acrylonitrile in
    aquatic organisms is not believed to be significant (Kenaga 1980). A steady-state bioconcentration factor
    U.S. EPA Region 6                                                              U.S. EPA
    Multimedia Planning and Permitting Division                                          Office of Solid Waste
    Center for Combustion Science and Engineering                                                        H-4
    

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    Protocol for Screening Level Ecological Risk Assessment
    lexicological Profile H-2;  Acrylonitrile	August 1999
    (BCF) of 48 was measured in bluegill sunfish (Barrows et al. 1978). The estimated average BCF for
    edible portions of freshwater and marine species was approximately 30 based on the relative proportion of
    fat in sunfish and other organisms (EPA 1980). Also, based on a low log K^,, acrylonitrile is estimated to
    show low bioconcentration in aquatic organisms (Verschueren 1983; Kenaga 1980).
    
    Acrylonitrile is readily absorbed into the body through lung and intestinal mucosa following inhalation,
    ingestion, or dermal contact (Clayton and Clayton 1982). Once absorbed into the body, acrylonitrile is
    distributed throughout the body to the major organs (Pilon et al. 1988a). Following a single oral dose of
    radiolabeled acrylonitrile, rapid distribution of acrylonitrile and its metabolites was shown in all tissues of
    rats (Ahmed et al. 1982, 1983; Silver et al. 1987; Young et al. 1968). Another metabolic pathway includes
    the formation of CO2 which is excreted via the lungs (Young et al. 1968).  The rate of acrylonitrile
    metabolism is inconclusive;  however, evidence suggests that it is rapid (Pilon et al. 1988b; Ghanayem and
    Ahmed 1982; Miller and Villaume 1978). Values representing the amount of acrylonitrile metabolized
    range from 4% to 30% (IARC 1979).
    
    No information was available on the fate of acrylonitrile after exposure by birds or plants.
    
    4.0    REFERENCES
    Ahmed A, Farooqui M, Upreti R, El-Shabrawy O. 1982. "Distribution and Covalent Interactions of
           [l(-14)c]acryolontrile in the Rat."  Toxicology 23:159-175.
    Ahmed A, Farooqui M, Upreti R, El-Shabrawy O. 1983. "Comparative Toxicokinetics of 2,3-(14)c- and
           l-(14)c-acrylonitrile in the Rat." J Appl Toxicol 3:39-47.
    ATSDR.  1990.  Toxicological Profile for Acrylonitrile. Agency for Toxic Substances and Disease
           Registry. December.
    Barrows M, Petrocelli S, Macek K, et al.  1978. "Bioconcentration and Elimination of Selected Water
           Pollutants by Bluegill Sunfish." Proc Am Chem See 18:345-346.
    Cherry A, Bagaccia A, Senn H.  1956. "The Assimilation Behavior of Certain Toxic Organic Compounds
           in Natural Water." Sewage Industrial Wastes 28:1137-1146.
    Clayton G, Clayton F. 1982. Patty's Industrial Hygiene and Toxicology.  3rded. Vol2c. John Wiley &
           Sons, New York. pp. 4863-4866.
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    lexicological Profile H-2; Acrylonitrile	August 1999
    
    EPA. 1980. Ambient Water Quality Criteria Document for Acrylonitrile.  EPA 440/5-80-017. Office of
           Water Regulations and Standards, Washington, DC.
    
    EPA. 1987. Health Assessment Document for Acrylonitrile.  Cincinnati, OH: US Environmental
           Protection Agency, Office of Research and Development. EPA 600/8-88/014. NTIS No.
           PB88-179411.
    
    Ghanayem B, Ahmed A.  1982.  "In Vivo Biotransformation and Biliary Excretion of l-14c-acrylonitrile in
           Rats."  Arch Toxicol 50:175-185.
    
    HSDB.  1997.  Hazardous Substance Data Bank.
    
    IARC. 1979. "Acrylonitrile,  Acrylic and Modacrylic Fibers, and Acrylonitrile-butadiene-styene and
           Styrene-acrylonitrileCopolymers." IARC monographs, Vol 19. IARC, Lyon. pp. 73-113.
    
    Kenaga E.  1980.  "Predicted Bioconcentration Factors and Soil Sorption Coefficients of Pesticides and
           Other Chemicals." Ecotoxicol Environ Safety 4:26-38.
    
    Klein E, Weaver J, Webre B.  1957.  "Solubility of Acrylonitrile in Aqueous Bases and Alkali Salts."  Ind
           EngChem2:DS72-75.
    
    Meylan W, Howard P. 1991.  Environ Toxicol Chem 10:1283-1293.  As cited in HSDB 1997.
    
    Miller L, Villaume J.  1978. Investigation of Selected Potential Environmental Contaminants:
           Acrylonitrile. Office of Toxic Substances.  U.S. Environmental Protection Agency. Washington,
           DC.
    
    Mills E, Stack V.  1954.  "Biological Oxidation of Synthetic Organic Chemicals."  Engineering Bulletin,
           Proceedings 8th Ind Waste Conf Ext Ser. 83:492-517. As cited in ATSDR 1990.
    
    Mills E, Stack V.  1955.  "Acclimation of Microorganisms for the Oxidation of Pure Organic Chemicals."
           Proceedings 9th Ind Waste Conf Ext Ser. 87:449-464. As cited in ATSDR 1990.
    
    NorrisM. 1967. Acrylonitrile. Encyclopedia of Industrial Chemical Analysis. Interscience Publ., New
           York. 4:368-371.
    
    Pilon D, Roberts A, Rickert D.  1988a.  "Effect of Glutathione Depletion on the Uptake of Acrylonitrile
           Vapors and on its Irreversible Association with Tissue Macromolecules." Toxicol Appl Pharmacol
           95:265-278.
    
    Pilon D, Roberts A, Rickert D.  1988b.  "Effect of Glutathione Depletion on the Irreversible Association of
           Acrylonitrile with Tissue Macromolecules after Oral Administration to Rats." Toxicol Appl
           Pharmacol 95:311-320.
    
    Silver E, Szabo S, Cahill M, Jaeger R. 1987.  'Time-course Studies of the Distribution of
           [l-14c]acrylonitrile in Rats after Intravenous Administration." J Appl Toxicol 7:303-306.
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    Stover E, Kincannon D. 1983.  "Biological Treatability of Specific Organic Compounds Found in
           Chemical Industry Wastewaters." J Water Pollut Control Fed 55:97-109.
    
    Thomas R.  1982.  "Volatilization from Water." In: Handbook of Chemical Property Estimation
           Methods. Environmental Behavior of Organic Compounds. McGraw-Hill, New York.  pp. 15.1
           to 15.34.
    
    Verschueren K.  1983.  Handbook of Environmental Data on Organic Chemicals. 2nded. VanNostrand
           Reinhold Co., New York. pp.  162-165.
    
    Young J,  Slauter R, Karbowski R.  1968.  The Pharmacokinetic and Metabolic Profile of
           14c-acrylonitrile Given to Rats by Three Routes. Dow Chemical Company, Toxicology Research
           Laboratory, Midland, MI. As  cited in ATSDR 1990.
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    Toxicological Profile H-3;  Ahimimim	August 1999
                                             ALUMINUM
    1.0    SUMMARY
    
    In nature, aluminum does not exist in the elemental state, but partitions between the liquid and solid phases
    by forming complexes with various compounds.  Aluminum adsorbs to clays and suspended solids in
    water.  Exposure routes for aquatic organisms include ingestion, gill uptake and dermal contact.
    Aluminum bioconcentrates in aquatic organisms. Exposure routes for mammals include ingestion,
    inhalation and dermal exposure; however, regardless of the route of exposure, aluminum is poorly absorbed
    by mammals. Aluminum is not readily metabolized. Aluminum causes pulmonary and developmental
    effects. Aluminum uptake by plants varies between species, resulting in differing rates of bioconcentration
    in plant tissues.
    
    The following is a profile of the fate of aluminum in soil, surface water and sediment; and the fate after
    uptake by ecological receptors. Section 2 discusses the environmental fate and transport in soil, surface
    water and sediment. Section 3  discusses the fate in ecological receptors.
    
    2.0    FATE IN SOIL, SURFACE WATER AND SEDIMENT
    
    Aluminum does not exist as a free metal in nature due to its reactivity, but rather partitions  between the
    solid and liquid phases by reacting with water, chloride, fluoride, sulfate, nitrate, phosphate, hurnic
    materials and clay (Bodek et al. 1988). Soils with a greater mineral content result in reduced mobility of
    aluminum (James and Riha 1989).
    
    In water, aluminum forms relatively water-insoluble complexes, or is found as a water-soluble complex.
    Aluminum adsorbs to suspended solids and sediment. If large amounts of organic matter or fulvic acid are
    present, aluminum binds to them (Brusewitz 1984). In water, aluminum undergoes hydrolysis to form
    hydroxy aluminum species (Snoeyink and Jenkins 1980). The pH of the water determines which hydrolysis
    products are formed.
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    Multimedia Planning and Permitting Division                                           Office of Solid Waste
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    Toxicological Profile H-3; Aluminum	August 1999
    
    3.0    ECOLOGICAL RECEPTORS
    Exposure routes for aquatic organisms include ingestion, gill uptake, and dermal absorption. Aluminum
    
    bioconcentrates in aquatic species (Cleveland et al. 1989).
    
    
    Exposure routes for mammals include ingestion, inhalation and dermal exposure. Aluminum is poorly
    
    absorbed.  Aluminum is distributed to the brain (Santos et al. 1987), bone, muscle and kidneys (Greger and
    
    Donnaubauer 1986). No studies were located that described excretion of aluminum in animals; however in
    
    humans, absorbed aluminum is excreted primarily through the kidney (Gorsky et al. 1979).
    
    
    Information was not available on the fate of aluminum in birds.
    
    
    Aluminum is taken up by plants (Brusewitz 1984). Some plants bioaccumulate aluminum in the root
    
    tissues. Plant uptake of aluminum and the transport to stems and leaves varies considerably between
    
    species (Kabata-Pendias and Pendias 1984).
    
    
    4.0    REFERENCES
    ATSDR. 1992. lexicological Profile for Aluminum. Agency for Toxic Substances and Disease
           Registry. July.
    
    Bodek I, Lyman W, Reehl W, et al., eds.  1988.  Environmental Inorganic Chemistry-properties,
           Processes, and Estimation Methods. Pergamon Press, New York. pp. 6.7-1 to 6.7-9.
    
    Brusewitz S.  1984. Aluminum. Vol 203. University of Stockholm, Institute of Theoretical Physics,
           Stockholm, Sweden, p 138.  As cited in ATSDR 1992.
    
    Cleveland L, Little E, Wiedmeyer R, Buckler D. 1989. "Chronic No-observed-effect Concentrations of
           Aluminum for Brook Trout Exposed in Low-calcium, Dilute Acidic Water." In: Lewis T, ed.
           Environmental Chemistry and Toxicology of Aluminum.  Lewis Publishers, Chelsea, MI.
           pp. 229-246.
    
    Gorsky J, Dietz A, Spencer H, Osis D. 1979. "Metabolic Balance of Aluminum Studied in Six Men."
           ClinChem 25:1739-1743.
    
    Greger J, Donnaubauer S. 1986. "Retention of Aluminum in the Tissues of Rats after the Discontinuation
           of Oral Exposure to Aluminum." Food ChemToxicol 24:1331-1334.
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    James B, Riha S. 1989. "Aluminum Leaching by Mineral Acids in Forest Soils: I. Nitric-sulfuric Acid
           Differences." Soil Sci Soc Am J 53:259-264.
    
    Kabata-Pendias A, Pendias H, eds.  1984. Trace Elements in Soils and Plants.  CRC Press, Boca Raton,
           FL. pp. 135-136.
    
    Santos F, Chan J, Yang M, Savory J, Wills M.  1987.  "Aluminum Deposition in the Central Nervous
           System. Preferential Accumulation in the Hippocampus in Weanling Rats."  MedBiol 65:53-55.
    
    Snoeyink V, Jenkins D, ed.  1980.  Water Chemistry. John Wiley and Sons, New York. pp. 209-210.
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    Toxicological Profile H-5; Arsenic	August 1999
                                            ANTIMONY
    1.0    SUMMARY
    Antimony binds to soil and particulates and is oxidized by bacteria in soil. Exposure routes for aquatic
    organisms include ingestion and gill uptake. Antimony bioconcentrates in aquatic organisms. Exposure
    routes for mammals include ingestion and inhalation.  It does not biomagnify in terrestrial food chains.
    Antimony is not significantly metabolized and is excreted in the urine and the feces. Antimony causes
    reproductive, pulmonary and hepatic effects in mammals. Antimony uptake by plants occurs following
    surface deposition.
    
    The following is a profile of the fate of antimony in soil, surface water and sediment; and the fate after
    uptake by ecological receptors. Section 2 discusses the environmental fate and transport in soil, surface
    water and sediment. Section 3 discusses the fate in ecological receptors.
    
    2.0    FATE IN SOIL, SURFACE WATER AND SEDIMENT
    
    Antimony binds to soil, particularly to particles containing iron,  manganese, or aluminum Ainsworth
    1988).  In water, antimony is oxidized when exposed to atmospheric oxygen (Parris and Brinckman 1976).
    
    3.0    ECOLOGICAL RECEPTORS
    
    Exposure routes for aquatic organisms include ingestion and gill uptake. Antimony bioconcentrates in
    aquatic organisms (ACQUIRE 1989; Callahan et al. 1979; EPA 1980).
    
    Exposure routes for mammals include ingestion and inhalation (Groth et al. 1986, EPA 1988). Dermal
    absorption is low (Myers et  al. 1978) and absorption from the respiratory tract is dependent on particle size
    (Thomas  et  al. 1973).  Following absorption, antimony is distributed to the liver, kidney, bone, lung, spleen
    and thyroid  (Sunagawa 1981; Ainsworth 1988). Antimony is excreted in the urine and the feces (Felicetti
    et al. 1974). Antimony does not biomagnify in the food chain (Ainsworth 1988). Data regarding the
    amount of antimony that reaches the site of action and assimilation efficiency were not available.
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    Information was not available on the fate of antimony in birds.
    Antimony is taken up by plants following surface deposition, with uptake from soil dependent on the
    
    solubility of the antimony in the soil (Ainsworth 1988).
    
    
    4.0    REFERENCES
    
    
    Acquire. 1989. Acquire database.  September?. As cited in ATSDR 1990.
    
    Ainsworth N.  1988.  Distribution and Biological Effects of Antimony in Contaminated Grassland.
           Dissertation. As cited in ATSDR 1990.
    
    ATSDR. 1990.  Toxicological Profile for Antimony. Agency for Toxic Substances and Disease Registry.
           October.
    
    Callahan M, Slimak M, Gabel N, et al.  1979.  Water-Related Environmental Fate of 129 Priority
           Pollutants.  Voll. EPA 440/4-79-029a.  Office of Water Planning and Standards, Washington,
           DC.  pp. 5-1 to 5-8.
    
    EPA. 1988.  Drinking Water Criteria Document for Antimony. EPA contract no. 68-03-3417. p. UI-16.
    
    EPA. 1980.  Ambient Water Quality Criteria for Antimony. EPA 440/5-80-020. Office of Water
           Regulations and Standards Criteria Division, Washington, DC.
    
    Felicetti S, Thomas R, McClellan R.  1974.  "Metabolism of Two Valence States of Inhaled Antimony in
           Hamsters."  Am Ind Hyg Assoc J 355:292-300.
    
    Groth D, Stettler L, Burg J. 1986. "Carcinogenic Effects of Antimony Trioxide and Antimony Ore
           Concentrate in Rats." J Toxicol Environ Health 18:607-626.
    
    Myers R, Homan E, Well C, et al.  1978.  Antimony Trioxide Range-finding Toxicity Studies. Ots206062.
           Carnegie-Mellon Institute of Research, Carnegie-Mellon University, Pittsburgh, Pa. Sponsored by
           Union Carbide.  As cited in ATSDR 1990.
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    Toxicological Profile H-5:  Arsenic	August 1999
    
    Parris G, Brinckman F. 1976. "Reactions Which Relate to the Environmental Mobility of Arsenic and
           Antimony.  li. Oxidation of Trimethylarsine and Trimethylstibine."  Environ Sci Technol
           10:1128-1134.
    
    SunagawaS.  1981. "Experimental Studies on Antimony Poisoning." Igaku Kenkyu 51: 129-142.
    
    Thomas R, Felicetti S, Lucchino R, McClellan R. 1973. "Retention Patterns of Antimony in Mice
           Following Inhalation of Particles Formed at Different Temperatures."  Proc Exp Biol Med
           144:544-550.
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    Toxicological Profile H-5; Arsenic	August 1999
                                               ARSENIC
    1.0     SUMMARY
    
    Arsenic, because of its complex chemistry, exists in the environment in many different inorganic and
    organic forms, which have different toxicological and physicochemical properties.  Inorganic arsenic exists
    as either the trivalent (3+) form or the pentavalent (5+) form. The inorganic trivalent arsenic forms are
    more toxic than the pentavalent forms. Elemental arsenic (the metalloid -Q+) is essentially nontoxic even at
    high intakes.
    
    Arsenic in soil is usually tightly bound.  The bioconcentration potential in soil invertebrates and aquatic
    species is  low. Biomagnification through the food chain is minimal because once ingested, arsenic is
    metabolized to methylated compounds that are rapidly excreted.  Absorbed arsenic is distributed to all
    tissues where it interferes with normal enzymatic activity or disrupts the functioning of other cellular
    macromolecules. Evaluation of the potential for toxicity from exposure to low levels of arsenic is
    complicated by the current understanding that arsenic is an essential element in some mammalian species,
    and that arsenic deficiency may result in adverse reproductive and developmental effects.
    
    The following is a  profile of the fate of arsenic in soil, surface water and sediment; and the fate after uptake
    by ecological receptors.  Section 2 discusses the environmental fate and transport in soil, surface water and
    sediment.  Section  3 discusses the fate in ecological receptors.
    
    2.0     FATE IN SOIL, SURFACE WATER, AND SEDIMENT
    
    The dominant form of arsenic in soil and its transport are largely dependent on the physical characteristics
    of the soil matrix.  Insoluble arsenic compounds, such as arsenic trioxide, bind tightly to organic matter in
    soil or sediment (EPA 1984; ATSDR 1993).  Various forms of arsenic in soil are interconverted by
    chemical reactions and microbial activity. Soil microorganisms convert small amounts of arsenic to
    volatile arsines.  These volatile arsines are released to the air, become adsorbed to particles, and are
    redeposited (ATSDR  1993) or, under certain conditions, react to form oxides (Ghassemi et al. 1981).
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    The bioavailability of arsenic in soil is inversely proportional to the organic carbon and clay content of the
    soil matrix.  Arsenic in soil is directly taken up by plants and soil microbes and invertebrates, and indirectly
    taken up by terrestrial receptors via ingestion.
    
    In surface water, soluble inorganic arsenate (As5+) predominates under normal conditions and is more
    stable than arsenite (EPA 1980a). Movement and partitioning of arsenic in water depends on the chemical
    form of arsenic and on interactions with other materials present (Callahan et al. 1979). Soluble forms of
    arsenic remain dissolved in the water column or adsorb onto sediments or soils, especially those containing
    clays, iron oxides, aluminum hydroxides, manganese compounds, and organic matter (Callahan et al. 1979;
    Welch et al. 1988).  Sediment bound arsenic is released back into the water by chemical or biological
    interconversions. This interconversion is influenced by the Eh (the oxidation-reduction potential), pH,
    temperature, other metals, salinity, and biota (Callahan et al. 1979). Arsenate is transformed by microbes
    to arsenite and methylated arsenicals (Benson 1989; Braman and Foreback 1973).
    
    3.0     ECOLOGICAL RECEPTORS
    
    Exposure routes for aquatic organisms include gill uptake, ingestion of arsenic suspended on particles in
    the water column or deposited in sediment, and ingestion of plant matter and lower trophic level aquatic
    species.  Arsenic bioconcentration in aquatic organisms is low (Spehar et al. 1980; EPA 1980b).  Fish and
    shellfish rapidly metabolize arsenic to non-toxic forms (EPA 1984, Garcia-Vargas and Cebrian 1996;
    ATSDR 1993). Biomagnification does not readily occur in aquatic food chains (Callahan et al. 1979).
    
    Soil invertebrates are directly exposed to arsenic found in soil and soil pore water.  Exposure routes for
    soil invertebrates include ingestion and dermal absorption. Arsenic bioconcentration in soil invertebrates is
    low (Rhett et al.  1988).
    
    The majority of ecological mammalian exposure occurs through ingestion.  The oral absorption efficiency
    is dependent on the form of arsenic, its solubility, and the media ingested.  Soluble arsenic compounds in
    aqueous solution are more readily absorbed from the gastrointestinal tract than insoluble compounds.
    Absorption from water ingested is approximately 85%. Inorganic arsenic in food sources is expected to be
    readily bioavailable with absorption rates of greater than 85% expected.  Once absorbed, arsenic is readily
    transported throughout the body with little tendency to accumulate preferentially in any one internal organ
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    Toxicological Profile H-5;  Arsenic	August 1999
    (ATSDR 1993). Dermal absorption is a minor route of exposure with absorption estimated at 0.1 %
    (ATSDR 1993).
    
    Metabolism of arsenic occurs primarily in the liver. The methylated metabolites are less toxic than the
    inorganic precursors, and metabolism results in lower tissue retention of inorganic arsenic (Marafante and
    Vahter 1984, 1986, 1987; Marafante et al. 1985). Inorganic arsenic and its methylated products are
    rapidly eliminated.
    
    The toxicokinetic data for arsenic indicate there is little potential for bioaccumulation in animal tissue
    exposed to doses that are below the level required to saturate detoxifying methylation reactions.  The level
    of biornagnification in mammals depends on the diet of the animal.  Herbivores have a low arsenic
    biomagnification rate due to the general lack of transport of arsenic from soil to above ground plant parts.
    Ornnivores have a higher biomagnification rate based on the higher proportion of soil invertebrates in their
    diet. Carnivores have the highest biomagnification rate due to their diet of aquatic invertebrates, small
    mammals, and fish and the incidental ingestion of soil. However, arsenic is rapidly metabolized in
    mammalian species, therefore, arsenic does not readily bioaccumulate in mammals.
    
    Exposure routes for avion receptors include ingestion of surface water, soil, soil and aquatic invertebrates,
    and plant material. Absorption studies specific to avian species are not available. Based on mammalian
    absorption (ATSDR 1993), avian absorption can be assumed to be 85% absorption from water, 30% to
    40% absorption from soil, and 85% absorption from food sources.
    
    Arsenic uptake by plants depends on the form of arsenic and the type of soil. The higher the soil's organic
    carbon and clay content the more the arsenic will bind to the soil and, therefore, less arsenic is available for
    uptake by plant roots. That which is readily taken up by the plant is accumulated in the roots.  Arsenite
    (3+) is highly toxic to cell membranes and, therefore, not readily translocated once taken up; arsenate (5+)
    is less toxic and, therefore, more readily translocated after uptake (ORNL 1996; Speer 1973). Rice, most
    legumes, and members of the bean family are sensitive to arsenic in most forms, with spinach being the
    most sensitive plant (Woolson et al 1975).
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    Multimedia Planning and Permitting Division                                           Office of Solid Waste
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    lexicological Profile H-5;  Arsenic	August 1999
    
    4.0    REFERENCES
    
    ATSDR. 1993.  Toxicological Profile for Arsenic.  Agency for Toxic Substances and Disease Registry.
           April.
    
    Benson A. 1989. "Arsonium Compounds in Algae." Proc Natl Acad Sci 86:6131-6132.
    
    Brarnan R, Foreback C. 1973.  "Methylated Forms of Arsenic in the Environment." Science
            182:1247-1249.
    
    Callahan M, Slimak M, Gabel N et al.  1979.  Water-related Environmental Fate of 129 Priority
           Pollutants.  Volume 1.  EPA/440/4-79-029a. Office of Water Planning and Standards,
           Washington, DC. As cited in ATSDR 1993.
    
    EPA.  1980a.  Ambient Water Quality Criteria for Arsenic. EPA 440/5-80-021. Office of Water
           Regulations and Standards, Washington, DC.
    
    EPA.  1980b.  Unpublished laboratory data. Environmental Research Lab, Narragansett, Rhode Island.
           As cited in EPA 1980a.
    
    EPA.  1984. Health Assessment Document for Inorganic Arsenic. EPA/600/8-83-021f. Office of Health
           and Environmental Assessment, Washington, DC.
    
    Garcia-Vargas G, Cebrian M.  1996. "Health Effects of Arsenic." In: Chang L, ed. Toxicology of
           Metals.  Lewis Publ., Boca Raton, FL. pp. 423-438.
    
    Ghassemi M, Fargo L, Painter P,  et al.  1981.  Environmental Fates and Impacts of Major Forest Use
           Pesticides. Prepared by TRW Environmental Division, Redondo Beach, CA.  Prepared for EPA,
           Office of Pesticides and Toxic Substances, Washington, DC.
    
    Marafante F, Vahter M. 1984.  "The Effect of Methyltransferase Inhibition on the Metabolism of [74as]
           Arsenite in Mice and Rabbits." Chem Biol Interact 50:49-57.
    
    Marafante E, Vahter M. 1986.  "The Effect of Dietary and Chemically Induced Methylation Deficiency on
           the Metabolism of Arsenate in the Rabbit." Acta Phannacol Toxicol 59(Suppl 7):35-38.
    
    Marafante E, Vahter M. 1987.  "Solubility, Retention, and Metabolism of Intratracheally and Orally
           Administered Inorganic Arsenic Compounds in the Hamster." Environ Res 42:72-82.
    
    Marafante E, Vahter M, Envall J. 1985.  "The Role of the Methylation in the Detoxication of Arsenate in
           the Rabbit."  Chem-Biol Interact 56:225-238.
    
    ORNL.  1996. Toxicological Benchmarks for Screening Potential Contaminants of Concern for Effects
           on Terrestrial Plants:  1995 Revision. ES/ER/TM-82-R2. Oak Ridge National Laboratory, Oak
           Ridge, TN.
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    Rhett RG, Simmers JW, Lee CR. 1988. Eisenia Foetida Used as a Biomonitoring Tool to Predict the
           Potential Bioaccumulation of Contaminants from Contaminated Dredging Material. SPB
           Academic Publishing.  Pp. 321-328.
    
    Speer, H.L.  1973. "The Effect of Arsenic and Other Inhibitors on Early Events During the Germination of
           Lettuce Seeds." Plant Physiology 52: 142-146.
    
    Spehar R, Fiandt J, Anderson R, Defoe D.  1980. "Comparative Toxicity of Arsenic Compounds and
           Their Accumulation in Invertebrates and Fish." Arch Environ Contam Toxicol 9:53-63.
    
    Welch A, Lico M, Hughes J.  1988.  "Arsenic in Groundwater of the Western United States." Ground
           Water 26:333-347.
    
    Woolson E.A., Axley J.H., and Kearney P.C.  1973.  "The Chemistry and Phytotoxicity of Arsenic in Soils
           li. Effects of Time and Phosphorus." Soil Science Society of America Proceedings 37:254-259.
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    Multimedia Planning and Permitting Division                                          Office of Solid Waste
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    Toxicological Profile H-6;  Beryllium	August 1999
                                             BERYLLIUM
    1.0    SUMMARY
    
    In environmental media, beryllium usually exists as beryllium oxide. Beryllium has limited solubility and
    mobility in sediment and soil.  Exposure routes for aquatic organisms include ingestion and gill uptake.
    Beryllium does not bioconcentrate in aquatic organisms. Beryllium is toxic to warm water fish, especially in
    soft water.  Exposure routes for mammalian species include inhalation.  Mammals exposed via inhalation
    exhibit pulmonary effects which may last long after exposure ceases.
    
    The following is a profile of the fate of beryllium in soil, surface water and sediment, and the fate after uptake
    by biological receptors. Section 2 discusses the environmental fate and transport in soil, surface water and
    sediment. Section 3 discusses the fate in ecological receptors.
    
    2.0    FATE IN SOIL, SURFACE WATER, AND SEDIMENT
    
    Beryllium adsorbs to clays at low pH, precipitates as insoluble complexes at higher pH, and has limited
    solubility in soil (Callahan et  al. 1979).  Chemical reactions in soil transform one beryllium compound into
    another (ATSDR 1993).   Reactions  in soil include  hydrolysis of soluble salts, anion exchange,  and
    complexation with ligands such as humic substances (ATSDR 1993).
    
    In water, beryllium is speciated often by hydrolysis in which soluble beryllium salts are hydrolyzed to form
    relatively insoluble beryllium hydroxide (Callahan et al.  1979).  Beryllium is not volatilized from water
    (ATSDR 1993).  Beryllium is retained in an insoluble and immobile form in sediment (EPA 1980).
    
    3.0    ECOLOGICAL RECEPTORS
    
    Beryllium uptake from water is low, resulting in low bioconcentration rates (EPA 1980; Callahan etal. 1979).
    Biomagnification of beryllium in aquatic food chains does not occur (Fishbein 1981).
    
    In mammals, beryllium compounds are absorbed primarily through the lung (ATSDR 1993).  Beryllium is
    poorly absorbed from the gastrointestinal tract, and is not absorbed through intact skin to any significant degree
    U.S. EPA Region 6                                                              U.S. EPA
    Multimedia Planning and Permitting Division                                          Office of Solid Waste
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    Protocol for Screening Level Ecological Risk Assessment
    Toxicological Profile H-6; Beryllium	August 1999
    
    (ATSDR 1993). Beryllium is distributed to the liver, skeleton, tracheobronchial lymph nodes, and blood (Finch
    
    et al. 1990). Beryllium is not biotransformed, but soluble beryllium salts are partially converted to less soluble
    
    forms in the lung (Reeves and Vorwald 1967).  Excretion is predominantly via the feces (Finch et al. 1990).
    
    Data regarding the amount of beryllium that reaches the site of action or assimilation efficiency were not
    
    located.
    
    
    Information was not available on the fate of beryllium in birds.
    
    
    Beryllium uptake by plants occurs when beryllium is present in the soluble form. The highest levels of
    
    beryllium are found in the roots, with lower levels in the stems and foliage (EPA 1985).
    
    
    4.0    REFERENCES
    
    
    ATSDR. 1993.  Toxicological Profile for Beryllium.  Agency for Toxic Substances and Disease
           Registry.
    
    Callahan M, Slimak M, Gabel N, et al. 1979.  Water-Related Environmental Fate of 129 Priority
           Pollutants. EPA-440/4-79-029a.  Vol 1. Office of Water Planning and Standards, Washington,
           DC. pp. 8-1 to 8-7.
    
    EPA. 1980. Ambient Water Quality Criteria for Beryllium. EPA 440/5-80-024. Office of Water
           Regulations and Standards, Washington, DC.
    
    EPA. 1985. Environmental Profiles and Hazard Indices for Constituents of Municipal Sludge:
           Beryllium.  Office of Water Regulations and Standards. Washington, DC.
    
    Finch G, Mewhinney J, Hoover M, Eidson A, Haley P, Bice D. 1990. "Clearance, Translocation, and
           Excretion of Beryllium Following Acute Inhalation of Beryllium Oxide by Beagle Dogs."
           Fundam Appl Toxicol 15:231-241.
    
    FishbeinL.  1981. "Sources,  Transport and  Alterations of Metal Compounds: an Overview. I. Arsenic,
           Beryllium, Cadmium, Chromium, and Nickel." Environ Health Perspect 40:43-64.
    
    Reeves A, Vorwald A.  1967.  "Beryllium Carcinogenesis. li.  Pulmonary Deposition and Clearance of
           Inhaled Beryllium Sulfate in the Rat." Cancer Res 27:446-451.
    U.S. EPA Region 6                                                             U.S. EPA
    Multimedia Planning and Permitting Division                                          Office of Solid Waste
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    Protocol for Screening Level Ecological Risk Assessment
    Toxicological Profile H-7;  Bis(2-Ethylhexyl)Phthalate	August 1999
                                 BIS(2-ETHYLHEXYL)PHTHALATE
    1.0     SUMMARY
    
    Bis(2-ethylhexyl)phthalate (BEHP) is a high molecular weight, semi-volatile organic compound.  BEHP
    adsorbs strongly to soil and sediment, and it may be biodegraded in aerobic environments. It has a low
    water solubility and low vapor pressure.  It does not undergo significant photolysis, hydrolysis, or
    volatilization in soil or water. Receptors may be exposed to BEHP by the oral, inhalation, and dermal
    routes.  BEHP bioconcentration in aquatic organisms is generally low, therefore significant food chain
    biomagnification in upper-trophic-level fish is unlikely. Mammalian and avian wildlife can metabolize and
    eliminate BEHP, therefore, it does not biomagnify in these receptors.
    
    The following summarizes the fate of BEHP in surface soil, surface water and sediment; and the fate after
    uptake by ecological receptors.  Section 2 discusses the environmental fate after released to surface soil,
    surface water, and sediment. Section 3 discusses the fate in ecological receptors.
    
    2.0     FATE IN SOIL, SURFACE WATER AND SEDIMENT
    
    BEHP adsorbs strongly to soil and does not undergo significant volatilization or photolysis (HSDB 1997).
    Limited information indicates that, under aerobic conditions, degradation in soil may occur (Hutchins et al.
    1983; Mathur 1974).  However, because BEHP adsorbs strongly to soil, biodegradation is slow (Warns
    1987). Biodegradation in anaerobic conditions is slower than under aerobic conditions (Johnson et al.
    1984).
    
    BEHP has a low water solubility. In surface water environments, adsorption is the major mechanism
    affecting the concentration of BEHP.  BEHP strongly adsorbs to suspended solids and sediments  (Al-
    Omran and Preston 1987; Sullivan et al.  1982; Wolfe et al. 1980).  However, in marine environments,
    adsorption to sediments may be decreased because BEHP is not as soluble in salt water when compared to
    fresh water (Al-Omran and Preston 1987).  BEHP may also form complexes with fulvic acid, potentially
    increasing its mobility in aquatic environments (Johnson et al. 1977).
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    Multimedia Planning and Permitting Division                                         Office of Solid Waste
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    Protocol for Screening Level Ecological Risk Assessment
    Toxicological Profile H-7; Bis(2-Ethylhexyl)Phthalate	August 1999
    In aquatic environments, biodegradation is the primary route of degradation.  BEHP is biodegraded in
    aerobic conditions; however, under anaerobic conditions, biodegradation is limited (OXTonnor et al. 1989;
    Tabek et al. 1981; OXJrady et al. 1985).  A half-life of approximately one month, due to microbial
    biodegradation has been reported for BEHP in river water (Warns 1987). BEHP does not undergo
    significant hydrolysis or photolysis in aquatic environments (Callahan et al. 1979). A hydrolysis half-life
    of 2,000 years has been estimated (Callahan et al. 1979); and in water a photolysis half-life of 143 days
    has been reported (Wolfe et al. 1980). BEHP does not significantly volatilize from water, with an half-life
    of 15 years reported (Callahan et al.  1979).
    
    3.0    FATE IN ECOLOGICAL RECEPTORS
    
    Aquatic receptors may be exposed through ingestion of contaminated food or water, dermal exposure, or in
    the case of fish, by direct contact of the gills with the surrounding water. Based on its low water solubility
    and high soil partition coefficient (ATSDR 1993), dietary uptake is the  most significant route of exposure
    anticipated for BEHP.
    
    Based on its high log Kow value, BEHP is expected to accumulate in aquatic species (Barrows et al.1980;
    Mayer 1977).  Invertebrates will bioconcentrate BEHP from surface water and from sediment. The level
    of bioconcentration is receptor-specific, because some invertebrates can metabolize BEHP, while some
    have limited capability (Sanders et al. 1973). Under continuous exposure conditions, fish will
    bioconcentrate BEHP to levels moderately higher than the concentration in surface water (Mehrle and
    Mayer 1976). BEHP has a short half-life in fish, indicating that it is quickly eliminated (Park et al.  1990).
    Fish eliminate BEHP by metabolizing it to polar byproducts, which are quickly excreted (Melancon and
    Lech 1977; Menzie 1980).  Therefore, food chain accumulation and biomagnification of BEHP in aquatic
    food webs is not significant (Callahan et al. 1979; Johnson et al. 1977; Wofford et al. 1981).
    
    BEHP is absorbed by mammals following oral (Astill 1989; Rhodes et al. 1986) or dermal exposure
    (Melnick et al. 1987), with oral exposure being the route with the greatest absorption efficiency in
    laboratory animals.  In laboratory animals, small amounts of BEHP have been shown to be absorbed
    following dermal exposure (Melnick et al. 1987). Following oral exposure, it has been reported that a
    portion of the BEHP is hydrolyzed in the small intestine to 2-ethylhexanol and mono(ethylhexyl)phthalate
    U.S. EPA Region 6                                                              U.S. EPA
    Multimedia Planning and Permitting Division                                           Office of Solid Waste
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    Protocol for Screening Level Ecological Risk Assessment
    Toxicological Profile H-7;  Bis(2-Ethylhexyl)Phthalate	August 1999
    
    which is subsequently absorbed (Albro, et al. 1982). Following absorption, BEHP is distributed primarily
    to the liver and kidney, and in some species, to the testes (Rhodes et al. 1986).
    
    
    In mammals, BEHP is metabolized by tissue esterases that hydrolyze one of the ester bonds resulting in the
    formation of mono(2-ethylhexyl)phthalate and 2-ethylhexanol. Small amounts of
    mono(2-ethylhexyl)phthalate may be further hydrolyzed to form phthalic acid; however, the majority
    undergoes aliphatic side chain oxidation followed by alpha- or beta-oxidation. These oxidized products
    may then be conjugated with glucuronic acid and excreted (Albro 1986). Metabolites of BEHP are
    excreted in both the urine and the feces (Astill 1989; Short et al.  1987; Eceda et al.  1980).
    
    
    BEHP may evaporate from the leaves of plants. In one study, using a closed terrestrial simulation
    chamber, BEHP was applied to the leaves of Sinapis alba. Evaporation rates from the leaves were
    <0.8 ng/cm2-hr for a time interval of 0-1 days and <0.5 ng/cnrMir for a time interval of 8-15 days (Loekke
    and Bro-Rasumussen  1981). Uptake of BEHP by plants has also been reported (Overcash et al. 1986).
    
    
    No data were available on the fate of BEHP in birds.
    
    
    4.0    REFERENCES
    Al-Omran L, Preston M.  1987. "The Interactions of Phthalate Esters with Suspended Paniculate Material
           in Fresh and Marine Waters." Environ Pollut 46:177-186.
    
    Albro P.  1986. "Absorption, Metabolism and Excretion of Di(2-ethyhexyl)phthalate by Rats and Mice."
           Environ Health Perspect 65:293-298.
    
    Albro PW, Hass JR, Peck CC, et al. 1982.  "Identification of Metabolites of Di(2-ethylhexyl)phthalate in
           Urine from the African Green Monkey." Drug Metab Dispos 9:223-225. As cited in ATSDR
           1993.
    
    Astill B.  1989. "Metabolism of Dehp: Effects of Prefeeding and Dose Variation, and Comparative Studies
           in Rodents and the Cynomolgus Monkey (CMS Studies)."  Drug Metab Rev 21:35-53.
    
    ATSDR.  1993. lexicological Profile for Di(2-ethylhexyl)phthalate. Agency for Toxic Substances and
           Disease Registry. April.
    
    Barrows M, Petrocelli S, Macel K, et al. 1980. "Bioconcentration and Elimination of Selected Water
           Pollutants by Bluegill Sunfish." In: Haque R, ed. Dynamics, Exposure Hazard Assessment of
           Toxic Chemicals. Ann Arbor Sci., Ann Arbor,  MI. pp. 379-392.
    
    U.S. EPA Region 6                                              ~~      ~~       U.S. EPA
    Multimedia Planning and Permitting Division                                           Office of Solid Waste
    Center for Combustion  Science and Engineering                                                       H-23
    

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    Protocol for Screening Level Ecological Risk Assessment
    lexicological Profile H-7; Bis(2-Ethylhexyl)Phthalate	August 1999
    
    Callahan M, Slimak M, Gabel N, et al.  1979.  Water-Related Environmental Fate of 129 Priority
           Pollutants. Vol. H. EPA-440/4-79-029b.  U.S. EPA, Office of Water Planning and Standards,
           Washington, DC. pp. 94-6 to 94-14.
    
    HSDB.  1997. Hazardous Substances Data Bank.
    
    Hutchins S, Tomson M, Ward C.  1983. "Trace Organic Contamination of Ground Water from Rapid
           Infiltration Site: A Laboratory-Field Coordinated Study."  Environ Toxicol Chem 2:195-216.
    
    Ikeda G, Sapienza P, Couvillion J, et al.  1980.  "Comparative Distribution, Excretion and Metabolism of
           Di-(2-ethylhexyl)phthalate in Rats, Dogs and Miniature Pigs."  Food Cosmet Toxicol 18:637-642.
           As cited in ATSDR 1993.
    
    Johnson B, Heitkamp M, Jones J.  1984. "Environmental and Chemical Factors Influencing the
           Biodegradation of Phthalic Acid Esters in Freshwater Sediments." Environ Pollut (Series
           6)8:101-118.
    
    Johnson B, Stalling D, Hogan J, et al. 1977. "Dynamics of Phthalic Acid Esters in Aquatic Organisms."
           In: Suffet I, ed. Fate of 'Pollutants in the Air and Water Environments. Part 2. John Wiley, New
           York.  pp. 283-300.
    
    Loekke H, Bro-Rasumussen F. 1981. "Studies of Mobility of Di-iso-butyl Phthalate (Dibp), Di-n-butyl
           Phthalate (Dbp), and Di-(2-ethyl Hexyl) Phthalate (Dehp) by Plant Foliage Treatment in a Closed
           Terrestrial Simulation Chamber." Chemosphere 10:1223-1235.
    
    Mathur S. 1974.  "Respirometric Evidence of the Utilization of Di-octyl and Di-2-ethylhexyl Phthalate
           Plasticizers." J Environ Qual 3:207-209.
    
    Mayer F.  1977.  J Fish Res Board Can 33:2610.
    
    Mehrle P, Mayer F.  1976. Trace Substances in Environmental Health,  pp.518. As cited in HSDB
    1997.
    
    Melancon M, Lech J.  1977.  "Metabolism of Di-2-ethylhexyl Phthalate by Subcellular Fractions from
           Rainbow Trout Liver." Drug Metab Dispos 5(1):29.
    
    Melnick R, Morrissey R, Tomaszewski  K.  1987.  "Studies by the National Toxicology Program on
           Di(2-ethylhexyl)phthalate." Toxicol Ind Health 3:99-118.
    
    MenzieC. 1980.  Metabolism of Pesticides. Update HI. U.S. Department of Interior, Fish and Wildlife
           Service,  p. 453.
    
    O'Connor O, Rivera M, Young L. 1989. "Toxicity and Biodegradation of Phthalic Acid Esters under
           Methanogenic Conditions." Environ Toxicol Chem 8:569-576.
    U.S. EPA Region 6                                                             U.S. EPA
    Multimedia Planning and Permitting Division                                          Office of Solid Waste
    Center for Combustion Science and Engineering                                                       H-24
    

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    Protocol for Screening Level Ecological Risk Assessment
    Toxicological Profile H-7; Bis(2-Ethylhexyl)Phthalate	August 1999
    
    O'Grady D, Howard P, Werner A.  1985. Activated Sludge Biodegradation of 12 Commercial Phthalate
            Esters. Report to Chemical Manufacturers Association by Syracuse Research Corporation.
            Contract no. PE-17.0-ET-SRC. SRC 11553-03.  As cited in ATSDR 1993.
    
    Overcash M, Weber J, Tucker W. 1986. Toxic and Priority Organics in Municipal Sludge Land
            Treatment Systems.  EPA/600/2-86/010. EPA, ORD, Cincinnati, OH NTIS PB86-50208.
    
    Park, C.W., O. Imamura, and T. Yoshida. 1990. "Uptake, Excretion, and Metabolism of 14C-labeled
            Di-2-ethylhexyl Phthalate by Mullet, Mugil cephalus" Bulletin of Korean Fish. Soc. 22:424-428.
    
    Rhodes C, Orton T, Pratt I, Batten P, Bratt H, Jackson S, Elcombe C. 1986. "Comparative
            Pharmacokinetics and Subacute Toxicity of Di(2-ethylhexyl)phthalate in Rats and Marmosets:
            Extrapolation of Effects in Rodents to Man."  Environ Health Perspect 65:299-308.
    
    Sanders H, Mayer F, Walsh D.  1973.  "Toxicity, Residues Dynamics, and Reproductive Effects of
            Phthalate Esters in Aquatic Invertebrates."  Environ Res 6:84-90.
    
    Short R, Robinson E, Lington A, Chin A.  1987.  "Metabolic and Peroxisome Proliferation Studies with
            Di(2-ethylhexylphthalate in Rats and Monkeys."  Toxicol Ind Health 3:185-195.
    
    Sullivan K, Atlas E, Giam C. 1982. "Adsorption of Phthalic Acid Esters from Seawater." Environ Sci
            Technol 16:428-432.
    
    Tabak H, Quave S, Mashni C, Earth E. 1981. "Biodegradability Studies with Organic Priority Pollutant
            Compounds." J Water Pollut Contr Fed 53:1503-1518.
    
    Warns T.  1987.  "Diethylhexylphthalate as a Environmental Contaminant-a Review." Sci Total Environ
            66:1-16.
    
    Wofford HW, Wilsey CD, Neff GS, et al.  1981. "Bioaccumulation and Metabolism of Phthalate Esters
           by Oysters, Brown Shrimp, and Sheepshead Minnows." Ecotoxicol Environ Safety 5:202-210. As
            cited in ATSDR 1993.
    
    Wolfe N, Burns L, Steen W.  1980. "Use of Linear Free Energy Relationships and an Evaluative Model to
            Assess the Fate and Transport of Phthalate Esters in the Aquatic Environment." Chemosphere
           9:393-402.
    U.S. EPA Region 6                                                             U.S. EPA
    Multimedia Planning and Permitting Division                                         Office of Solid Waste
    Center for Combustion Science and Engineering                                                      H-25
    

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    Protocol for Screening Level Ecological Risk Assessment
    lexicological Profile H-8:  Cadmium	August 1999
                                             CADMIUM
    1.0    SUMMARY
    
    Cadmium exists in the elemental (0+) state or the 2+ valance state in nature.  Exposure routes for aquatic
    organisms include ingestion and gill uptake.  Freshwater biota are the most sensitive organisms to cadmium
    exposure, with toxiciry inversely proportional to water hardness.  Cadmium bioaccumulates in both aquatic
    and terrestrial animals, with higher bioconcentration in aquatic organisms. Exposure routes for ecological
    mammalian species include ingestion and inhalation. Cadmium interferes with the absorption and
    distribution of other metals and causes renal toxicity in vertebrates.
    
    The following is a profile of the fate of cadmium in soil, surface water and sediment, and the fate after
    uptake by biological receptors.  Section 2 discusses the environmental fate and transport in soil, surface
    water and sediment. Section 3 discusses the fate in ecological receptors.
    
    2.0    FATE IN SOIL, SURFACE WATER AND SEDIMENT
    
    Cadmium has a low vapor pressure and is released from soil to air by entrainment with soil particles (EPA
    1980; OHM/TADS 1997). Cadmium compounds in soil are stable and are not subject to degradation
    (ATSDR 1993).  Cadmium compounds can be transformed by precipitation,  dissolution, complexation, and
    ion exchange (McComish and Ong 1988).
    
    Cadmium compounds in aquatic environments are not affected by photolysis, volatilization, or biological
    methylation (Callahan et al. 1979). Precipitation and sorption to mineral surfaces and organic materials
    are important removal processes for cadmium compounds (ATSDR 1993). Concentrations of cadmium are
    generally higher in sediments than in overlying water (Callahan et al. 1979).
    
    3.0    ECOLOGICAL RECEPTORS
    
    Cadmium bioconcentrates in aquatic organisms, primarily in the liver and kidney (EPA 1985). Cadmium
    accumulated from water is slowly excreted, while cadmium accumulated from food is eliminated more
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    Protocol for Screening Level Ecological Risk Assessment
    Toxicological Profile H-8; Cadmium	August 1999
    rapidly (EPA 1985). Metal-binding, proteinaceous, metallothionens appear to protect vertebrates from
    deleterious effects of high metal body burdens (Eisler 1985).
    
    Exposure routes in ecological mammalian species include ingestion and inhalation, while dermal absorption
    is negligible (Goodman and Oilman 1985). Absorption and retention of cadmium decreases with prolonged
    exposure. Cadmium absorption through ingestion is inversely proportional to intake of other metals,
    especially iron and calcium (Friberg 1979).  Cadmium accumulates primarily in the liver and kidneys
    (IARC 1973).  Cadmium crosses the placental barrier (Venugopal 1978). Cadmium does not undergo
    direct metabolic conversion, but the ionic (+2 valence) form binds to proteins and other molecules
    (Nordberg et al. 1985). Absorbed cadmium is excreted very slowly, with urinary and fecal excretion being
    approximately equal (Kjellstrom and Nordberg 1978).
    
    Freshwater aquatic species are most sensitive to the toxic effects of cadmium, followed by marine
    organisms, birds, and mammals.
    
    4.0    REFERENCES
    
    ATSDR.  1993. Toxicological Profile for Cadmium. Agency for Toxic Substances and Disease Registry.
    Callahan M, Slimak M, Gable N, et al. 1979. Water-Related Fate of 129 Priority Pollutants.
           EPA-440/4-79-029a.  Vol 1. Office of Water Planning and Standards, Washington, DC.  pp. 9-1
           to 9-20.
    Eisler 1985. Cadmium Hazards to Fish, Wildlife, and Invertebrates: A Synoptic Review. U. S. Fish and
           Wildlife Service, U.S. Department of the Interior. Biological Report 85 (1.2).
    EPA. 1980. Fate of Toxic and Hazardous Materials in the Air Environment. Environmental Sciences
           Research Laboratory, Research Triangle Park, NC.
    EPA. 1985. Cadmium Contamination of the Environment: an Assessment of Nationwide Risk. EPA
           600/8-83/025f. Office of Water Regulations and Standards, Washington, DC.
    Friberg L.  1979. Handbook of the Toxicity of Metals. As cited in HSDB 1997.
    Goodman L, Oilman A, eds. • 1985.  The Pharmacological Basis of Therapeutics.  7th ed.  Macmillan
           Publ., New York. pp. 1617-1619.
    HSDB.  1997.  Hazardous Substance Data Base.
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    Protocol for Screening Level Ecological Risk Assessment
    Toxicological Profile H-8:  Cadmium	August 1999
    
    IARC. 1973. IARC monographs. 2:74-99.
    
    Kjellstrom T, Nordberg G. 1978. "A Kinetic Model of Cadmium Metabolism in the Human Being."
           Environ Res 16:248-269.
    
    McComish MF, Ong JH.  1988.  "Trace Metals." In: Bodek I, Lyman W, Reehl W, Rosenblatt DH eds.
           Environmental Inorganic Chemistry: Properties, Processes, and Estimation Methods.
           Pergammon Press, New York.  pp. 7.5.1 to 7.5.12. As cited in ATSDR 1993.
    
    Nordberg G, Kjellstrom T, Nordberg M.  1985.  "Kinetics and Metabolism." In: Friberg L,Elinder C,
           Kjellstrom T, et al., eds. Cadmium and Health: A Toxicological and Epidemiological Appraisal.
           Vol 1. CRC Press, Boca Raton, FL.  pp. 103-178. As cited in ATSDR 1993.
    
    OHM/TADS. 1997. Oil and Hazardous Materials/Technical Assistance Data System.
    
    Venugopal.  1978. Metal Toxicity in Mammals 2. pp. 78, 83. As cited in HSDB 1997.
    U.S. EPA Region 6                                                            U.S. EPA
    Multimedia Planning and Permitting Division                                         Office of Solid Waste
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    Protocol for Screening Level Ecological Risk Assessment
    Toxicological Profile H-9;  Chromium	August 1999
                                             CHROMIUM
    1.0     SUMMARY
    
    Chromium exists primarily in the Cr3+ and Cr6+ valence forms in environmental and biological media.  It
    exists in soil primarily in the form of insoluble oxides with very limited mobility. In the aquatic phase,
    chromium may be in the soluble state or attached to clay-like or organic suspended solids.
    
    Exposure routes for aquatic organisms include ingestion, gill uptake, and dermal absorption.
    Bioaccumulation occurs in aquatic receptors; biomagnification does not occur in aquatic food chains.
    Exposure routes for ecological mammalian species include ingestion, inhalation, and dermal absorption.
    Chromium is not truly metabolized, but undergoes various changes in valence states and binding with
    ligands and reducing agents in vivo. Elimination of chromium is slow.
    
    The following is a profile of the fate of chromium in soil, surface water and sediment, and the fate after
    uptake by biological receptors. Section 2 discusses the environmental fate and transport in soil, surface
    water and sediment. Section 3 discusses the fate in ecological receptors.
    
    2.0     FATE IN SOIL, SURFACE WATER, AND SEDIMENT
    
    In soil, chromium 3+ is readily hydrolyzed and precipitated as chromium hydroxide. It exists in soil
    primarily as insoluble oxide with very limited mobility (EPA 1984a, b).
    
    In water, chromium 6+ occurs in the soluble state or as suspended solids adsorbed onto clay-like materials,
    organics, or iron oxides. Cr6+ persists in water for long periods of time, but is eventually reduced to
    chromium 3+ by organic matter or other reducing agents in water (Gary 1982).
    
    3.0     ECOLOGICAL RECEPTORS
    
    Exposure routes for aquatic organisms include ingestion, gill uptake, and dermal absorption. Chromium
    bioconcentrates in aquatic organisms (ATSDR 1993; OHM/TADS 1997; EPA 1985; EPA 1984a). The
    U.S. EPA Region 6                                                             U.S. EPA
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    lexicological Profile H-9;  Chromium	August 1999
    biomagnification and toxicity of chromium 3+ is low relative to chromium 6+ because of its low membrane
    permeability and noncorrosivity. Chromium is not significantly biomagnified in aquatic food chains.
    
    In vertebrates, chromium 3+ is an essential nutrient needed to produce glucose tolerance factor (GTF),
    which is required for regulation of glucose levels (ATSDR 1993).  Exposure routes for ecological
    mammalian species include ingestion, inhalation, and dermal absorption.  Chromium is poorly absorbed
    from the gastrointestinal tract after oral exposure, but fasting increases the absorption (Chen et al. 1973).
    Absorbed chromium is distributed to various organs including the liver and spleen (Maruyama 1982 as
    cited in ATSDR 1993; Witmer et al. 1989, 1991, as cited in ATSDR 1993).
    
    Following inhalation exposure,  chromium is distributed to the lung, kidney, spleen, and erythrocytes
    (Weber 1983; Baetjer et al. 1959). Following dermal exposure, chromium is readily absorbed and is
    distributed to the blood, spleen, bone marrow, lymph glands, urine, and kidneys. Chromium is not truly
    metabolized, but undergoes various changes in valence states and binding with ligands and reducing agents
    in vivo.  Elimination of chromium is slow (Langard et al. 1978).
    
    A large degree of accumulation by aquatic and terrestrial plants and animals in the lower trophic levels has
    been documented, however, the mechanism of this accumulation remains  unknown.
    
    4.0    REFERENCES
    ATSDR. 1993. Toxicological Profile for Chromium. Agency for Toxic Substances and Disease
           Registry.
    Baetjer A Damron C, Budacz V. 1959. "The Distribution and Retention of Chromium in Men and
           Animals." Arch Ind Health 20:136-150.
    CaryE. 1982. "Chromium in Air, Soil and Natural." In: Langard S, ed.  Topics in Environmental
           Health 5: Biological and Environmental Aspects of Chromium. Elsevier Science, New York.
           pp. 49-64.
    Chen N, Tsai A, Dyer I.  1973.  "Effect of Chelating Agents on Chromium Absorption in Rats." J Nutr
            103:1182-1186.
    EPA. 1985. Ambient Water Quality Criteria for Chromium. Office of Water Regulations and Standards.
           EPA 440/5-84-029.
    U.S. EPA Region 6                                                             U.S. EPA
    Multimedia Planning and Permitting Division                                         Office of Solid Waste
    Center for Combustion Science and Engineering                                                       H-30
    

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    Protocol for Screening Level Ecological Risk Assessment
    Toxicological Profile H-9;  Chromium	August 1999
    
    EPA. 1984a. Health Assessment Document for Chromium. Research Triangle Park, NC: Environmental
           Assessment and Criteria Office. US Environmental Protection Agency. EPA-600/8-81-014F.
    
    EPA. 1984b. Health Assessment Document for Chromium. Final report. As cited in ATSDR 1993.
    
    Langard S, Gundersen N, Tsalev D, Gylseth B. 1978. "Whole Blood Chromium Level and Chromium
           Excretion in the Rat after Zinc Chromate Inhalation." Acta Pharmacol et Toxicol 42:142-149.
    
    Maruyama Y. 1982. "The Health Effect of Mice Given Oral Administration of Trivalent and Hexavalent
           Chromium over a Long-term." Acta Scholae Med Univ Gifu 31:24-46. As cited in ATSDR 1993.
    
    OHM/TADS. 1997. Oil and Hazardous Materials/Technical Assistance Data System.
    
    Weber H. 1983.  "Long-term Study of the Distribution of Soluble Chromate-51 in the Rat after a Single
           Intratracheal Administration." J Toxicol Environ Health 11:749-764.
    
    Witmer C, Harris R, Shupack S. 1991. "Oral Bioavailability of Chromium from a Specific Site." Environ
           Health Perspect 92:105-110.
    
    Witmer C, Park H-S, Shupack S.  1989. "Mutagenicity and Disposition of Chromium."  Sci Total Environ
           86:131-148.
    U.S. EPA Region 6                                                            U.S. EPA
    Multimedia Planning and Permitting Division                                         Office of Solid Waste
    Center for Combustion Science and Engineering                                                      H-31
    

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    Protocol for Screening Level Ecological Risk Assessment
    Toxicological Profile H-10;  Copper	August 1999
                                               COPPER
    1.0    SUMMARY
    
    Copper binds to soils and sediment. Copper is not biodegraded or transformed. Exposure routes for
    aquatic organisms include ingestion, gill uptake, and dermal absorption. In aquatic organisms, exposures
    to copper are associated with developmental abnormalities. Copper bioconcentrates in aquatic organisms,
    however, biomagnification does not occur.  Exposure routes for ecological mammalian species include
    ingestion, inhalation, and dermal absorption. Copper is associated with adverse hematological, hepatic,
    developmental, immunological, and renal effects in mammals.  Copper does not bioaccumulate in
    mammals.
    
    The following is a profile of the fate of copper in soil, surface water and sediment; and the fate after uptake
    by ecological receptors. Section 2 discusses the environmental fate and transport in soil, surface water and
    sediment.  Section 3 discusses the fate in ecological receptors.
    
    2.0    FATE IN SOIL, SURFACE WATER AND SEDIMENT
    
    Copper occurs naturally in many animals and plants and is an essential micronutrient.  Copper may exist in
    two oxidation states: +1 or +2.  Copper (+1) is unstable and, in aerated water over the pH range of most
    natural waters (6 to 8), oxidizes to the +2 state. In the aquatic environment, the fate of copper is
    determined by the formation of complexes,  especially with humic substances, and sorption to hydrous metal
    oxides, clays, and organic materials. The amount of copper able to remain in solution is directly dependent
    on water chemistry, especially pH and temperature, and the concentration of other chemical species
    (Callahan et al. 1979; Tyler and McBride 1982; Fuhrer 1986).
    
    The majority of copper released to surface waters settles out or adsorbs to sediments (Harrison and Bishop
    1984). Copper is affected by photolysis (Moffett and Zika 1987).  Some copper complexes undergo
    metabolism however, biotransformation of  copper is low (Callahan 1979).
    U.S. EPA Region 6                                                              U.S. EPA
    Multimedia Planning and Permitting Division                                           Office of Solid Waste
    Center for Combustion Science and Engineering                                                       H-32
    

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    Protocol for Screening Level Ecological Risk Assessment
    Toxicological Profile H-10;  Copper	August 1999
    
    3.0    ECOLOGICAL RECEPTORS
    Copper bioconcentrates in aquatic organisms. Copper does not biomagnify in aquatic food chains (Heit
    
    and Klusek 1985; Perwack et al. 1980).
    
    
    Copper is absorbed by mammals following ingestion, inhalation, and dermal exposure (Batsura 1969; Van
    
    Campen and Mitchell 1965; Crampton et al. 1965).  Once absorbed, copper is distributed to the liver
    
    (Marceau et al. 1970). Copper is not metabolized.  Copper exerts its toxic effects by binding to DNA
    
    (Sideris et al. 1988) or by generating free radicals (EPA 1985). Copper does not bioaccumulate in
    
    mammals and is excreted primarily in the bile (Bush et al. 1955).
    
    
    Copper is known to inhibit photosynthesis and plant growth. Because copper is an essential micronutrient
    
    for plant  nutrition, most adverse effects result from copper deficiency (Adriano 1986).
    
    
    4.0    REFERENCES
    
    
    Adriano D.C. 1986.  Trace elements in the terrestrial environment. Springer-Verlag. New York.
    
    ATSDR.  1990.  Toxicological Profile for Copper.  Agency for Toxic Substances and Disease Registry.
           December.
    
    Batsura Y.  1969. "Electron-microscopic investigation of penetration of copper oxide aerosol from the
           lungs into the blood and internal organs." Bull Exp Biol Med 68:1175-1178.
    
    Bush J, Mahoney J, Markowitz H, Gubler C, Cartwright G, Wintrobe M.  1955. "Studies on copper
           metabolism. XVI. Radioactive copper studies in normal subjects and in patients with
           hepatolenticular degeneration." J  Clin Invest 34:1766-1778..
    
    Callahan  M, Slimak M, Gabel N, et al.  1979. Water-Related Environmental Fate of 129 Priority
           Pollutants.  Vol. 1&2. EPA-440/4-79-029. Office of Water Planning and Standards,
           Washington, DC.  11-1 to 11-19.
    
    Crampton R, Matthews D, Poisner R.  1965.  "Observations on the mechanism of absorption of copper by
           the small intestine." J Physiol  178:111-126.
    
    EPA. 1985. Drinking Water Criteria Document for Copper. Final draft.  EPA-600/X-84-190-1.
           P. VH-1.
    U.S. EPA Region 6                                                              U.S. EPA
    Multimedia Planning and Permitting Division                                          Office of Solid Waste
    Center for Combustion Science and Engineering                                                      H-33
    

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    Protocol for Screening Level Ecological Risk Assessment
    lexicological Profile H-10;  Copper	August 1999
    
    Fuhrer G. 1986.  "Extractable cadmium, mercury, copper, lead, and zinc in the lower Columbia River
           estuary, Oregon and Washington." In: U.S. geological survey water-resources investigations
           report. U.S. Department of the Interior. 86:4088.
    
    Harrison F, Bishop D.  1984.  A review of the impact of copper released into freshwater environments.
           Prepared for Division of Health, Siting and Waste Management, Office of Nuclear Regulatory
           Research. U.S. Nuclear Regulatory Commission, Washington, DC. As cited in ATSDR 1990.
    
    Heit M, Klusek C. 1985. "Trace element concentrations in the dorsal muscle of white suckers and brown
           bullheads from two acidic Adirondack lakes." Water Air Soil Pollut 25:87-96.
    
    HSDB. 1997. Hazardous Substance Data Base.
    
    Marceau N, Aspin N, Sass-Kortsak A.  1970. "Absorption of copper 64 from gastrointestinal tract of the
           rat." Am J Physiol 218:377-383.
    
    Moffett J, Zika R.  1987. "Photochemistry of copper complexes in sea water." In: Zika R, Copper W,  ed.
           ACS Symposium Series, Washington, DC. 327:116-130.  As cited in ATSDR 1990.
    
    Perwak J, Bysshe S, Goyer M, et al.  1980. Exposure and risk assessment for copper. EPA
           400/4-81-015.  EPA, Cincinnati, OH. NTIS PB85-211985. As cited in ATSDR 1990.
    
    Sideris E, Sylva C, Charalambous AT, and Katsaros N. 1988. "Mutagenesis; Carcinogenisis and the
           metal elements - DNA interaction." Prog Clin Biol Res 259:13-25.
    
    Tyler L, McBride M.  1982.  "Mobility and extractability of cadmium, copper, nickel, and zinc in organic
           and mineral soil columns." Soil Sci 134:198-205.
    
    Van Campen D, Mitchell E.  1965. "Absorption of Cu64, Zn66, Mo",  and Fe59 from ligated segments of the
           rat gastrointestinal tract." J Nutr 86:120-124.
    U.S. EPA Region 6                                                             U.S. EPA
    Multimedia Planning and Permitting Division                                         Office of Solid Waste
    Center for Combustion Science and Engineering                                                      H-34
    

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    Protocol for Screening Level Ecological Risk Assessment
    Toxicological Profile H-ll;  Crotonaldehyde	August 1999
                                        CROTONALDEHYDE
    1.0     SUMMARY
    
    Crotonaldehyde is a highly volatile, water-soluble, low molecular weight, organic compound.
    Volatilization is the major fate process for crotonaldehyde in surface water and surface soil.
    Crotonaldehyde does not bioconcentrate in aquatic organisms and does not accumulate in wildlife.
    Therefore, food chain transfer is insignificant.
    
    The following summarizes information about the fate of crotonaldehyde in soil, surface water, and
    sediment; and the fate after uptake by ecological receptors. Section 2 discusses the environmental fate and
    transport in soil, water and sediment. Section 3 discusses the fate in ecological receptors.
    
    2.0     FATE IN SOIL, SURFACE WATER, AND SEDIMENT
    
    Crotonaldehyde has a low K^. value, therefore it will not strongly adsorb to soils (Irwin 1988 as cited in
    ATSDR 1990), and may dissolve in soil water.  Crotonaldehyde has a short half-life (Lyman 1982) and it
    will quickly volatilize from surface soils.
    
    Crotonaldehyde is completely rniscible in water and does not dissolve in oils. However, based on its
    volatilization half-life of about 1 to 2 days (Bowmer et al. 1974; Thomas 1982), crotonaldehyde is
    expected to quickly volatilize from surface water. The adsorption of crotonaldehyde to suspended solids
    and sediment is not expected to be significant because of its low K^. value (Lyman 1982).
    
    Aerobic biodegradation may degrade crotonaldehyde at low concentrations in natural water (Bowmer and
    Higgins 1976; Callahan et al. 1979; Tabak et al. 1981). In addition, data suggest that persistence of
    crotonaldehyde in aerobic aquatic environments for moderate to long periods of time will not occur
    (Jacobson and Smith 1990 as cited in ATSDR 1990).
    
    3.0     FATE IN ECOLOGICAL RECEPTORS
            Based on its short volatilization half life and low bioconcentration factor (Bysshe 1982; Hansch
    and Leo 1985), crotonaldehyde will not concentrate in aquatic organisms.
    U.S. EPA Region 6                                                             U.S. EPA
    Multimedia Planning and Permitting Division                                          Office of Solid Waste
    Center for Combustion Science and Engineering                                                      H-35
    

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    Protocol for Screening Level Ecological Risk Assessment
    Toxkological Profile H-ll; Crotonaldehyde	August 1999
    
    Little information was available on the fate of crontonaldehyde in mammals.  Because crotonaldehyde has a
    low soil adsorption coefficient and strongly volatilizes, inhalation is the primary exposure route for
    mammals. Studies have indicated that inhaled crotonaldehyde is quickly absorbed by the upper and lower
    respiratory tracts (Egle 1972).  Studies also suggest that absorbed crotonaledhyde is quickly metabolized
    (Alarcon  1976; Kaye 1973; Patel et al. 1980).
    
    
    No information was available on the fate of crotonaldehyde in birds or plants.
    
    
    4.0    REFERENCES
    Alarcon R.  1976. "Studies on the in vivo formation of acrolein. 3-hydroxypropylmercapturic acid as an
           index of cyclophosphamide (nsc-26271) activation." Cancer Treat Rep 60:327-335.
    
    ATSDR.  1990. Toxicological Profile for Acrolein. Agency for Toxic Substances and Disease Registry,
           Atlanta, GA.  December.
    
    Bowmer K, Higgins M.  1976. "Some aspects of the persistence and fate of acrolein herbicide in water."
           Arch Environ Contam Toxicol 5:87-96.
    
    Bowmer K, Lang A Higgins M, et al. 1974. "Loss of acrolein from water by volatilization and
           degradation." Weed Res 14:325-328.
    
    Bysshe S.  1982. "Bioconcentration factor in aquatic organisms."  In: Lyman W, Reehl W, Rosenblatt D,
           eds. Handbook of Chemical Property Estimation Methods. McGraw-Hill Book Co., New York.
           pp 5-1  to 5-30. As cited in ATSDR 1990.
    
    Callahan M, Slimak M, Gabel N, et al. 1979.  Water-Related Environmental Fate of 129 Priority
           Pollutants. Vol 1 & 2.  EPA-440/4-79-029a.  USEPA Washington, DC.
    
    Egle J. 1972.  "Retention of inhaled formaldehyde, propionaldehyde, and acrolein in the dog." Arch
           Environ Health 25:119-124.
    
    Hansch C, Leo A. 1985. Medchem Project Issue No.  26, Pomona College, Claremont, CA.  As cited in
           ATSDR 1990.
    
    Irwin K.  1988. Soil Adsorption Coefficient For Acrolein (Magnicide, H Herbicide And Magnicide, B
           Microbiocide). Prepared by SRI International, Menlo Park, CA for Baker Performance
           Chemicals, Houston, TX. SRI Project No. PYU 3562. As cited in ATSDR 1990.
    
    Jacobson B, Smith J.  1990.  Aquatic Dissipation for Acrolein. Prepared by Analytical Bio-Chemistry
           Laboratories, Inc., Columbia, MI, for Baker Performance Chemicals, Houston, TX.  ABC Final
           Report No. 37891.  As cited in ATSDR 1990.
    U.S. EPA Region 6                                                             U.S. EPA
    Multimedia Planning and Permitting Division                                          Office of Solid Waste
    Center for Combustion Science and Engineering                                                      H-36
    

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    Protocol for Screening Level Ecological Risk Assessment
    lexicological Profile H-ll;  Crotonaldehyde	August 1999
    
    Kaye C.  1973. "Biosynthesis of mercapturic acids from allyl alcohol, allyl esters, and acrolein." Biochem
           1134:1093-1101.
    
    Lyman W.  1982.  "Adsorption coefficient for soils and sediments."  In: Lyman W, Reehl W, Rosenblatt
           D, eds. Handbook of Chemical Property Estimation Methods. McGraw-Hill Book Co., New
           York, pp 4-1 to 4-33.
    
    Patel J, Wood J, Leibman K. 1980. "The biotransformation of allyl alcohol and acrolein in rat liver and
           lung preparations." Drug Metab Dispos 8:305-308.
    
    Tabak H, Quave S, Mashni C, et al.  1981.  "Biodegradability studies with organic priority pollutant
           compounds." J Water Pollut Cont Fed 53:1503-1518.
    
    Thomas R.  1982.  "Volatilization from water." In: Lyman W, Reehl W, Rosenblatt D, eds.  Handbook of
           Chemical Property Estimation Methods.  McGraw-Hill Book Company, New York, pp 15-1 to
           15-34.
    U.S. EPA Region 6                                                             U.S. EPA
    Multimedia Planning and Permitting Division                                          Office of Solid Waste
    Center for Combustion Science and Engineering                                                      H-37
    

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    Protocol for Screening Level Ecological Risk Assessment
    Toxicological Profile H-12;  Cumene (Isopropylbenzene)	August 1999
                                  CUMENE aSOPROPYLBENZENE)
    1.0    SUMMARY
    
    1-methylethylbenzene is also called cumene.  Cumene and its superoxidized form, cumene hydroperoxide,
    are moderately volatile organic compounds. Cumene released to soil and surface water will rapidly
    dissipate through biodegradation and volatilization. Routes of exposure for cumene and cumene
    hydroperoxide include inhalation, ingestion, and dermal exposure.  However, due to its high potential to
    volatilize, inhalation is  the major exposure route for wildlife receptors.  Bioconcentration of cumene is not
    likely in aquatic organisms. No information was available regarding the environmental fate of cumene
    hydroperoxide in air, water, or soil. However, degradation in soil and water is expected to be very rapid
    based on the high reactivity of cumene hydroperoxide with multivalent metal ions and free radicals.
    
    The following is a profile of the fate of cumene and cumene hydroperoxide in soil, surface water and
    sediment; and the fate after uptake by ecological receptors. Section 2 discusses the environmental fate and
    transport in soil, surface water and sediment. Section 3 discusses the fate in ecological receptors.
    
    2.0    FATE IN SOIL, SURFACE WATER, AND SEDIMENT
    
    The primary removal process for cumene in soil is expected to be through biodegradation in surface soil,
    and volatilization (HSDB 1997). Based on its log K^. value (Lyman 1982), cumene that does not volatilize
    is expected to strongly  adsorb to soil.
    
    The environmental fate of cumene hydroperoxide in soil is unknown. However, based on its high reactivity
    with multivalent metal  ions and free radicals, degradation in soil is expected to be very rapid (HSDB
    1997).
    In surface water, cumene is expected to have a relatively  short half-life.  The primary removal processes
    for cumene when released in water are volatilization and biodegradation (GEMS 1986; HSDB 1997).
    Based on different water characteristics, volatilization half-lives ranging from a few hours to a few days
    have been estimated (GEMS 1986). Cumene is amenable to biodegradation (Price et al.  1974; Kappeler
    and Wuhrmann 1978), and biodegrades in 10 to 30 days  (Walker and Colwell 1975; Price et al. 1974).
    U.S. EPA Region 6                                                              U.S. EPA
    Multimedia Planning and'Permitting Division                                          Office of Solid Waste
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    Protocol for Screening Level Ecological Risk Assessment
    Toxicological Profile H-12;  Cumene (Isopropylbenzene)	August 1999
    
    The environmental fate of cumene hydroperoxide in water is unknown. However, based on its high
    reactivity with multivalent metal ions and free radicals, degradation in water is expected to be very rapid
    
    (HSDB 1997).
    
    
    3.0    FATE IN ECOLOGICAL RECEPTORS
    
    
    Cumene is reported to have relatively low bioconcentration in fish (TTC/EPA 1984; Geiger 1986;).
    
    
    In wildlife, cumene and cumene hydroperoxide enter the body primarily via inhalation and dermal
    
    absorption (Lefaux 1968; HSDB 1997). Cumene is readily absorbed in mammalian systems and oxidized
    
    (Clayton and Clayton 1982).  In the event that cumene is ingested, it is readily metabolized and excreted
    
    (Robinson et al. 1955).  Long-term exposure by mammals results in cumene distribution to many tissues
    
    and organs (Gorban et al. 1978).
    
    
    4.0    REFERENCES
    
    
    Clayton G, Clayton F, eds. 1982. Patty's Industrial Hygiene and Toxicology.  Srded  Vol2. John Wiley
           & Sons, New York. pp. 3309-3310.
    
    Geiger. 1986. Acute Tox Org Chem to Minnows. Vol HI. p.213. As cited in HSDB 1997.
    
    GEMS.  1986.  Graphical Exposure Modeling System. Fate of atmospheric pollution. EPA, Office of
           Toxic Substances.
    
    Gorban G, et al. 1978. Gig Sanit 10:113. As cited in HSDB 1997.
    
    HSDB. 1997. Hazardous Substance Data Bank,
    
    ITC/EPA. 1984.  Information review #464. Draft.  Cumene. pp. 10; 23.  As cited in HSDB 1997.
    
    Kappeler T, Wuhrmann K. 1978. "Microbial degradation of the water-soluble fraction of gas oil~n.
           Bioassayw with pure strains."  Water Res 12:335-342.
    
    Lefaux.  1968.  Practox of plastics, p. 166. As cited in HSDB 1997.
    
    Lyman W. 1982.  "Adsorption coefficient for soils and sediments." In: Lyman W, Reehl W, Rosenblatt
           D, eds. Handbook of Chemical Property Estimation Methods. McGraw Hill Book Co., New
           York. pp. 4-1 to 4-33.
    U.S. EPA Region 6                                                            U.S. EPA
    Multimedia Planning and Permitting Division                                         Office of Solid Waste
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    Protocol for Screening Level Ecological Risk Assessment
    Toxicological Profile H-12:  Cumene (Isopropylbenzene)	August 1999
    
    Price K, Waggy G, Conway R. 1974. "Brine shrimp bioassay and seawater BOD of petrochemicals."
           J Water Pollut Cont Fed 46:63-77.
    
    Robinson D, Smith J, Williams R.  1955.  "Studies in detoxication." Biochem J 59:153-159.
    
    Walker J, ColwellR. 1975. J Gen Appl Microbiol 21:27-39.
    U.S. EPA Region 6                                                            U.S. EPA
    Multimedia Planning and Permitting Division                                         Office of Solid Waste
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    Protocol for Screening Level Ecological Risk Assessment
    Toxicological Profile H-13;  DDE	August 1999
                                                 DDE
    1.0     SUMMARY
    
    Dichlorodiphenyldichloroethane (DDE) is a high molecular weight, chlorinated pesticide. It is also a
    congener of dichlorodiphenyltrichloroethane (DDT), a full-spectrum pesticide. DDE is stable,
    accumulates in soil and sediment, and concentrates in fatty tissue. DDE has a low water solubility, and is
    adsorbed strongly in soils and sediments. Soil and benthic organisms accumulate DDE from soil and
    sediment.  Wildlife will accumulate DDE in fatty tissue. Following chronic exposure by wildlife to DDE,
    an equilibrium between absorption and excretion may occur; however, concentrations will continue to
    increase because accumulation is related to fat content, which increases with age.
    
    The following summarizes the fate of DDE in surface soil, surface water, and sediment; and the fate after
    uptake by ecological receptors.  Section 2 discusses the environmental fate and transport in soil, water, and
    sediment.  Section 3 discusses the fate  in ecological receptors.
    
    2.0     FATE IN SOIL, SURFACE WATER, AND SEDIMENT
    
    DDE absorbs strongly to soil and is only slightly soluble in water.  Under normal environmental conditions,
    DDE does not hydrolyze or biodegrade. In soils with low organic content, evaporation from the surface of
    soil may be significant (HSDB 1997).
    
    DDE is bioavailable to plants and soil  invertebrates despite being highly bound to soil. DDT has been
    found to accumulate in grain, maize, and rice plants with the majority located in the roots. Mobilization of
    soil-bound DDT by earthworms to more bioavailable forms has also been reported (Verma and Pillai
    1991).
    
    DDE is very persistent in the aquatic environment, has  a very low water solubility, and is highly soluble in
    lipids.  Compounds with these characteristics tend to partition to the organic carbon fraction of sediments
    and lipid fraction of biota (EPA 1986). DDE absorbs very strongly to sediment,  and bioconcentrates in
    aquatic organisms (HSDB 1997). In aquatic environments, the small fraction of dissolved DDE may be
    photolyzed.
    U.S. EPA Region 6                                                              U.S. EPA
    Multimedia Planning and Permitting Division                                          Office of Solid Waste
    Center for Combustion Science and Engineering                                                       H-41
    

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    Protocol for Screening Level Ecological Risk Assessment
    Toxicological Profile H-13:  DDE	August 1999
    3.0    FATE IN ECOLOGICAL RECEPTORS
    
    In general, DDE will bioconcentrate in lower-trophic-level organisms and will accumulate in food chains.
    Fish and other aquatic organisms readily take up pesticides, including DDE. Pesticides are taken up by
    organisms through the gills, by direct contact with the contaminant in the water, or by ingestion of
    contaminated food, sediment, or water.  The lipophilic nature and extremely long hah0 life of DDE result in
    bioaccumulation when it is present in ambient water. DDE will bioconcentrate in freshwater and marine
    plankton, insects, mollusks and other invertebrates, and fish (Oliver and Niimi 1985). When these
    organisms are consumed by other receptors, DDE is transferred up food chains. Following absorption,
    either through the gills or by ingestion, pesticides appear in the blood and may be distributed to tissues of
    all soft organs (Nimmo 1985).
    
    DDE is accumulated to high concentrations in fatty tissues of carnivorous receptors. Elimination and
    absorption of DDE may occur simultaneously once an equilibrium is reached. This equilibrium may be
    disturbed by high concentrations of DDE, but termination of exposure usually results in elimination of the
    stored substance. This elimination occurs in two phases—an initial rapid phase followed by a much slower
    gradual loss (Nimmo 1985).
    
    DDE can be introduced into mammals through oral, dermal, and inhalation exposure. Inhalation
    absorption is considered minor because the large particle size of DDE precludes entry to the deeper spaces
    of the lung; DDE is deposited in the upper respiratory tract and, through mucociliary action, is eventually
    swallowed and absorbed in the gastrointestinal tract. Gastrointestinal absorption following oral exposure
    has been shown in experimental animals (Hayes 1982).  Dermal absorption is limited and the toxic effects
    are less than those seen following oral exposure.  The highest concentration of DDE and metabolites has
    been found in adipose tissue, followed by reproductive organs, liver, kidneys, and brain (EPA 1980).
    
    The metabolism of DDE in animals is similar to that in humans. DDE metabolism and elimination occurs
    very slowly. The primary route of elimination is in the urine (Gold and Brunk 1982, 1983, 1984);
    however, DDE may also be eliminated through the feces, semen, or breast milk. When exposure ceases,
    DDE is slowly eliminated from the body (Murphy 1986).  The biological half-life of DDE is 8 years (NAS
    1977).
    U.S. EPA Region 6                                                               U.S. EPA
    Multimedia Planning and Permitting Division                                           Office of Solid Waste
    Center for Combustion Science and Engineering                                                       H-42
    

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    lexicological Profile H-13; DDE	August 1999
    
    Bioaccumulation has been reported in one Alaskan study of two raptor species—the Rough-legged hawk
    and the Peregrine falcon.  Higher tissue residues were reported in the peregrine falcon than in the
    rough-legged hawk. It was believed that these differences may have been due to the different feeding habits
    of the birds (Matsumura 1985).
    
    
    No information was available on the fate of DDE taken up by plants.
    
    
    4.0     REFERENCES
    ATSDR. 1994. Toxicological Profile for p,p'-DDT, p,p'-DDE, and p,p'-DDD.  Agency for Toxic
           Substances and Disease Registry. April.
    
    EPA.  1980. Ambient Water Quality Criteria for DDT. EPA 440/5-80-038. EPA, Office of Water
           Regulations and Standards, Washington, DC.  October. 95 PP.
    
    EPA.  1986. Superfund Public Health Evaluation Manual. EPA 540/1-86/000.  Office of Emergency and
           Remedial Response, Washington, DC.
    
    Gold B, Brunk G.  1982. "Metabolism of 1,1, l-trichloro-2,2-bis(p-chlorophenyI)-ethane and
           l,l-dichloro-2,2-bis(p-chlorophenyl)ethane in the mouse."  Chem-Biol Interact 41:327-339.
    
    Gold B, Brunk G.  1983. "Metabolism of l,l,-trichloro-2,2-bis(p-chlorophenyl)ethane (DDT),
           l,l-dichloro-2,2-bis(p-chlorphenyl)ethane, and l-chloro-2,2-bis(p-chlorophenyl)ethene in the
           hamster."  Cancer Res 43:2644-2647.
    
    Gold B, Brunk G.  1984. "A mechanistic study of the metabolism of 1, l-dichloro-2,2-bis(p-chloropheny
           l)ethane (ODD) to 2,2-bis(p-chlorophenyl)acetic acid (DDA)." Biochem Pharmacol 33:979-982.
    
    Hayes W.  1982. "Chlorinated hydrocarbon insecticides."  In: Pesticides Studied in Man. Williams and
           Wilkins, Baltimore, MD..  pp. 180-195.
    
    HSDB.  1997.  Hazardous Substances Data Bank.
    
    Matsumura F.  1985.  Toxicology of Insecticides. 2nded.  Plenum Press, New York.
    
    Murphy S.  1986.  "Toxic effects of pesticides." In: Klaassen C, et al., eds. Casarett andDoull's
           Toxicology. 3rded  MacMillan Publishing Company, New York,  pp 519-580.
    
    NAS.  1977. Drinking Water and Health. Safe Drinking Water Committee, National Research Council.
           National Academy of Sciences, Washington, DC. p. 576.
    U.S. EPA Region 6                                                             U.S. EPA
    Multimedia Planning and Permitting Division                                          Office of Solid Waste
    Center for Combustion Science and Engineering                                                      H-43
    

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    Protocol for Screening Level Ecological Risk Assessment
    lexicological Profile H-13; DDE	August 1999
    
    NimmoD.  1985.  "Pesticides." In: Fundamentals of Aquatic Toxicology Methods and Applications.
           Hemisphere Publishing Corp. pp. 335-373.
    Oliver B, Niimi A.  1985.  "Bioconcentration factors of some halogenated organics for rainbow trout:
           Limitations in their use for prediction of environmental residues." Environ Sci Technol
           19:842-849.
    
    Verma A, Pillai M. 1991. "Bioavailability of soil-bound residues of DDT and HCH to earthworms."
           Curr Sci 61(12):840-843.  As cited in ATSDR 1994.
    U.S. EPA Region 6                                                             U.S. EPA
    Multimedia Planning and Permitting Division                                         Office of Solid Waste
    Center for Combustion Science and Engineering                                                      H-44
    

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    Protocol for Screening Level Ecological Risk Assessment
    Toxicological Profile H-14: Dichlorofluoromethane	August 1999
                                  DICHLOROFLUOROMETHANE
    1.0    SUMMARY
    
    Dichlorofluoromethane (DCFM) is a highly volatile hydrocarbon.  It has a high vapor pressure and low soil
    adsorption coefficient; therefore, volatilization is the main fate process for DCFM released to surface soil
    and surface water. For terrestrial animals, inhalation is the main exposure route and ingestion is a minor
    exposure route. DCFM is not expected to bioconcentrate in fish; however, it can accumulate in tissues of
    mammals. DCFM is not expected to move up food chains.
    
    The following information summarizes the fate of dichlorofluoromethane in soil, surface water and
    sediment; and the fate after uptake by ecological receptors.  Section 2 discusses the environmental fate and
    transport in soil, water and sediment. Section 3 discusses the fate in ecological receptors.
    
    2.0    FATE IN SOIL, SURFACE WATER, AND SEDIMENT
    
    If released to soil, DCFM, an inert gas at room temperature, is expected to volatilize into the air due to its
    low soil adsorption coefficient (K^ value (Lyman et al. 1982). Because it does not have a strong affinity
    for organic carbon, it may dissolve in soil pore water, thus becoming bioavailable. Photooxidation,
    hydrolysis, and biodegradation are not likely to be significant removal processes for DCFM in soil due to
    its high volatility and minimal reactivity (HSDB 1997).
    
    Based on its high water solubility and low soil adsorption coefficient, DCFM does not adsorb strongly to
    suspended solids or sediment.  Based on a reported half-life of less than 1 day, DCFM is expected to
    rapidly volatilize from water (Lyman et al. 1982). The hydrolysis of DCFM is reported to be very low
    (<0.01 g/1 of water-yr) (Du Pont de Nemours Co. 1980).
    
    3.0    FATE IN ECOLOGICAL RECEPTORS
    
    DCFM is not expected to bioconcentrate in aquatic organisms, based on its low log K^, value (Hansch and
    Leo 1985) and low estimated BCF value (Lyman et al. 1982).
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    Multimedia Planning and Permitting Division                                          Office of Solid Waste
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    Protocol for Screening Level Ecological Risk Assessment
    Toxicological Profile H-14;  Dichlorofluoromethane	August 1999
    
    Information was not available on the fate of DCFM in mammals, birds, or plants.
    4.0    REFERENCES
    Du Pont de Nemours Company.  1980. Freon Product Information B-2. DuPont de Nemours and
           Company, Wilmington, DE. As cited in HSDB 1997.
    
    Hansch C, Leo A. 1985.  Medchem Project Issue No. 26, Pomona College, Claremont, CA.  As cited in
           HSDB 1997.
    
    HSDB. 1997. Hazardous Substance Data Bank.
    
    Lyman W.  1982. "Adsorption coefficient for soils and sediments." In: Lyman W, Reehl W, Rosenblatt
           D, eds.  Handbook of Chemical Property Estimation Methods. McGraw-Hill Book Co., New
           York, pp 4-1 to 4-33.
    U.S. EPA Region 6                                                          U.S. EPA
    Multimedia Planning and Permitting Division                                        Office of Solid Waste
    Center for Combustion Science and Engineering                                                    H-46
    

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    Protocol for Screening Level Ecological Risk Assessment
    Toxicological Profile H-15: Dichloroethene, 1,1-	August 1999
                                       DICHLOROETHENE, 1,1-
    1.0     SUMMARY
    
    1,1-dichloroethene is a hydrophillic, low molecular weight, chlorinated hydrocarbon.  It has a short half-life
    in the environment, thus acute exposures by ecological receptors are the main concern. Evaporation and
    biodegradation are major fate processes for 1,1-dichloroethene in soil, surface water, and sediment. It will
    also adsorb to detritus in soils and sediments. Ingestion and respiratory uptake are the significant direct
    exposure routes for ecological receptors exposed to 1,1-dichloroethene. Metabolic intermediates are
    responsible for the toxicity of 1,1-dichloroethene to upper trophic level receptors.  Indirect (food chain)
    exposure through ingestion of contaminated food is minor because it is readily biotransformed and
    excreted. Hence, the biomagnification potential is very low.
    
    The following is a profile of the fate of 1,1-dichloroethene in soil, surface water and sediment; and the fate
    after uptake by ecological receptors.  Section 2 discusses the environmental fate and transport in soil, water
    and sediment. Section 3 discusses the fate in ecological receptors.
    
    2.0     FATE IN SOIL, SURFACE WATER AND SEDIMENT
    
    If released onto the soil surface, the majority of 1,1-dichloroethene will quickly evaporate.  Depending on
    the hydrogeology of a site, some may leach into ground water. Based on its high water solubility and small
    KO,. value, 1,1-dichloroethene may migrate through soils by adsorbing to dissolved organic carbon (EPA
    1982). Studies have also documented that 1,1-dichloroethene will biodegrade in soils (HSDB 1997). A
    bioaccumulation factor  for 1,1-dichloroethene in soil was not reported. However,  based on its volatility
    and polarity, 1,1-dichloroethene is not expected to significantly bioaccumulate in soil (Callahan et al.
    1979).
    
    Evaporation is the major fate of 1,1-dichloroethene in surface water, with a short half-life of 1-6 days.
    Only a small quantity of 1,1-dichloroethene will be lost by adsorption onto the sediment (HSDB 1997).
    1,1-dichloroethene also  quickly biodegrades in aqueous environments. Degradation studies showed that
    45-78% was lost in 7 days, when incubated with a wastewater inoculum. A large amount was also lost
    due to volatilization (Patterson and Kodukala 1981). In anaerobic environments, 1,1-dichloroethene
    U.S. EPA Region 6                                                               U.S. EPA
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    Protocol for Screening Level Ecological Risk Assessment
    Toxicological Profile H-15;  Dichloroethene. 1,1-	August 1999
    degrades (through reductive dechlorination) to vinyl chloride. Anaerobic degredation is slower that aerobic
    degradation. Approximately 50-80% of 1,1-dichloroethene underwent degradation in 6 months in a
    simulated groundwater environment (Barrio-Lage et al. 1986;  Hallenetal. 1986). Photo-oxidation and
    hydrolysis are not expected to be significant removal processes for 1,1-dichloroethene (Callahan et al.
    1979; Mabey et al. 1981; Cline and Delfino 1987). A bioaccumulation factor for 1,1-dichloroethene in
    water and sediment was not reported. However, based on its volatility and polarity, 1,1-dichloroethene is
    not expected to significantly bioaccumulate in water or sediment (Callahan et al.  1979).
    
    3.0     FATE IN ECOLOGICAL RECEPTORS
    
    Aquatic receptors may be directly exposed to dissolved 1,1-dichloroethene through gill respiration or
    through ingestion of suspended particles. Because  1,1-dichloroethene generally is not persistent in surface
    water, exposures are expected to be of short duration.  1,1-dichloroethene is not expected to bioconcenrrate
    in fish or aquatic invertebrates, based on its low log K,^ value (Tute 1971; HSDB 1997). Due to limited
    bioconcentration,  1,1-dichloroethene is not expected to biomagnifiy in terrestrial or aquatic food chains
    (Barrio-Lage et al. 1986; Wilson et al. 1986).
    
    1,1-dichloroethene is readily absorbed following inhalation (Dallas et al. 1983; McKenna et al. 1978a) or
    oral exposure, and is rapidly distributed in the body. Following inhalation exposure to 1,1-dichloroethene,
    uptake is dependent upon the duration of the exposure and the dose. Until equilibrium is reached, as
    exposure concentration increases, the percentage of 1,1-dichloroethene uptake decreases.  Studies show that
    2 minutes after inhalation exposure, substantial amounts of 1,1-dichloroethene were found in the venous
    blood of rats. Concentrations of 150 ppm or less of 1,1-dichloroethene showed a linear cumulative uptake.
    However, at 300 ppm steady state was not achieved, indicating saturation at high concentrations (Dallas et
    al. 1983).
    
     Following oral administration of 1,1-dichloroethene in corn oil, rapid and almost  complete absorption from
    the gastrointestinal tract of rats and mice was observed (Jones and Hathway 1978a; Putcha et al. 1986).
    Recovery of radio-labeled 1,1-dichloroethene was 43.55, 53.88, and 42.11%, 72  hours following oral
    administrations of 0.5, 5.0, and 50 rag/kg, respectively, to rats (Reichert et al. 1979). Also, 14.9-22.6%
    1,1 dichloroethene was recovered in expired air, 42.11-53.88% in urine, 7.65-15.74% in feces, 2.77-5.57%
    in the carcass, and 5.91-9.8% in the cage rinse (Reichert et al. 1979).
    U.S. EPA Region 6                                                               U.S. EPA
    Multimedia Planning and Permitting Division                                           Office of Solid Waste
    Center for Combustion Science and Engineering                                                        H-48
    

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    Protocol for Screening Level Ecological Risk Assessment
    lexicological Profile H-15: Dichloroethene, 1,1-	August 1999
    1,1-dichloroethene is distributed mainly to the liver and kidneys following inhalation or oral exposure.  In
    rodents, the highest levels of 1,1-dichloroethene are found in the liver and kidneys. Rats that were fasted
    and exposed to 1,1-dichloroethene showed significantly greater tissue burden than nonfasted rats (McKenna
    et al. 1978b; Jones and Hathway 1978b).
    
    1,1-dichloroethene does not appear to be stored or accumulated in tissues, but is metabolized by the hepatic
    microsomal cytochrome P-450 system  This reaction produces reactive intermediates responsible for the
    toxicity of 1,1-dichloroethene. These reactive intermediates are detoxified through hydroxylation or
    conjugation with GSH, which is the primary biotransformation pathway in the rat.   Excretion of
    unmetabolized 1,1-dichloroethene is through exhaled air, and metabolites are excreted via urine and exhaled
    air (Fielder et al. 1985; ATSDR 1994).
    
    Avian receptors may be directly exposed to  1,1-dichloroethene through the ingestion of surface water and
    soil.  Absorption studies specific to avian species were not identified in the literature.
    
    Data on the fate of 1,1-dichloroethene in plant receptors were not identified in the literature.  However,
    based on the low probability of significant bioaccumulation, uptake by plant receptors is expected to be
    minimal.
    
    4.0    REFERENCES
    
    ATSDR. 1994.  Toxicological Profile for 1,1-Dichloroethene. Agency for Toxic Substances and Disease
           Registry.
    Barrio-Lage G, Parsons F, Nassar R, Lorenzo P. 1986. "Sequential Dehalogenation of Chlorinated
           Ethenes." Environ Sci Technol 20:96-99.
    Callahan M, Slimak M, Gabel N,  et al.  1979.  Water-Related Environmental Fate of 129 Priority
           Pollutants.  Vol2. EPA-440/4-79-029b. USEPA, Washington, DC. pp. 50-1 to 50-10.
    Cline P, Delfino J.  1987.  Am Chem  Soc Div Environ Chem preprint.  New Orleans, LA. 27:577-579.
           As cited in HSDB 1997.
    Dallas C, Weir R, Feldman S, et al.  1983.  "The Uptake and Disposition of 1,1-dichloroethene in Rats
           During Inhalation Exposure." Toxicol Appl Pharmacol 68:140-151.
    U.S. EPA Region 6                                                               U.S. EPA
    Multimedia Planning and Permitting Division                                           Office of Solid Waste
    Center for Combustion Science and Engineering                                                        H-49
    

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    Protocol for Screening Level Ecological Risk Assessment
    lexicological Profile H-15;  Dichloroethene, 1,1-	August 1999
    
    EPA. 1982. Aquatic Fate Process Data for Organic Priority Pollutants. Washington, DC: US
           Environmental Protection Agency. Code of Federal Regulations 40 CFR 61.65.
    
    Fielder R, Dale E, Williams S.  1985.  Toxicity Review 13: Vinylidene Chloride. Her Majesty's
           Stationary Office, London, England. As cited in ATSDR 1994.
    
    Hallen R, et al. 1986. "Am Chem Soc Div Environ Chem, 26th Natl Mtg." 26:344-346. As cited in
           HSDB 1997.
    
    HSDB 1997.  Hazardous Substance Data Base. June 1997.
    
    Jones B, Hathway D. 1978a.  "Differences in Metabolism of Vinylidene Chloride Between Mice and
           Rats." Br J Cancer 37:411-417.
    
    Jones B, Hathway D. 1978b.  "The Biological Fate of Vinylidene Chloride in Rats." Chem-Biol Interact
           20:27-41.
    
    Mabey W, Smith J, Podoll R, et al.  1981. Aquatic Fate Process Data for Organic Priority Pollutants.
           EPA 440/4-81-014. EPA Office of Water Regulations and Standards, Washington, DC.
    
    McKenna M, Zempel J, Madrid E,  et al.  1978a. "Metabolism and Pharmacokinetic Profile of Vinylidene
           Chloride in Rats Following Oral Administration." Toxicol Appl Pharmacol 45:821-835.
    
    McKenna M, Zempel J, Madrid E,  et al.  1978b. "The Pharmacokinetics of [14c]vinylidene Chloride in
           Rats Following Inhalation Exposure."  Toxicol Appl Pharmacol 45:599-610.
    
    Patterson J, Kodukala P.  1981.  "Biodegradation of Hazardous Organic Pollutants." Chem Eng Prog
           77:48-55.
    
    Putcha L, Bruchner J, D'Soyza R, et al.  1986.  "Toxicokinetics and Bioavailability of Oral and
           Intravenous 1,1-dichloroethene."  Fundam Appl Toxicol 6:240-250.
    
    Reichert D, Werner H, Metzler M, et al.  1979.  "Molecular Mechanism of 1,1-dichloroethene Toxicity:
           Excreted Metabolites Reveal Different Pathways of Reactive Intermediates." Arch Toxicol
           42:159-169.
    
    Tute M.  1971. Adv Drug Res 6:1-77. As cited in HSDB 1997.
    
    Wilson B, Smith  G, ReesJ. 1986. "Biotransformations of Selected Alkylbenzenes and Halogenated
           Aliphatic Hydrocarbons in Methanogenic Acquifer Material; a Microcosm Study."  Environ Sci
           Technol 20:997-1002.
    U.S. EPA Region 6                                                             U.S. EPA
    Multimedia Planning and Permitting Division                                          Office of Solid Waste
    Center for Combustion Science and Engineering                                                      H-50
    

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    Protocol for Screening Level Ecological Risk Assessment
    Toxicological Profile H-16;  Dim'trotohienes	August 1999
                                          DINITROTOLUENES
    1.0     SUMMARY
    
    2,4-dinitrotoluene and 2,6-dinitrotoluene are semi-volatile, nitrogen-substituted, organic compounds. They
    are moderately persistent in soil and have short half-lives in aqueous environments due to high rates of
    photolysis. Evidence also indicates that they are biodegraded in soil, surface waters and sediment. For
    wildlife, all routes of exposure are significant. Dinitrotoluenes are not expected to bioconcentrate in
    aquatic organisms and bioaccumulation is not expected in animal tissues. The major target organs
    following exposure to 2,4-dinitrotoluene are the liver and kidney.  2,6-dinitrotoluene is distributed to
    various organs following uptake.  Evidence indicates that upper-trophic-level receptors rapidly metabolize
    2,4-dinitrotoluene to innocuous by-products that are readily excreted. 2-6-dinitrotoluene is metabolized to
    a highly electrophilic ion that is capable of reacting with DNA and other biological nucleophiles.
    
    The following summarizes the fate of 2,4-dinitrotoluene and 2,6-dinitrotoluene in soil, surface water and
    sediment; and the fate after uptake by ecological receptors. Section 2 discusses the environmental fate and
    transport in soil, water and sediment.  Section 3 discusses the fate in ecological receptors.
    
    2.0     FATE IN SOIL, SURFACE WATER, AND SEDIMENT
    
    2,4-dinitrotoluene is expected to be slightly mobile in soil, based on its estimated K^. value (Lyman et al
    1982; Kenaga 1980).  Information on the biodegradation of 2,4-dinitrotoluene in soil was not located;
    however, biodegradation is thought to occur in both aerobic and anaerobic zones of soil, based on aqueous
    biodegradation experiments (HSDB 1997).
    
    2,6-dinitrotoluene readily biodegrades when released into the soil. Half-lives of 73 and 92 days were
    reported, when tested in two soils, with degradation rates of 0.5 to 0.7 mg/kg/day reported (Loehr 1989).
    Based on the calculated K^. value (Lyman et al. 1982) and the estimated log K^ value (GEMS 1984), 2,6-
    dinitrotoluene is expected to be slightly mobile in soil (Kenaga 1980).
    U.S. EPA Region 6                                                               U.S. EPA
    Multimedia Planning and Permitting Division                                           Office of Solid Waste
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    Toxicological Profile H-16; Dinitrotoluenes	August 1999
    Volatilization of dinitrotoluenes from surface soil is expected to be negligible due to very low vapor
    pressures of these compounds (Banerjee et al. 1990). Hydrolysis is not a significant removal process for
    nitroaromatic hydrocarbons (Lyman et al. 1982).
    
    2,4-dinitrotoluene and 2,6-dinitrotoluene have a slight tendency to sorb to sediments, suspended solids, and
    biota, based on measured log K,,w values (GEMS 1984).  In surface water, photolysis is the primary
    removal process for 2,4-dinitrotoluene and 2,6-dinitrotoluene. Reported half-lives range from a few
    minutes to a few hours (Spanggord et al. 1980; Zepp et al.  1984). Hydrolysis is not a removal process for
    nitroaromatics (Lyman et al.  1982).
    
    Dinitrotoluenes do not readily volatilize in surface water. Volatilization half-lives of 2-4 dinitrotoluene
    from distilled water were 248 and 133 hours, which correspond to the volatilization rate constants of
    0.0028 and 0.0052/hour (Smith et al. 1981). Davis et al. (1981), reported a 0.3 percent loss of 2,6-
    dinitrotoluene in a model waste stabilization pond.  Empirical evidence indicates that dinitrotoluenes are
    expected to biodegrade in surface waters (Uchimura and Kido 1987; Umeda et al. 1985; Kondo et al. 1988;
    Tabaketal. 1981).
    
    3.0     FATE IN ECOLOGICAL RECEPTORS
    
    Aquatic organisms take up 2,4-dinitrotoluene, however, it does not bioconcentrate because it is readily
    eliminated. Measured BCF values for dinitrotoluenes are low indicating that bioconcentration does not
    occur in aquatic organisms (Deneer et al. 1987; EPA 1980).
    
    Evidence indicates that once it is ingested by wildlife, 2,4-dinitrotoluene is rapidly absorbed into the
    bloodstream (Rickert et al. 1983). 2,4-dinitrotoluene is quickly distributed, with the highest concentrations
    in the liver and kidney (Rickert and Long 1981).  The metabolism of 2,4-dinitrotoluene occurs in the liver
    and the intestine (via intestinal microflora), and it is quickly eliminated through the urine and feces (Lee et
    al. 1978; Long and Rickert 1982; Rickert and Long 1981;  Schut et al. 1983). Based on the low log P value
    for 2,4-dinitrotoluene, bioaccumulation in animal tissues is not expected (Callahan et al. 1979; Mabey et
    al. 1981).
    U.S. EPA Region 6                                                                U.S. EPA
    Multimedia Planning and Permitting Division                                            Office of Solid Waste
    Center for Combustion Science and Engineering                                                         H-52
    

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    Protocol for Screening Level Ecological Risk Assessment
    Toxicological Profile H-16:  Dinitrotoluenes	August 1999
    
    Dinitrotoluenes are expected to be readily taken up by plants, based on structural analogies with
    1,3-dinitrobenzene and p-nitrotoluene (McFarlane et al. 1987; Nolt 1988).
    
    
    4.0    REFERENCES
    ATSDR. 1989. Toxicological Profile for 2,4-Dinitrotoluene, 2,6-Dinitrotoluene. Agency for
           Toxicological Substances and Disease Registry.
    
    Banerjee S, et al.  1990.  Chemosphere 21:1173-1180. As cited in HSDB 1997.
    
    Callahan M, Slimak M, Gabel N, et al.  1979. Water-Related Environmental Fate of 129 Priority
           Pollutants.  Vol2. EPA-440/4-79-029b. USEPA, Washington, DC..  PP. 81-1 TO 82-8.
    
    Davis E, etal.  1981. Water Res 15:1125-1127. As cited in HSDB 1997.
    
    Deneer J, et al. 1987. Aquatic Toxicol 10:115-129. As cited in HSDB 1997.
    
    EPA. 1980. Ambient Water Quality Criteria for Dinitrotoluene. EPA 440/5-80-045. Office of Water
           Regulations and Standards, Washington, DC.  P. C-6.
    
    GEMS. 1984. Graphical Exposure Modeling System. CLOGP3.  Office of Toxic Substances. As cited
           in HSDB 1997.
    
    HSDB.  1997.  Hazardous Substances Data Bank.
    
    Kenaga E.  1980. "Predicted bioconcentration factors and soil sorption coefficients of pesticides and other
           chemicals." Ecotoxicol Environ Safety 4:26-38. As cited in HSDB 1997.
    
    KondoM, etal. 1988. EiseiKagaku 34:115-122.  As cited in HSDB 1997.
    
    Lee C, Ellis H, Kowalski J, et al.  1978. Mammalian Toxicity of Munitions Compounds. Phase II.
           Effects of Multiple Doses.  Part II: 2,4-Dinitrotoluene. DAMD  17-74-C-4073.  Midwest
           Research Institute, Kansas City, MO.  As cited in ATSDR 1989.
    
    LoehrR. 1989. Treatability Potential for EPA Listed Hazardous Wastes in Soil. EPA 600/2-89-011.
           Robert S. Kerr Environ Res Lab, Ada, OK. As cited in HSDB 1997.
    
    Long L, Rickert D.  1982. "Metabolism and Excretion of 2,6-dinitro-[14c]toluene in Vivo and in Isolated
           Perfused Rat Livers."  Drug Metab Dispos 10:455-458. As cited in ATSDR 1989.
    
    Lyman W, Reehl W, Rosenblatt D, eds. 1982. Handbook of Chemical Property Estimation Methods.
           McGraw-Hill, New York.
    
    Mabey W, Smith J, Podoll R, et al. 1982. Aquatic Fate Process Data for Organic Priority Pollutants.
           EPA 440/4-81-014.  EPA Office of Water Regulations and Standards,  Washington, DC.
    
    U.S. EPA Region 6                                                             U.S. EPA
    Multimedia Planning and Permitting Division                                          Office of Solid Waste
    Center for Combustion Science and Engineering                                                      H-53
    

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    Protocol for Screening Level Ecological Risk Assessment
    Toxicological Profile H-16;  Dinitrotoluenes	August 1999
    
    McFarlane C, Nolt C, Wickliff C, et al.  1987. "The uptake, distribution and metabolism of four organic
           chemicals by soybean plants and barley roots." Environ Toxicol Chem 6:874-856. As cited in
           ATSDR 1989.
    
    Nolt C.  1988. Uptake and Translocation of Six Organic Chemicals in a Newly-Designed Plant Exposure
           System and Evaluation of Plant Uptake Aspects of the Prebiologic Screen for Ecotoxicologic
           Effects.  Master's Thesis. Cornell Univ., Ithaca, NY.  As cited in ATSDR 1989.
    
    Rickert D, Long R.  1981. "Metabolism and excretion of 2,4-dinitrotoluene in male and female
           Fischer-344 rats after different doses." Drug Metab Dispos 9(3):226-232.  As cited in ATSDR
           1989.
    
    Rickert D, Schnell S, Long R.  1983. "Hepatic macromolecular covalent binding and intestinal disposition
           of 2,4-(14C)dinitrotoluene." J Toxicol Environ Health 11:555-568.  As cited in ATSDR 1989.
    
    Schut H, et al. 1983. J Toxicol Environ Health 12(4-6):659-670. As cited in ATSDR 1989.
    
    Smith J, et al. 1981. Chemosphere 10:281-289. As cited in HSDB 1997.
    
    Spanggord R, et al.  1980. Environmental Fate Studies on Certain Munitions Wastewater Constituents.
           NTIS AD A099256.
    
    Tabak H, Quave S, Mashni C, et al. 1981. "Biodegradability studies with organic priority pollutant
           compounds." J Water Pollut Cont Fed 53:1503-1518..
    
    Uchimura Y, Kido K. 1987. KogaitoTaisaku23:1379-1384. As cited in HSDB 1997.
    
    Umeda H, et al.  1985. Hyogo-Ken Kogai Kenkysho Kenkyu Hokoku 17:76-82.
    
    ZeppR, etal. 1984. "Dynamics of pollutant photoreactions in the hydrosphere."  Fresenius Z Anal Chem
           319:119-125.
    U.S. EPA Region 6                                                            U.S. EPA
    Multimedia Planning and Permitting Division                                         Office of Solid Waste
    Center for Combustion Science and Engineering                                                      H-54
    

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    Protocol for Screening Level Ecological Risk Assessment
    Toxicological Profile H-17:  Di(N)octylphthalate	August 1999
                                      DI(N)OCTYLPHTHALATE
    1.0     SUMMARY
    
    Di(n)octylphthalate (DOP) is a high-molecular-weight, semi-volatile compound. It has a low water
    solubility and low vapor pressure, therefore it adsorbs strongly to the soil and sediment.  Biodegradation is
    possible under aerobic conditions, but is slow under anaerobic conditions.  DOP also undergoes hydrolysis
    in water. DOP may be absorbed following oral (dietary), inhalation, or dermal exposures, however dietary
    exposure is the most significant route of exposure. DOP may accumulate to increasing concentrations in
    algae, aquatic invertebrates, and fish, and accumulate to low levels in terrestrial wildlife.  However, higher-
    trophic-level receptors will quickly metabolize it, therefore it does not biomagnify in food chains.
    
    The following is a profile of the fate of DOP in soil, surface water and sediment; and the fate after uptake
    by ecological receptors. Section 2 discusses the environmental fate and transport in soil, water and
    sediment.  Section 3 discusses the fate in ecological receptors.
    
    2.0     FATE IN SOIL, SURFACE WATER AND SEDIMENT
    
    DOP has a very high K^ value; therefore, it should adsorb strongly and remain immobile in soil (Wolf et
    al. 1980).  Degradation in soil is slow, especially under anaerobic conditions (HSDB 1997).
    
    Following release into aquatic environments, DOP adsorbs strongly to sediments and particulate material
    suspended in the water column (HSDB 1997). DOP has a moderate half-life in aquatic environments;
    losses are due to both volatilization and microbial degradation.  Slow degradation is possible in aerobic
    conditions; however, DOP is resistant to anaerobic degradation (HSDB 1997).  Approximately 50%
    degradation was observed within 5 days  in a model terrestrial-aquatic ecosystem, with the monoester and
    phthalic acids the primary degradation products (Sanborn et al. 1975). DOP may bioconcentrate in aquatic
    organisms (Sanborn et al.  1975).                       •
    U.S. EPA Region 6                                                               U.S. EPA
    Multimedia Planning and Permitting Division                                           Office of Solid Waste
    Center for Combustion Science and Engineering                                                       H-55
    

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    Protocol for Screening Level Ecological Risk Assessment
    Toxicological Profile H-17;  Di(N)octylphthalate	August 1999
    
    3.0    FATE IN ECOLOGICAL RECEPTORS
    Sanborn et al. (1975) evaluated the bioconcentration and trophic transfer of DOP in model aquatic
    ecosystems containing phytoplankton, zooplankton, snails, insects, and fish. Evidence showed that the
    algae and invertebrates bioconcentrated DOP. Fish accumulated DOP to low levels, indicating that these
    receptors readily eliminate DOP.
    
    
    DOP may be absorbed following oral, inhalation or dermal exposures (EPA 1980a); however, due to low
    volatility of DOP, inhalation is not a significant route of exposure (Meditext 1997). Following absorption,
    DOP is rapidly distributed with the highest amounts concentrated in the liver, kidney and bile (EPA
    1980b). DOP is rapidly metabolized to water-soluble derivatives (Gosselin et al. 1984) prior to and after
    absorption (EPA 1980b). These metabolites are then excreted through the urine and the bile (Dceda et al.
    1978).
    
    No information was available on the fate of DOP in birds or plants.
    
    
    4.0    REFERENCES
    EPA 1980a. Ambient Water Quality Criteria Document for Phthalate Esters. EPA 440/5-80-067.
           Office of Water Regulations and Standards, Washington, DC.  pp. B-8; C-12.  As cited in HSDB
           1997.
    
    EPA. 1980b. Atlas Document for Phthalate Esters.  EPA/ECAO. XI-2; XI-5; XI-21. As cited in HSDB
           1997.
    
    Gosselin R, Smith R, Hodge H.  1984.  Clinical Toxicology of Commercial Products.  Vol H.  5th ed.
           Williams and Wilkins, Baltimore, MD. p. 204. As cited in ATSDR 1993, Meditext 1997, and
           ATSDR 1993.
    
    HSDB.  1997. Hazardous Substances Data Bank.
    
    Ikeda G, Sapienza P, Couviffion J, Farber T, Smith C, Inskeep P, Marks E, Cerra F, van Loon E.  1978.
           "Distribution and excretion of two phthalate esters  in rats, dogs and miniature pigs." Fd Cosmet
           Toxicol 16:409-413. As cited in HSDB 1997.
    
    Meditext.  1997. Medical Management Data Base.
    U.S. EPA Region 6                                                             U.S. EPA
    Multimedia Planning and Permitting Division                                          Office of Solid Waste
    Center for Combustion Science and Engineering                                                      H-56
    

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    Protocol for Screening Level Ecological Risk Assessment
    Toxicological Profile H-17;  Di(N)octylphthalate	August 1999
    
    Sanborn J, Metcalf R, Yu C-C, Lu P-Y.  1975.  "Plasticizers in the environment: The fate of di-n-octyl
            phthalate (DOP) in two model ecosystems and uptake and metabolism of DOP by aquatic
            organisms." Arch Environ Contain Toxicol 3:244-255.
    Wolfe N, Burns L, Steen W.  1980.  "Use of linear free energy relationships and an evaluative model to
            assess the fate and transport of phthalate esters in the aquatic environment." Chemosphere
            9:393-02.
    U.S. EPA Region 6                                                              U.S. EPA
    Multimedia Planning and Permitting Division                                          Office of Solid Waste
    Center for Combustion Science and Engineering                                                       H-57
    

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    Protocol for Screening Level Ecological Risk Assessment
    Toxicological Profile H-18;  Dioxane. 1,4-	August 1999
                                            DIOXANE, 1,4-
    1.0    SUMMARY
    
    1,4-dioxane is a highly water-soluble, moderately volatile organic compound. In soil, surface water, and
    sediment environments, 1,4-dioxane is not persistent because it is volatile and because it has a low affinity
    for adsorption to organic carbon.  It has a low potential to bioconcentrate in aquatic receptors. Wildlife
    can be exposed to 1,4-dioxane through ingestion, inhalation, and dermal contact. It does not bioaccumulate
    in food chains.
    
    The following is a profile of the fate of 1,4-dioxane in soil, surface water and sediment; and the fate after
    uptake by ecological receptors. Section 2 discusses the environmental fate and transport in soil, water and
    sediment. Section 3 discusses the fate in ecological receptors.
    
    2.0    FATE IN SOIL, SURFACE WATER AND SEDIMENT
    
    Based on an estimated log K^ value (Lyman et al. 1982), 1,4-dioxane is expected to have a low affinity for
    organic carbon in soil, thus having a high potential to leach out of surface soils (HSDB 1997). This
    reduces the exposure potential for vegetation (through root uptake) and soil invertebrates.   In addition,
    because of its moderate vapor pressure, volatilization is expected to be a significant fate process in soil
    (Verschueren 1983). Based on the volatility of 1,4-dioxane, biaccumulation is not considered to be a
    significant fate process in soil.
    
    1,4-dioxane is infinitely soluble in water (Lange 1967). However, because 1,4-dioxane has a moderate
    vapor pressure at 25 °C, volatilazation from water is a significant removal process (Verschueren 1983;
    HSDB 1997). 1,4-dioxane is not expected to adsorb to suspended sediments or detritus due to the
    estimated K^ value (HSDB 1997).  Based on its high volatility in water and low absorption to sediments,
    bioaccumulation is not expected to be a significant fate process for 1,4-dioxane in water and sediment.
    
    3.0    FATE IN ECOLOGICAL RECEPTORS
    Because it is highly soluble in water, aquatic receptors can take up 1,4-dioxane through direct exposure,
    however, it is not expected to bioconcentrate based on its low KOW value (Hansch and Leo 1985).
    U.S. EPA Region 6                                                               U.S. EPA
    Multimedia Planning and Permitting Division                                           Office of Solid Waste
    Center for Combustion Science and Engineering                                                       H-58
    

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    Protocol for Screening Level Ecological Risk Assessment
    Toxicological Profile H-18; Dioxane, 1,4-	August 1999
    Information suggests that 1,4-dioxane has a low potential to be biodegraded in aerobic aquatic
    environments.  Biodegradation experiments with activated sludge showed a negligible biochemical oxygen
    demand for 1,4-dioxane, therefore, classifying 1,4-dioxane as relatively undegradable (Mills 1954;
    Alexander 1973; Heukelekian and Rand 1955; Fincher and Payne 1962; Lyman et al. 1982; Kawasaki
    1980).
    
    No information was available on the fate of 1,4-dioxane after uptake by aquatic receptors. However, its
    low bioconcentration factor suggests that 1,4-dioxane is readily eliminated after uptake (Hansch 1985).
    
    The metabolism of 1,4-dioxane in rats has been studied, and information indicates that at high daily doses,
    1,4-dioxane can induce its own metabolism.  There is an apparent threshold of toxic effects of 1,4-dioxane
    that coincides with saturation of the metabolic pathway for its detoxification (Young et al. 1978).
    1,4-dioxane is highly toxic via all routes of exposure (OHM/TADS 1997), and is readily absorbed through
    intact skin (Gosselin 1984). Once 1,4-dioxane enters the body, it is distributed throughout the tissues,
    including the liver, kidney, spleen, lung, colon, and skeletal muscle (Woo et al. 1977).  The excretion of
    1,4-dioxane is primarily through the urine, in which approximately 85% of excreted material is in the form
    of beta-hydroxyethoxyacetic acid, a metabolic byproduct. The remaining material is excreted as
    unchanged dioxane (Braun & Young 1977).
    
    Information was not available on the fate of 1,4-dioxane in birds or plants.
    
    4.0    REFERENCES
    Alexander M.  1973.  "Nonbiodegradable and Other Recalcitrant Molecules." Biotechnol Bioeng
            15:611-647.
    Braun W, Young J. 1977.  "Identification of B-hydroxyethoxyacetic Acid as the Major Urinary Metabolite
            of 1,4-dioxane in the Rat." Toxicol Appl Pharmacol 39:33-38.
    Fincher E, Payne W.  1962. "Bacterial Utilization of Ether Glycols." Appl Microbiol 10:542-547.
    Gosselin R, Smith R,  Hodge H. 1984.  Clinical Toxicology of Commercial Products.  5th ed. Vol E.
            Williams and Wilkins, Baltimore, MD.  p. 408.
    Hansch C, Leo A. 1985. Medchem Project Issue No. 26, Pomona College, Claremont, CA. As cited in
            ATSDR 1990.
    
    U.S. EPA Region 6                                                              U.S. EPA
    Multimedia Planning and Permitting Division                                           Office of Solid Waste
    Center for Combustion Science and Engineering                                                       H-59
    

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    Protocol for Screening Level Ecological Risk Assessment
    lexicological Profile H-18:  Dioxane, 1,4-	August 1999
    
    Heukelekian H, Rand M. 1955.  "Biochemical Oxygen Demand of Pure Organic Compounds."  J Water
           Pollut Contr Assoc 27:1040-1053.
    
    HSDB.  1997. Hazardous Substances Data Bank. June 1997.
    
    Kawasaki M.  1980. "Experiences with the Test Scheme under the Chemical Control Law of Japan: an
           Approach to Structure-activity Correlations." Ecotox Environ Safety 4:444-454.
    
    LangeN. 1967. Handbook of Chemistry.  10th ed. McGraw-Hill, New York. p. 523.
    
    LymanW, Reehl W, Rosenblatt D, eds.. 1982. Handbook of Chemical Property Estimation Methods.
           McGraw-Hill, New York.  pp. 7-4; 9-64.
    
    Mills E, Stack V. 1954. Proceedings 8th Ind Waste Conf Ext Ser. 83:492-517.
    
    OHM/TADS. 1997. Oil and Hazardous Materials/Technical Assistance Data System. June 1997.
    
    Verschueren K.  1983.  Handbook of Environmental Data on Organic Chemicals.  2nd ed. Van Nostrand
           Reinhold, New York. pp. 578-580.
    
    Woo Y-T, Argus M, Arcos J.  1977. "Tissue and Subcellular Distribution of 3h-dioxane in the Rat and
           Apparent Lack of Microsome-catalyzed Covalent Binding in the Target Tissue." Life Sci
           21(10):1447-1456.
    
    Young J, Braun w, Gehring P. 1978. "Dose-dependent Fate of 1,4-dioxane in Rats." J Toxicol Enivom
           Health 4(5-6):709-726.
    U.S. EPA Region 6                                                            U.S. EPA
    Multimedia Planning and Permitting Division                                         Office of Solid Waste
    Center for Combustion Science and Engineering                                                      H-60
    

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    Protocol for Screening Level Ecological Risk Assessment
    Toxicological Profile H-19;  Dibenzo-p-Dioxins	August 1999
                                        DIBENZO-p-DIOXINS
    1.0    SUMMARY
    Dibenzo-p-dioxins (dioxins) are a group of high molecular weight chlorinated compounds that are highly
    soluble in fatty tissues. The congener tetrachlorodibenzodioxin (TCDD) is commonly used as a surrogate
    for estimating the fate of dioxins in the environment and in ecological receptors. Dioxins have low water
    solubilities and adsorb strongly to organic carbon in sediment and soil. Dioxins bioaccumulate in aquatic
    organisms and wildlife, and biomagnify in food chains because of their affinity for lipids. Biomagnification
    of TCDD appears to be significant between fish and fish-eating birds, but not between fish and their food
    (other fish).
    
    The following is a profile of the fate of dioxins in soil, surface water, and sediment; and the fate after
    uptake by ecological receptors.  Section 2 discusses the environmental fate and transport in soil, water, and
    sediment. Section 3 discusses the fate in ecological receptors.
    
    2.0    FATE IN SOIL, SURFACE WATER, AND SEDIMENT
    
    TCDD adsorbs strongly to soils (HSDB 1997).  TCDD in soil may be susceptible to photodegradation.
    Volatilization from soil surfaces during warm months may be a major mechanism by which TCDD is
    removed from soil.  Various biological screening studies have demonstrated that TCDD is generally
    resistant to biodegradation.  The half-life of TCDD in surface soil varies from less than 1 year to 3 years.
    Half-lives in deeper soils may be as long as 12 years (EPA 1993).
    
    TCDD is very persistent in the aquatic environment, has a very low aqueous solubility, and is highly
    soluble in lipids. Aquatic sediments are an important reservoir for dioxins, and may be the ultimate
    environmental sink  for all global releases of TCDD (HSDB 1997).  TCDD may be removed from water
    through either photolysis or volatilization. The photolysis half-life at surface level has been estimated to
    range from 21 hours in summer to 118 hours in winter (HSDB 1997). These rates increase significantly
    with increasing water depths. Therefore, many bottom sediments may not be susceptible to significant
    photodegradation.  The volatilization half-life from the water column of an environmental pond has been
    estimated to be 46 days, and may be as high as 50 years if adjusted for the effects of sediment adsorption.
    U.S. EPA Region 6                                      ~~                       U.S. EPA
    Multimedia Planning and Permitting Division                                          Office of Solid Waste
    Center for Combustion Science and Engineering                                                        H-61
    

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    Protocol for Screening Level Ecological Risk Assessment
    Toxicological Profile H-19;  Dibeiizo-p-Dioxiiis	August 1999
    Various biological screening studies have demonstrated that TCDD is generally resistant to biodegradation.
    The persistent half-life of TCDD in lakes has been estimated to be in excess of 1.5 years (HSDB 1997).
    
    3.0    FATE IN ECOLOGICAL RECEPTORS
    
    Ecological exposures to TCDD can occur via ingestion of contaminated soils, water, and sediment, dermal
    exposure to soil and water, and to a much lesser extent via inhalation of airborne vapors and particulates.
    It should be noted that, unlike toxicokinetic and toxicodynamic studies where exposures are closely
    controlled, environmental exposure to dioxin occurs as a complex mixture of congeners, including TCDD.
    It is generally understood that persistent, lipophilic compounds accumulate in fish in proportion to the lipid
    content and age of each animal (Gutenmann et al. 1992).  Also, it has been demonstrated that the influence
    of biotransformation on bioaccumulation increases as a function of the K,,w of the compound (de Wolf et al.
    1992). The dependence of metabolic rate on TCDD dose and length of exposure is not well understood,
    but time-course studies of P-450 induction in rainbow trout by p-napthoflavone demonstrate that different
    toxicity responses can occur over time depending on the frequency and duration of exposure (Zhang et al.
    1990).
    
    Dioxins readily  bioconcentrate in aquatic organisms (Branson et al. 1985; Mehrle et al. 1988; Cook et al.
    1991; and Schmieder et al. 1992).  Evidence indicates that dioxins will distribute in fish tissues in
    proportion to the total lipid content of the tissues (Cook et al 1993). Dioxins are metabolized and
    eliminated very  slowly from fish (Kleeman et al.  1986a,b; Opperhuizen and Sijm 1990; Kuehl et al. 1987).
    
    Several studies in a wide range of mammalian and aquatic species indicate that TCDD is metabolized to
    more polar metabolites (Ramsey et al.  1979; Poiger and Schlatter 1979; Olson et al. 1980; Olson 1986;
    Poiger et al. 1982; Sijm et al. 1990; Kleeman et al. 1986a,b, 1988; Gasiewicz et al. 1983; Ramsey et al.
    1982). The metabolism of TCDD and related compounds is required for urinary and biliary elimination
    and plays an important role in regulating the rate of excretion of these compounds.
    
    Dioxins are transferred through food chains, biomagnifying in upper-trophic-level receptors, especially
    birds. Biomagnification of TCDD appears to be significant between fish and fish-eating birds but not
    between fish and their food (Carey et al. 1990).  The lack of apparent biomagnification between fish and
    their prey is probably due to the influence of biotransformation of TCDD by the fish. Limited data for the
    U.S. EPA Region 6                                                              U.S. EPA
    Multimedia Planning and Permitting Division                                          Office of Solid Waste
    Center for Combustion Science and Engineering                                                       H-62
    

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    Protocol for Screening Level Ecological Risk Assessment
    lexicological Profile H-19;  Dibenzo-jp-Dioxins	August 1999
    base of the Lake Ontario lake trout food chain indicates little or no biomagnification between zooplankton
    and forage fish (Whittle et al. 1992). BMFs based on fish consuming invertebrate species probably are
    close to 1.0 because of the TCDD biotransformation by forage fish.
    
    Oral absorption of dioxin related compounds in laboratory animals has been reported to be contingent on
    species, test compound, administered dose, and vehicle. Typical oral absorption values range from 50 to
    90 percent (EPA 1994). Because TCDD in the environment is likely to be adsorbed strongly to soil, the
    oral bioavailability of TCDD varies significantly from laboratory values.  Studies have shown that oral
    bioavailability of TCDD in soil is lower by as much as 50 percent as compared to oral bioavailability of
    TCDD administered in corn oil over a 500-fold dose range (EPA 1994). Moreover, oral bioavailability of
    TCDD may be significantly lower in different soil types, with values as low as 0.5 percent bioavailability
    reported (Umbreit et al. 1986 a,b).
    
    Dermal absorption of TCDD has been studied extensively in laboratory animals. Dermal absorption has
    been demonstrated to depend on applied dose, with lower relative absorption (percentage of administered
    dose) decreasing at higher doses (Brewster et al. 1989). Dermal absorption rates in laboratory rats ranged
    from 17 to 40 percent of administered dose (Brewster et al. 1989). Percent bioavailability of TCDD
    following dermal absorption is significantly lower than bioavailability following oral absorption by as
    much as 60 percent (Poiger and Schlatter 1980).  As with oral absorption of TCDD in soil, percent
    bioavailability following dermal exposure to TCDD in soil was significantly lower than percent
    bioavailability following an equivalent oral dose (approximately 1  percent of an administered dose) (Shu et
    al. 1988).
    
    Transpulmonary absorption of TCDD has been studied in laboratory animals following intratracheal
    instillation of the compound in various vehicles (Nessel et al. 1990, 1992).  Systemic effects characteristic
    of TCDD exposures, including hepatic microsomal cytochrome p-450 induction, were observed after
    inhalation exposures, indicating that transpulmonary absorption does occur and that inhalation may be an
    important route of TCDD exposure. Transpulmonary bioavailability was estimated at approximately 92
    percent of administered dose, very similar to that observed after oral exposures (Diliberto et al. 1992). It
    should be noted that in an environmental setting, inhalation exposures to TCDD in fly ash, dust and soil
    particulates may be associated with very different absorption and bioavailability patterns.
    U.S. EPA Region 6                                                                U.S. EPA
    Multimedia Planning and Permitting Division                                           Office of Solid Waste
    Center for Combustion Science and Engineering                                                        H-63
    

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    Protocol for Screening Level Ecological Risk Assessment
    Toxicological Profile H-19:  Dibenzo-p-Dioxins	August 1999
    
    Tissue distribution studies in laboratory rats and mice indicate that TCDD is distributed preferentially to
    adipose tissue and liver (EPA 1994). TCDD is distributed to other organs as well, but to a lesser extent.
    Also, tissue distribution of TCDD has been demonstrated to be time and dose-dependent, with increasing
    levels of TCDD distributing to adipose and liver associated with higher doses and increased latency period
    from time of dosage (EPA 1994).
    
    
    Plants will take up TCDD through root uptake from soil and through foliar uptake from air (EPA 1994).
    No other information was available on the fate of dioxins after uptake by plants.
    
    
    No information was available on the fate of dioxins in birds.
    
    
    4.0    REFERENCES
    Branson D, Takahashi I, Parker W, Blau G. 1985. "Bioconcentration of
           2,3,7,8-tetrachlorodibenzo-p-dioxin in rainbow trout." Environ Toxicol Chem 4:779-788.
    
    Brewster D, Banks Y, Clark A-M, Bimbaum L.  1989. "Comparative dermal absorption of
           2,3,7,8-tetrachlorodibenzo-p-dioxin and three polychlorinated dibenzofurans." Toxicol Appl
           Pharmacol 97:156-166.
    
    Carey A, Shifrin N, Cook P.  1990.  "Derivation of a Lake Ontario bioaccumulation factor for
           2,3,7,8-TCDD." In:  Lake Ontario TCDD bioaccumulation study, final report, Chapter 9.  EPA,
           Region E, New York. As cited in EPA 1993.
    
    Cook et al. 1991. As cited in EPA 1993. Interim Report on Data and Methods for Assessment of
           2,3,7,8-Tetracholorodibenzo-p-dioxin Risks to Aquatic Life and Associated Wildlife. EPA
           600/R-93/055. Office of Research and Development, Washington, DC.
    
    Cook P, Nichols J, Berini C, Libal J. 1993. Disposition of2,3,7,8-tetrachlorodibenzo-p-dioxin and
           co-planar chlorinated biphenyls in tissue of male lake trout following ingestion of food. EPA,
           Duluth, MN. As cited in EPA 1993.
    
    de Wolf W, de Bruijn J, Seinen W, Hermens J.  1992. "Influence of biotransformation on the relationship
           between bioconcentration factors and octanol-water partition coefficients."  Environ Sci Technol
           26:1197-1201.
    
    Diliberto J, Jackson J, Birnbaum L.  1992.  "Disposition and absorption of intratracheal, oral, and
           intravenous 3H-TCDD in male Fischer rats." Toxicologist 12:79.
    U.S. EPA Region 6                                                             U.S. EPA
    Multimedia Planning and Permitting Division                                          Office of Solid Waste
    Center for Combustion Science and Engineering                                                      H-64
    

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    Protocol for Screening Level Ecological Risk Assessment
    Toxicological Profile H-19;  Dibenzo-/?-Dioxins	August 1999
    
    EPA. 1993. Interim report on data and methods for assessment of 2,3,7,8-tetrachlorodibenzo-p-dioxin
            risks to aquatic life and associated wildlife.  EPA 600/r-93/055.  Office of Research and
            Development, Washington, DC.
    
    EPA. 1994. Health Assessment Document for 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and related
            compounds. EPA/600/bp-92/001. Office of Research and Development, Washington, DC.
    
    Gasiewicz T, Olson J, Geiger L, Neal R.  1983. "Absorption, distribution and metabolism of
            2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in experimental animals." In: Tucker R, Young A,
            Gray A, eds. Human and Environmental Risks of Chlorinated Dioxins and Related Compounds.
            Plenum Press, New York pp. 495-525. As cited in EPA 1994.
    
    Gutenmann W, Ebel J, Kuntz H, Yourstone K, Lisk D.  1992. "Residues  of p,p'-DDE and mercury in lake
            trout as a function of age." Arch Environ Contam Toxicol 22:452-455.
    
    HSDB.  1997. Hazardous Substance Data Bank.
    
    Kleeman J, Olson J, Chen S, Peterson R.  1986a. "2,3,7,8-tetrachlorodibenzo-p-dioxin metabolism and
            disposition in yellow perch." Toxicol Appl Pharmacol 83:401-411.
    
    Kleeman J, Olson J, Chen S, Peterson R.  1986b. "Metabolism and disposition of
            2,3,7,8-tetrachlorodibenzo-p-dioxin in rainbow trout." Toxicol Appl Pharmacol 83:391-401.
    
    Kleeman J, Olson J, Peterson R.  1988. "Species differences in 2,3,7,8-tetrachlorodibenzo-p-dioxin
            toxicity and biotransformation in fish." Fundam Appl Toxicol 10:206-213.
    
    Kuehl D, Cook P, Batterman A, Lothenbach D, Butterworth B. 1987. "Bioavailability of polychlorinated
            dibenzo-p-dioxins and dibenzofurans from contaminated Wisconsin river sediment to carp."
            Chemosphere 16(4):667-679.
    
    Mehrle P, Buckler D, Little E, et al. 1988. "Toxicity and bioconcentration of
            2,3,7,8-tetrachlorodibenzodioxin and 2,3,7,8-tetrachlorodibenzofuran in rainbow trout." Environ
            Toxicol Chem 7:47-62.
    
    Nessel C, Amoruso M, Umbreit T, Gallo M. 1990.  "Hepatic aryl hydrocarbon hydroxylase and
            cytochrome P450  induction following the transpulmonary absorption of TCDD from
            intratracheally instilled particles."  Fundam Appl Toxicol 15:500-509.
    
    Nessel C, Amoruso M, Umbreit T, Meeker R, Gallo M. 1992.  "Pulmonary bioavailability and fine
            particle enrichment of 2,3,7,8-tetrachlorodibenzo-p-dioxin in respirable soil particles." Fundam
            Appl Toxicol 19:279-285.
    
    Olson J. 1986. "Metabolism and disposition of 2,3,7,8-tetrachlorodibenzo-p-dioxin in guinea pigs."
            Toxicol Appl Pharmacol 85:263-273.
    U.S. EPA Region 6                                                              U.S. EPA
    Multimedia Planning and Permitting Division                                          Office of Solid Waste
    Center for Combustion Science and Engineering                                                       H-65
    

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    Protocol for Screening Level Ecological Risk Assessment
    Toxicological Profile H-19:  Dibenzo-p-Dioxins	August 1999
    
    Olson J, Gasiewicz T, Neal R. 1980.  "Tissue distribution, excretion, and metabolism of
           2,3,7,8-tetrachlorodibenz o-p-dioxin (TCDD) in the golden Syrian hamster." Toxicol Appl
           Pharmacol 56:78-85.
    
    Opperhuizen A, Sijm D. 1990. "Bioaccumulation and biotransformation of polychlorinated
           dibenzo-p-dioxins and dibenzofurans in fish." Environ Toxicol Chem 9:175-186.
    
    Poiger H, Buser H-R, Weber H, Zweifel U, Schlatter C.  1982. "Structure elucidation of mammalian
           TCDD-metabolites." Experientia 38:484-486.
    
    Poiger H, Schlatter C.  1979. "Biological degradation of TCDD in rats." Nature 281:706-707.
    
    Poiger H, Schlatter C.  1980. "Influence of solvents and adsorbents on dermal and intestinal absorption of
           TCDD."  FDCosmet Toxicol 18:477-481.
    
    Ramsey J, Hefner J, Karbowski R, Braun W, Gehring P.  1979.  "The in vivo biotransformation of
           2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in the rat." Toxicol Appl Pharmacol 42:A162.
    
    Ramsey J, Hefner J, Karbowski R, Braun W, Gehring P.  1982.  "The in vivo biotransformation of
           2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in the rat." Toxicol Appl Pharmacol 65:180-194.
    
    Schmieder P, Lothenbach D, Johnson R, Erickson R, Tietge J. 1992.  "Uptake and elimination kinetics of
           3H-TCDD hi medaka." Toxicologist 12:138. As cited in EPA 1993.
    
    Shu H, Teitelbaum P, Webb A, et al.  1988.  "Bioavailability of soil-bound TCDD: Dermal bioavailability
           in the rat." Fund Appl Toxicol 10:335-343.
    
    Sijm D, Tarechewski A, Muir D, Webster G, Seinen W, Opperhuizen A. 1990.  "Biotransformation and
           tissue distribution of 1,2,3,7-tetrachlorodibenzo-p-dioxin, 1,2,3,4,7-pentachlorodibenzo-p-dioxin,
           2,3,4,7,8-pentachlorodibenzofuran in rainbow trout."  Chemosphere 21(7):845-866.
    
    Umbreit T, Hesse E, Gallo M. 1986a. "Bioavailability of dioxin in soil from a 2,4,5-T manufacturing
            site." Science 232:497-499.
    
    Umbreit T, Hesse E, Gallo M. 1986b. "Comparative toxicity of TCDD contaminated soil from Times
           Beach, Missouri, and Newark, New Jersey." Chemosphere 15:2121-2124.
    
    Whittle D, Sergent D, Huestis S, Hyatt W. 1992.  "Foodchain accumulation of PCDD and PCDF isomers
           in the Great Lakes aquatic community." Chemosphere 25:181-184.
    
    Zhang Y, Anderson T, Forlin L.  1990.  "Induction of hepatic xenobiotic biotransformation enzymes in
            rainbow trout by beta-napthoflavone." Tune-course studies. Comp Biochem Physiol
            956:247-253.
    U.S. EPA Region 6                                                             U.S. EPA
    Multimedia Planning and Permitting Division                                         Office of Solid Waste
    Center for Combustion Science and Engineering                                                      H-66
    

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    Protocol for Screening Level Ecological Risk Assessment
    Toxicological Profile H-20;  Dibenzofurans	August 1999
                                          DIBENZOFURANS
    1.0    SUMMARY
    
    Polychlorinated dibenzofurans (PCDF) are a class of hydrophobia chlorinated compounds that adsorb
    strongly to soils and sediments.  Like dioxins, PCDFs are persistent in the environment, bioconcentrate in
    aquatic organisms, and biomagnify in some food chains. Because PCDFs are associated with organic
    material in abiotic media, direct contact by soil and sediment receptors, and ingestion by bottom-feeding
    fish and upper trophic level wildlife, are the most important exposure routes.
    
    Since PCDFs are structurally similar to, and behave in the environment like dioxins, fate of PCDFs is
    inferred from information about dioxins. Most of the description on the fate of PCDFs is based on the
    behavior of tetrachlorodibenzofuran (TCDF), one of the most toxic PCDF congeners. The following is a
    profile of the fate of polychlorinated dibenzofurans (PCDFs) in soil, water, and sediment; and the fate after
    uptake by ecological receptors.  Section 2 discusses the environmental fate and transport in soil, surface
    water, and sediment. Section 3 discusses the fate in ecological receptors.
    
    2.0    FATE IN SOIL, SURFACE WATER, AND SEDIMENT
    
    TCDF adsorbs strongly to soils. Based upon its high K^ value, TCDF is expected to sorb very strongly in
    soil and not be susceptible to leaching under most soil conditions.  No data are available regarding the
    biological degradation of TCDF in soil (HSDB 1997).
    
    TCDF in the water column can be expected to partition strongly to sediment and suspended particulate
    matter. Volatilization from the water column can be important, however the significance of this fate
    process is limited by strong sorption to sediments (HSDB 1997).  Bioconcentration in aquatic organisms
    may be significant.  Aquatic hydrolysis is not expected to be important. Data on biodegradation of TCDF
    are unavailable (HSDB 1997).
    U.S. EPA Region 6                                                              U.S. EPA
    Multimedia Planning and Permitting Division                                          Office of Solid Waste
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    Protocol for Screening Level Ecological Risk Assessment
    Toxicological Profile H-20; Dibenzofurans	August 1999
    
    3.0    FATE IN ECOLOGICAL RECEPTORS
    Based on high Kow values, PCDFs are expected to accumulate in aquatic receptors (Gutenmann et al.
    1992).
    
    
    Based on its similar structure to dioxins, PCDFs are expected to accumulate to high concentrations in
    
    aquatic and semi-aquatic mammals and in fish-eating birds.
    
    
    Information was not available on the disposition of PCDFs in plants.
    
    
    4.0    REFERENCES
    Gutenmann W, Ebel J, Kuntz H, Yourstone K, Lisk D.  1992.  "Residues of p,p'-DDE and mercury in lake
           trout as a function of age."  Arch Environ Contain Toxicol 22:452-455.
    
    HSDB. 1997. Hazardous Substance Data Bank.
    U.S. EPA Region 6                                                           U.S. EPA
    Multimedia Planning and Permitting Division                                        Office of Solid Waste
    Center for Combustion Science and Engineering                                                     H-68
    

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    Protocol for Screening Level Ecological Risk Assessment
    Toxicological Profile H-21:  Hexachlorobenzene	August 1999
                                      HEXACHLOROBENZENE
    
    1.0    SUMMARY
    
    Hexachlorobenzene (HCB) is a persistent chemical that adsorbs strongly to soil and sediment. It is
    relatively stable in the environment and is resistant to hydrolysis, photolysis, and oxidation, with relatively
    no metabolism by microorganisms. Due to its high affinity for organic carbon, HCB will accumulate in
    sediments. Soil invertebrates and benthic invertebrates will take up HCB directly from these media. For
    higher-trophic-level receptors, indirect (food chain) exposure is anticipated to be the most significant
    pathway because HCB is resistant to metabolism and is very soluble in fat. The major toxic effect that has
    been observed across all species tested is porphyria.
    
    The following is a profile of the fate of HCB in soil, surface water and sediment; and the fate after uptake
    by ecological receptors. Section 2 discusses the environmental fate and transport in soil, water and
    sediment.  Section 3 discusses the fate in ecological receptors.
    
    2.0    FATE IN SOIL, SURFACE WATER, AND SEDIMENT
    
    Due to a long half-live in soil and its strong affinity for organic carbon, HCB released  to soil is likely to
    remain there for extended periods of time (Beck and Hansen 1974). Minimal biodegradation occurs,
    depending on the organic carbon content of the soil.  Some evaporation from surface soil to air may occur,
    again depending on the organic carbon content of the soil (Gile and Gillett 1979).
    
    Once released to water, HCB will either evaporate rapidly or adsorb to sediments, with very little dissolved
    in water (HSDB 1997; Kelly et al. 1991). Limited degradation of HCB is expected, since it appears to be
    stable to hydrolysis, photolysis, and oxidation (Callahan et al. 1979). Since HCB adsorbs strongly to
    sediments, it may build up in bottom sediments.
    
    3.0    FATE IN ECOLOGICAL RECEPTORS
    
    Aquatic organisms may be exposed to HCB through ingestion of contaminated water, soil, sediment, or
    food.  Empirical information indicates that HCB bioconcentrates in fish and invertebrates (Giam et al.
    U.S. EPA Region 6                                                              U.S. EPA
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    Protocol for Screening Level Ecological Risk Assessment
    lexicological Profile H-21;  Hexachlorobenzene	August 1999
    1980; Konemann and Vanleeuwen 1980; Veith et al. 1979; Oliver and Niimi 1983; Parrish et al. 1978;
    Kosian et al. 1978; Neely et al. 1974; Zitko and Hutzinger 1976; Laseter et al. 1976).
    
    HCB can be transferred through aquatic food chains. Knezovich and Harrison (1988) reported that
    chironomid larvae, a common food item of young fish and other aquatic receptors, rapidly bioaccumulate
    HCB and other chlorobenzenes from contaminated sediments, achieving steady state within 48 hours.
    Information was not available about metabolism of HCB by fish.
    
    Ingestion of contaminated media and food is the main route of mammalian exposure to HCB (HSDB 1997;
    ATSDR 1994; Edwards et al. 1991). Following ingestion, HCB is readily absorbed and is distributed
    through the lymphatic system to all tissues. It accumulates in fatty tissues and persists for many years
    since it is highly lipophilic and is very slowly metabolized (Weisenberg 1986; Mathews 1986).
    
    HCB is slowly metabolized by the hepatic cytochrome P-450 system, conjugated with glutathione, or
    reductively  dechlorinated (ATSDR 1994).  The metabolites of HCB in laboratory animals include
    pentachlorophenol, pentachlorobenzene, tetrachlorobenzene, traces of trichlorophenol, a number of sulfur
    containing compounds, and some unidentified compounds (Mehendale et al. 1975; Renner and Schuster
    1977, 1978; Renner et al.  1978; Edwards et al.  1991).
    
    Plants take  up relatively minimal amounts of HCB from soils (EPA 1985; Carey et al. 1979).
    Information was not available on the fate of HCB in birds.
    
    4.0    REFERENCES
    ATSDR. 1994. Toxicological Profile for Hexachlorobenzene.  Agency for Toxic Substances and Disease
           Registry.  August.
    Beck J, Hansen K. 1974.  The degradation of quintozene, pentachlorobenzene, hexachlorobenzene and
           pentachloranihne in soil. Pestic Sci 5:41-48. As cited in ATDSR 1994.
    Callahan M, Slimak M, Gabel N, et al.  1979. Water-Related Environmental Fate of 129 Priority
           Pollutants. EPA-440/4-79-029b.  Office of Water Planning and Standards, Washington, DC.
           p. 77-1 to 77-13.
    U.S. EPA Region 6                                                            U.S. EPA
    Multimedia Planning and Permitting Division                                         Office of Solid Waste
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    Protocol for Screening Level Ecological Risk Assessment
    Toxicological Profile H-21;  Hexachlorobenzene	August 1999
    
    Carey A, Gowen J, Tai H, Mitchell W, Wiersma G. 1979. Pesticide residue levels in soils and crops from
            37 states, 1972-National soils monitoring program (IV).  Pestic Monit J 12:209-229.
    
    Edwards I, Ferry D, Temple W.  1991. Fungicides and related compounds. In: Hayes W, laws E,eds.
            Handbook of Pesticide Toxicology. Vol 3. Classes of Pesticides.  Academic Press, New York.
            pp. 1409-1470.
    
    EPA. 1985. Environmental Profiles and Hazard Indices for Constituents of Municipal Sludge:
            Hexachlorobenzene. Office of Water Regulations and Standards, Washington, DC. June.
    
    Giam C, Murray HE, Lee ER, Kira S.  1980. Bioaccumulation of hexachlorobenzene in killifish (Fundulus
            similis).  Bull Environ Contam Toxicol 25:891-897.
    
    Gile J, Gillett J.  1979. Fate of selected fungicides in a terrestrial laboratory ecosystem. J Agric Food
            Chem27(6):l 159-1164.
    
    HSDB.  1997.  Hazardous Substance Data Bank.
    
    Kelly T, Czuczwa J, Sticksel P, Sverdrup G. 1991. Atmospheric and tributary inputs to toxic substances
            to Lake Erie. J Great Lakes Res 14(4):504-516.
    
    Knezovich P, Harrison F.  1988.  The bioavailability of sediment-sorbed chlorobenzenes to larvae of the
            midge, Chironomus decorus. Ecotoxicol Environ Saf 15(2):226-241.
    
    Konemann H, Van Leeuwen K.  1980.  Toxicokinetics in fish: Accumulation and elimination of six
            chlorobenzenes by guppies. Chemosphere 9:3-19.
    
    Kosian P, Lemke A, Studders K, Veith G.  1981. The precision of the ASTM bioconcentration test. EPA
            600/3-81-022.  Environmental Research Lab, Duluth, MN. As cited in HSDB 1997.
    
    Laseter J, et al.  1976.  Govt rept announce index.  NTIS PB-252671. 76:66. As cited in HSDB 1997.
    
    MathewsH.  1986. IARC Sci Publ 77:253-260. As cited in HSDB 1997.
    
    Mehendale H, Fields M, Matthews H.  1975. Metabolism and effects of hexachlorobenzene on hepatic
            microsomal enzymes in the rat. J Agric Food Chem 23:261-265.
    
    Neely W, Branson D, Blau G.  1974. Partition coefficient to measure bioconcentration potential of organic
            chemicals in fish.  Environ Sci Technol 8:1113-1115.
    
    Oliver B, Niimi A.  1983.  Bioconcentration of chlorobenzenes from water by rainbow trout: Correlations
            with partition coefficients and environmental residues. Environ Sci Technol 17:287-291.
    
    Parrish P, et al. 1978.  Chronic toxicity of chlordane, trifluralin, and pentachlorophenol to sheepshead
            minnows (cyprinodon variegatus). EPA-600/3-78-010. Environmental Research Laboratory,  pp.
            35-40.
    U.S. EPA Region 6                                                             U.S. EPA
    Multimedia Planning and Permitting Division                                         Office of Solid Waste
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    Toxicological Profile H-21;  Hexachlorobenzene	August 1999
    
    Renner G, Schuster K. 1977. 2,4,5-trichlorophenol, a new urinary metabolite of hexachlorobenzene.
           Toxicol Appl Pharmacol 39:355-356.
    
    Renner G, Richter E, Schuster K. 1978.  N-acetyl-s-(pentachlorophenyl)cysteine, a new urinary metabolite
           of hexachlorobenzene. Chemosphere 8:663-668.
    
    Renner G, Schuster K. 1978. Synthesis of hexachlorobenzene metabolites. Chemosphere 8:669-674.
    
    Veith G, Defoe D, Bergstedt B.  1979.  Measuring and estimating the bioconcentration factor of chemicals
           in fish. J Fish Res Board Can 36:1040-1048.
    
    WeisenbergE.  1986. Hexachlorobenzene in human milk: A polyhalogenated risk. lARCSciPubl
           77:193-200.
    
    Zitko V, Hutzinger D.  1976.  Bull Environ Contain Toxicol 16:665-673.
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    Multimedia Planning and Permitting Division                                          Office of Solid Waste
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    Protocol for Screening Level Ecological Risk Assessment
    Toxicological Profile H-22; Hexachlorobutadiene	August 1999
                                    HEXACHLOROBUTADIENE
    1.0    SUMMARY
    
    Hexachlorobutadiene (HCBD) is a moderately volatile, high molecular weight, chlorinated compound.  In
    surface soil and sediment, it will adsorb to organic carbon. It is moderately soluble in water.  In surface
    water, it will adsorb to suspended material; however, it has a tendency to volatilize. In aerobic
    environments, in will biodegrade.  Exposure routes for aquatic organisms include ingestion, gill uptake, and
    dermal contact. HCBD bioconcentrates in aquatic life. For mammalian and avian wildlife, HCBD can be
    taken up through oral, inhalation,  and dermal exposure routes. HCBD is not expected to bioaccumulate to
    high levels in upper-trophic-level receptors.  HCBD metabolites cause adverse effects.
    
    The following is a profile of the fate of HCBD in soil, surface water and sediment; and the fate after uptake
    by ecological receptors.  Section 2 discusses the environmental fate and transport in soil, water and
    sediment. Section 3 discusses the fate in ecological receptors.
    
    2.0    FATE IN SOIL, SURFACE WATER, AND SEDIMENT
    
    HCBD has a high soil partition coefficient, and would, therefore, be expected to adsorb to soils with a high
    organic content (Montgomery and Welkom 1990); however, in sandy soils with a low organic content,
    HCBD is more mobile and will be found in soil pore water (Piet and Zoeteman 1980).  HCBD also has a
    moderate potential to evaporate from surface soils, unless it is bound to organic carbon (Pearson and
    McConnel 1975). HCBD is expected to biodegrade in aerobic soils (Tabak et al. 1981), but not in
    anaerobic environments (Johnson and Young 1983).
    
    Following release into water, HCBD will either quickly volatilize or adsorb to sediments and suspended
    material (Montgomery and Welkom 1990). HCBD will accumulate concentrations in sediments (Elder et
    al. 1981; EPA 1976; Oliver and Charlton 1984). Biodegradation is a significant removal process for
    HCBD in aerobic environments (Tabak et al. 1981).  However, under anaerobic conditions biodegradation
    does not occur (Johnson and Young 1983).
    U.S. EPA Region 6                                                             U.S. EPA
    Multimedia Planning and Permitting Division                                          Office of Solid Waste
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    Protocol for Screening Level Ecological Risk Assessment
    Toxicological Profile H-22; Hexachlorobutadiene	August 1999
    3.0    FATE IN ECOLOGICAL RECEPTORS
    HCBD dissolved in surface water is expected to bioconcentrate in aquatic organisms, including algae,
    benthic macroinvertebrates (such as worms and bivalves), detritivore (crayfish), and plantivorous fish
    (EPA 1976, Oliver and Niimi 1983). HCBD also accumulates in carnivorous fish (EPA 1976). In fish,
    HCBD will distribute to fatty tissue, especially the liver (Pearson and McConnell 1975 as cited in ATSDR
    1994).
    
    Mammals may be exposed to HCBD through (1) ingestion of soil and exposed sediment while foraging for
    food, grooming,  and soil covering plant matter, (2) ingestion of drinking water, and (3) indirect ingestion of
    contaminated plant and animal matter.  Based on HCBD's affinity for soil and sediment, and its potential to
    be bioconcentrated, it is anticipated that indirect exposure will be the most significant exposure route for
    mammals. Once ingested, HCBD is readily absorbed in the gastrointestinal tract (Reichert et al. 1985).
    Following absorption, HCBD is distributed primarily to the kidney, liver, adipose tissue, and brain (Dekant
    et al. 1988; Nash et al. 1984; Reichert et al. 1985).
    
    HCBD does not  appear to be metabolized by the hepatic mixed function oxidase system; however, it does
    undergo conjugation with glutathione in the liver (Garle and Fry 1989).  Metabolic derivatives of these
    conjugates are believed to be responsible for the renal damage associated with exposure to HCBD (Dekant
    et al. 1991;.Koob and Dekant 1992).
    
    In gravid birds, low levels of HCBD will be transferred to eggs (Dow Chemical Co. 1972).
    
    Information was not available on the fate of HCBD in plants.
    
    4.0    REFERENCES
    ATSDR. 1994. Toxicological Profile for Hexachlorobutadiene. Agency for Toxic Substances and
           Disease Registry, Atlanta, GA.
    Dekant W, Schrenk D, Vamvakas S, et al. 1988. "Metabolism of hexachloro-l,3-butadiene in mice: in
           vivo and in vitro evidence for activation by glutathione conjugation."  Xenobiotica 18:803-816. As
           cited in ATSDR 1994.
    U.S. EPA Region 6                                                             U.S. EPA
    Multimedia Planning and Permitting Division                                         Office of Solid Waste
    Center for Combustion Science and Engineering                                                      H-74
    

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    Protocol for Screening Level Ecological Risk Assessment
    Toxicological Profile H-22;  Hexachlorobutadiene	August 1999
    
    Dekant W, Urban G, Gorsman C, et al. 1991. "Thioketene formation from haloalkenyl 2-nitrophenyl
           disulfides: models for biological reactive intermediates of cytotoxic S-conjugates." J Am Chem
           Soc 113:5120-5122.
    
    Dow Chemical Company. 1972. Analysis of Quail Eggs for Hexachlorobutadiene by Gas Liquid
           Chromatography.  EPA Document No. 878211372, Fiche No. OTS0206136.  As cited in HSDB
           1997.
    
    Elder V, Proctor B, Kites R. 1981.  "Organic compounds  found near dump sites in Niagara Falls, New
           York."  Environ Sci Technol 15:1237-1243.
    
    EPA. 1976. An Ecological Study of Hexachlorobutadiene (HCBD).  EPA/560/6-76-010. Office of
           Toxic Substances, Washington, DC.
    
    Garle M, Fry J. 1989.  "Detection of reactive metabolites  in vitro." Toxicology 54:101-110. As cited in
           ATSDR 1994.
    
    HSDB.  1997. Hazardous Substances  Data Base.
    
    Johnson L, Young J. 1983. "Inhibition of anaerobic digestion by organic priority pollutants." J Water
           Pollut Control Fed 55:1141-1149.
    
    Koob M, Dekant W. 1992. "Biotransformation of the hexachlorobutadiene metabolites
           l-(glutathione-S-yl)-pentachlorobutadiene and l-(cystein-S-yl)-pentachlorobutadiene in the isolated
           perfused rat liver." Xenobiotica 22:125-138. As cited in ATSDR 1994.
    
    Montgomery J, Welkom L. 1990. Groundwater Chemicals Desk Reference.  Lewis Publications,
           Chelsea, ML pp. 334-336.  As cited in ATSDR 1994.
    
    Nash J, King L, Lock E, et al.  1984. "The metabolism and disposition of hexachloro-l,3-butadiene in the
           rat and its relevance to nephrotoxicity."  Toxicol Appl Pharmacol 73:124-137. As cited in
           ATSDR 1994.
    
    Oliver B, Charlton M.  1984.  "Chlorinated organic contaminants on settling particulates in the Niagara
           River vicinity of Lake Ontario." Environ Sci Technol 18:903-908.
    
    Oliver B, Niimi A.  1983.  "Bioconcentration of chlorobenzenes from water by rainbow trout: Correlations
           with partition coefficients and environmental residues." Environ Sci Technol 17:287-291.
    
    Pearson C, McConnell G. 1975. "Chlorinated Cl and C2 hydrocarbons in the marine environment." Proc
           Royal Soc Lond Biol 189:305-332. As cited in HSDB 1997 and ATSDR 1994.
    
    Piet G, Zoeteman B. 1980. "Organic water quality changes during sand bank and dune filtration of
           surface waters in the Netherlands." J Am Water Works Assoc 72:400-404. As cited in ATSDR
           1994.
    U.S. EPA Region 6                                                             U.S. EPA
    Multimedia Planning and Permitting Division                                         Office of Solid Waste
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    Protocol for Screening Level Ecological Risk Assessment
    Toxicological Profile H-22;  Hexachlorobutadiene	August 1999
    
    Reichert D, Schutz S, Metzler M.  1985. "Excretion pattern and metabolism of hexachlorobutadiene in the
           rats: Evidence for metabolic activation by conjugation reactions." Biochem Pharmacol 34:499-
           505. As cited in ATSDR 1994.
    
    Tabak H, Quave S, Mashni C, et al.  1981.  "Biodegradability studies with organic priority pollutant
           compounds".  J Water Pollut Cont Fed 53:1503-1518.
    U.S. EPA Region 6                                                              U.S. EPA
    Multimedia Planning and Permitting Division                                          Office of Solid Waste
    Center for Combustion Science and Engineering                                                       H-76
    

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    Protocol for Screening Level Ecological Risk Assessment
    Toxicological Profile H-23; Hexachlorocyclopentadiene	August 1999
                                HEXACHLOROCYCLOPENTADIENE
    1.0     SUMMARY
    
    Hexachlorocyclopentadiene (HCCP) is a semi-volatile, chlorinated compound. If HCCP is released as an
    emission product, it has been shown to exist mostly in the vapor phase, with photolysis resulting in rapid
    degradation. HCCP in soil will adsorb to soil particles. Degradation of HCCP may also occur in the
    environment by chemical hydrolysis and biodegradation by soil biota.  Depending on the route of exposure,
    HCCP may distribute mainly to the lungs, kidneys, and liver. HCCP could potentially bioaccumulate in
    some aquatic organisms depending upon the species.  The respiratory system is the major site of toxicity
    following inhalation exposure, while, depending on the species, the kidney or the liver are the major sites of
    toxicity following oral exposure.
    
    The following is a profile of the fate of HCCP in soil, surface water and sediment, and the fate after uptake
    by ecological receptors. Section 2 discusses the environmental fate and transport in soil, water and
    sediment.  Section 3 discusses the fate in ecological receptors.
    
    2.0     FATE IN SOIL, SURFACE WATER, AND SEDIMENT
    
    HCCP deposited to soil is expected to adsorb strongly to organic carbon in the soil (HSDB 1997).
    Volatilization from soil surfaces is expected to be minor. In moist soil, hydrolysis and biodegradation
    under aerobic and anaerobic conditions may occur (HSDB 1997). HCCP on the surface of soil may be
    subject to photolysis.
    
    HCCP present in surface water will degrade primarily by photolysis and chemical hydrolysis. The half-life
    of HCCP from photodegradation is very short; Wolfe et al.(l 982) reported a half-life of less than 15
    minutes in the top of the water column. In unlit or deep, turbid water, the degradation of HCCP occurs by
    chemical hydrolysis.  Hydrolytic half-lives for HCCP range from several hours to 2-3 weeks, depending on
    the temperature of the water (Chou et al. 1981; Zepp and Wolfe 1987). HCCP has the potential to adsorb
    to suspended solids in surface water and sediments; however, this adsorption does not affect the rate of
    hydrolysis (Wolfe et al. 1982).
    U.S. EPA Region 6                                                              U.S. EPA
    Multimedia Planning and Permitting Division                                           Office of Solid Waste
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    Protocol for Screening Level Ecological Risk Assessment
    Toxicological Profile H-23; Hexachlorocyclopentadiene	August 1999
    Volatilization from water is also expected to be a significant removal mechanism; however, adsorption to
    suspended solids and sediments may interfere with this process.  (EPA 1987).
    
    3.0    FATE IN ECOLOGICAL RECEPTORS
    
    HCCP is expected to be moderately bioconcentrated by algae, invertebrates, and fish. (Lu et al. 1975;
    Spehar et al. 1979; Veith et al.  1979; Podowski and Khan 1984; Freitag et al. 1982) (Geyer et al. 1981).
    HCCP taken up by freshwater fish (goldfish) is readily distributed, stored, and metabolized (Podowski et
    al. 1991). In fish, HCCP is excreted in the bile. The biological half-life of HCCP in the goldfish was
    approximately 9 days (Podowski and Khan 1984).
    
    Inhalation is the main exposure route for HCCP toxicity in mammals. HCCP is less absorbed following
    ingestion (Lawrence and Dorough 1981). Following ingestion, HCCP will move primarily to the liver and
    the kidney (Lawrence and Dorough 1981), which appear to be the main sites of toxicity (Abdo et al. 1984;
    Southern Research Inst 1981).
    
    Limited information was available regarding the metabolism of HCCP. Some degradation may occur in the
    gut following oral administration (Dorough and Ranieri  1984; Mehendale 1977).
    
    Information was not available on the fate of HCCP in birds or plants.
    
    4.0    REFERENCES
    Abdo K, Montgomery C, Kluwe W, Farnell D, Prejean J.  1984.  "Toxicity of Hexachlorocyclopentadiene:
            Subchronic (13-week) administration by gavage to F344 rats and B6C3F mice." J Appl Toxicol
            42(2):75-81.
    Chou S, et al. 1981. Aqueous chemistry and adsorption of hexachlorocyclopentadiene by earth
            materials. NTIS PB81-173882. As cited in HSDB 1997.
    Dorough H, Ranieri T.  1984. "Distribution and elimination of hexachlorocyclopentadiene in rats and
            mice." Drug Chem Toxicol 7(l):73-89.
    EPA. 1987. Exams II. Computer simulation. As cited in HSDB 1997.
    U.S. EPA Region 6                                                             U.S. EPA
    Multimedia Planning and Permitting Division                                         Office of Solid Waste
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    Protocol for Screening Level Ecological Risk Assessment
    lexicological Profile H-23: Hexachlorocyclopentadiene	August 1999
    
    Freitag D, Geyer H, Kraus A, Viswanathan R, Kotzias D, Attar A, Klien W, Korte F.  1982.
            "Ecotoxicological profile analysis. VE. Screening chemicals for their environmental behavior by
            comparative evaluation." Ecotox Environ Safety 6:60-81.
    
    Geyer H, Viswanathan R, Freitag D, Korte F. 1981. "Relationship between water solubility of organic
            chemicals and their bioaccumulation by the alga chlorella."  Chemosphere 10:1307-1313.
    
    HSDB. 1997. Hazardous Substance Data Bank.
    
    Lawrence L, Dorough H. 1981. "Retention and fate of inhaled hexachlorocyclopentadiene in the rat."
            Bull Environ Contain Toxicol 26(5):663-668.
    
    Lu P, Metcalf R, Hirwe A, Williams J. 1975. "Evaluation of environmental distribution and fate of
            hexachlorocyclopentadiene, chlordane, heptachlor, and heptachlor epoxide in a laboratory model
            ecosystem." J Agric Food Chem 23:967-973.
    
    Meditext.  1997. Medical Management Data Base.
    
    Mehendale H. 1977. "Chemical reactivity-absorption, retention, metabolism, and elimination of
            hexachlorocyclopentadiene." Environ Health Perspect 21:275-278.
    
    Podowski A Khan M. 1984. "Fate of hexachlorocyclopentadiene in water and goldfish." Arch Environ
            Contain Toxicol 13(4):471-481.
    
    Podowski A, Sclove S, Pilipowicz A, Khan M.  1991. "Biotransformation and disposition of
            hexachlorocyclopentadiene in fish." Arch Environ Contain Toxicol 20(4):488-496.
    
    Southern Research Institute.  1981.  Subchronic toxicity report on report hexachlorocyclopentadiene
            (C53607) in rats and mice. EPA Document No. 40-8349130, Fiche No. OTS0507497.  As cited
            in HSDB 1997.
    
    Spehar R, Veith G, DeFoe D, Bergstedt B. 1979. "Toxicity and bioaccumulation of
            hexachlorocyclopentadiene, hexachloronorbornadiene and heptachloronorbornene in larval and
            early juvenile fathead minnows, Pimephales promelas."  Bull Environ Contain Toxicol
            21(4-5):576-583.
    
    Veith G, Defoe D, Bergstedt B.  1979. "Measuring and estimating the bioconcentration factor of chemicals
            in fish." J Fish Res Board Can 36:1040-1048.
    
    Wolfe N, Zepp RG, Schlotzhauer, Sink M. 1982. "Transformation pathways of
            hexachlorocyclopentadiene in the aquatic environment." Chemosphere 11:91-101.
    
    Zepp R, Wolfe N.  1987. Aquatic Surf Chem Vol:423-455. As cited in HSDB 1997.
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    Multimedia Planning and Permitting Division                                          Office of Solid Waste
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    Protocol for Screening Level Ecological Risk Assessment
    Toxicological Profile H-24;  Hexachlorophene	August 1999
                                       HEXACHLOROPHENE
    1.0    SUMMARY
    
    Hexachlorophene is a persistent organic chemical that is highly soluble in lipids and adsorbs strongly to soil
    and sediment  In surface soils and the euphoric (light-penetrating) zone of surface waters, hexachlorophene
    is degraded by photolysis. Hexachlorophene may be bioconcentrated by aquatic and soil organisms.  In
    upper-trophic-level receptors, hexachlorophene may be absorbed following oral or dermal exposure and is
    distributed throughout all body tissues.  Due to its high lipid solubility, hexachlorophene has the potential
    to be transferred significantly in food chains. In mammals, the nervous system is the major site of toxicity
    for hexachlorophene; however, reproductive and developmental effects have also been reported. Exposure
    to hexachlorophene may result in decreased egg production in birds.
    
    The following is a profile of the fate of hexachlorophene in soil, surface water, and sediment; and the fate
    after uptake by ecological receptors. Section 2 discusses the environmental fate and transport in soil,
    water, and sediment. Section 3 discusses the fate in ecological receptors.
    
    2.0    FATE IN SOIL, SURFACE WATER, AND SEDIMENT
    
    Hexachlorophene adsorbs strongly to soil and once bound does not tend to leach from soil or mobilize in
    soil. Hexachlorophene does not undergo significant hydrolysis or evaporation from the soil; however, slow
    photodegradation may occur if exposed to light above 290 nm (Kotzias et al.  1982).
    
    Hexachlorophene does not undergo hydrolysis, evaporation or volatilization in water; however,  slow
    photodegradation may occur. Hexachlorophene adsorbs strongly to sediments and has been identified in
    the humic acid portion of sediment. The half-life of hexachlorophene in water is expected to be greater
    than 50 years with a half-life of 290 days reported in sediment.  Hexachlorophene has been reported to
    bioconcentrate in aquatic organisms (Kotzias et al. 1982; Hansch and Leo 1985; Lyman et al. 1982).
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    Protocol for Screening Level Ecological Risk Assessment
    lexicological Profile H-24;  Hexachlorophene	August 1999
    3.0    FATE IN ECOLOGICAL RECEPTORS
    Based on its high octanol-water partition coefficient, hexachlorophene is expected to bioconcentrate in
    aquatic life living in the water column and in the sediment. Bioconcentration has been measured in
    mosquito fish and snail (Hansch and Leo 1985; Lyman et al. 1982).
    
    Hexachlorophene is absorbed rapidly following oral exposure (Hatch 1982).  Hexachlorophene may also be
    absorbed following dermal exposure with blood levels peaking approximately 6 to 10 hours post-
    application (Meditext 1997). Hexachlorophene is highly lipid-soluble. After entering the bloodstream, it
    distributes into adipose tissue and tissue with a high lipid content including the central nervous system.
    Hexachlorophene binds preferentially to myelin (Meditext 1997). Transplacental transfer of
    hexachlorophene has also been reported (Hatch 1982). Target organs include the nervous system, the
    gastrointestinal system, and skin (Meditext 1997).
    
    Hexachlorophene has been reported to have low volatility from plant leaves (Goetchius et al. 1986).
    Additional data regarding the potential effects of hexachlorophene on plants were not located  Information
    was not available on the fate of hexachlorophene in exposed birds.
    
    4.0    REFERENCES
    Goetchius P, et al.  1986. Health and environmental effect profile on hexachlorophene.  SR-TR-220.
           Syracuse Research Corporation,  pp. 2-1 to 3-1. As cited in HSDB 1997.
    Hansch C, Leo A.  1985. Medchem project issue no. 26, Pomona College, Claremont, CA.
    Hatch R. 1982. Veterinary toxicology. In: Booth N, McDonald L, eds.  Veterinary Pharmacology and
           Therapeutics.  5th ed.  Iowa State University Press, Ames, IA. pp. 927-1021.
    HSDB. 1997. Hazardous Substance Data Base.
    Kotzias D, Parlar H, Korte F.  1982. "Photoreaktivitat organischer chemikalien in wabrigen systemen in
           gegenwart von nitraten und nitriten." Naturwiss 69:444-445.  As cited in HSDB  1997.
    Lyman W, Reehl W, Rosenblatt D, eds.  1982.  Handbook of Chemical Property Estimation Methods.
           McGraw Hill Book Company, New York.
    Meditext (r).  1997. Medical Management Data Base..
    U.S. EPA Region 6                                                              U.S. EPA
    Multimedia Planning and Permitting Division                                          Office of Solid Waste
    Center for Combustion Science and Engineering                                                       H-81
    

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    Protocol for Screening Level Ecological Risk Assessment
    Toxicological Profile H-25;  Hydrazine	August 1999
                                             HYDRAZINE
    1.0    SUMMARY
    
    Hydrazine is a reactive, nitrogen-containing compound.  It is readily biodegraded after release to soil and
    surface water.  Volatilization may also be a significant removal process.  Hydrazine is readily absorbed
    following  inhalation, ingestion, and dermal absorption. Mammals rapidly break down and excrete
    hydrazine.
    
    The following is a profile of the fate of hydrazine in soil, surface water and sediment; and the fate after
    uptake by ecological receptors. Section 2 discusses the environmental fate and transport in soil, surface
    water, and sediment. Section 3 discusses the fate in ecological receptors.
    
    2.0    FATE IN SOIL, SURFACE WATER, AND SEDIMENT
    
    Studies show that hydrazine is expected to biodegrade in soils high in organic carbon, and to adsorb to soils
    high in clay content (Braun and Zirrolli 1983; Sun et al. 1992). For dry surface soil, volatilization may be
    a significant process (HSDB 1997).
    
    Hydrazine is expected to have a relatively short half-life of 8.3 days in pond water (Braun and Zirrolli
    1983). Hydrazine has been reported to react with dissolved oxygen at a rate inversely proportional to its
    concentration (Slonim and Gisclard 1976);  its degradation rate increases with increasing temperature,
    dissolved oxygen, and the presence of microorganisms (Sun et al. 1992).
    
    3.0    FATE IN ECOLOGICAL RECEPTORS
    
    Hydrazine is absorbed rapidly from the lungs, gastrointestinal tract, and through skin (ACGIH 1991).
    Hydrazine is reported to be neurotoxic, hepatotoxic and nephrotoxic hi rodents (Lambelt and Shank 1988).
    Hydrazine is rapidly metabolized in the liver and eliminated (Jenner and Timbrell 1995).
    
    Information was not available on the fate of hydrazine in exposed birds, aquatic life, or plants.
    U.S. EPA Region 6                                                              U.S. EPA
    Multimedia Planning and Permitting Division                                           Office of Solid Waste
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    Protocol for Screening Level Ecological Risk Assessment
    Toxicological Profile H-25;  Hydrazine	August 1999
    
    4.0    REFERENCES
    ACGIH.  1991.  Documentation of TLVs. 6th ed. p. 761.
    
    Braun B, Zirrolli J.  1983. Environmental fate of hydrazine fuels in aqueous and soil environments. Air
           Force Report No. ESLTR-82-45. NTIS AD-A125813. As cited in HSDB  1997.
    
    HSDB.  1997. Hazardous Substance Data Bank.
    
    Jenner A, Timbrell J. 1995.  "In vitro microsomal metabolism of hydrazine." Xenobiotica 25(6):599-609.
    
    Lambelt C, Shank R. 1988.  "Role of formaldehyde hydrazone and catalase in hydrazine-induced
           methylation of DNA guanine." Carcinogenesis 9(1):65-70.
    
    SlonimA, GisclardJ.  1976. Bull Environ Contain Toxicol 16:301-309. As cited in HSDB 1997.
    
    SunH, etal.  1992.  Huanjing Kexue 13:35-39.  As cited in HSDB 1997.
    U.S. EPA Region 6                                                            U.S. EPA
    Multimedia Planning and Peimitting Division                                         Office of Solid Waste
    Center for Combustion Science and Engineering                                                      H-83
    

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    Protocol for Screening Level Ecological Risk Assessment
    Toxicological Profile H-26;  Mercury	August 1999
                                              MERCURY
    1.0    SUMMARY
    
    Mercury is a highly toxic compound with no known natural biological function. Mercury exists in three
    valence states: mercuric (Hg2+), mercurous (Hgl+), and elemental (HgO+) mercury. It is present in the
    environment in inorganic and organic forms. Inorganic mercury compounds are less toxic than
    organomercury compounds, however, the inorganic forms are readily converted to organic forms by
    bacteria commonly present in the environment. The organomercury compound of greatest concern is
    methylmercury.
    
    Mercury sorbs strongly to soil and sediment. Elemental mercury is highly volatile. In aquatic organisms,
    mercury is primarily absorbed through the gills. In aquatic and terrestrial receptors, some forms of
    mercury, especially organomercury compounds, bioaccumulate significantly and biomagnify in the food
    chain. In all receptors, the target organs are the kidney and central nervous system.  However, mercury
    causes numerous other effects including teratogenicity and mutagenicity.
    
    The following is a profile of the fate of mercury in soil, surface water and sediment, and the fate after
    uptake by biological receptors.  Section 2 discusses the environmental fate and transport in soil, surface
    water and sediment.  Section 3 discusses the fate in ecological receptors.
    
    2.0    FATE IN SOIL, SURFACE WATER,  AND SEDIMENT
    
    In soil, mercury exists in the mercuric (Hg2+) and mercurous (Hgl+) states.  Mercury adsorbs to soil or is
    converted to volatile forms (Krabbenhoft and Babiarz 1992; Callahan et al. 1979). Mercury can migrate
    by volatilization from aquatic and terrestrial sources through the reduction of metallic mercury to complex
    species and by the deposition in reducing sediments. Atmospheric transport is a major environmental
    distribution pathway.
    
    Mercury 2+ is the predominant form of mercury in surface waters (ATSDR 1993). Nonvolatile mercury in
    surface water binds to organic matter and sediment particles (Lee and Iverfeldt 1991).
    U.S. EPA Region 6                                                              U.S. EPA
    Multimedia Planning and Permitting Division                                           Office of Solid Waste
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    Protocol for Screening Level Ecological Risk Assessment
    lexicological Profile H-26; Mercury	August 1999
    Sorption to suspended and bed sediments is one of the most important processes determining the fate of
    mercury in aquatic systems; sorption onto organic materials is the strongest for mercury 2+. As a result,
    mercury is generally complexed to organic compounds and is not readily leached from either organic-rich
    or mineral-rich soils (Rosenblatt et al 1975). Most mercury compounds can be remobilized in aquatic
    systems by microbial conversion to methyl and dimethyl forms.  Conditions reported to enhance microbial
    conversion include large amounts of available mercury, large numbers of bacteria, absence of strong
    complexing agents, near neutral pH, high temperatures, and moderately aerobic conditions.
    
    3.0     ECOLOGICAL RECEPTORS
    
    Sorption at the gill surface is the major pathway of mercury entry in aquatic organisms (EPA 1984). In
    aquatic organisms, bioaccumulation is rapid and elimination is slow. Biomagnification occurs in the
    aquatic food chain (NRCC 1979). Absorbed mercury is distributed to the blood and ultimately the internal
    organs. Mercury which is not absorbed is eliminated rapidly in the feces (Eisler 1987).  The biological
    half-life of mercury in fish is approximately 2 to 3 years (EPA 1985). In general, mercury accumulation is
    enhanced by elevated water temperatures, reduced water hardness or salinity, reduced water pH, increased
    age of the organism, reduced organic matter content of the medium, and the presence of zinc, cadmium, or
    selenium in solution.
    
    Mercury is readily absorbed by terrestrial species following oral and inhalation exposure. Elemental and
    organomercury compounds are readily transferred across the placenta and blood-brain barrier.  Mercury is
    bioaccumulated primarily in the kidney (Rothstein and Hayes 1964; Nielsen and Andersen 1991), and
    mercury is biomagnified in mammals (Eisler 1987).  Retention of mercury in mammals is longer for
    organomercury compounds (especially methylmercury) than for inorganic forms. Mercury elimination
    occurs via the urine, feces, expired air, and breast milk (Clarkson 1989; Yoshida et al. 1992).
    
    All mercury compounds interfere with metabolism in organisms, causing inhibition or inactivation of
    proteins containing thiol ligands and ultimately leading to miotic disturbances (Das et al 1982; Elhassani
    1983). Mercury also binds strongly with sulfhydryl groups. Phenyl and methyl mercury compounds are
    among the strongest known inhibitors of cell division (Birge et al 1979). In mammals, methyl mercury
    irreversibly destroys the neurons of the central nervous system.
    U.S. EPA Region 6                                                              U.S. EPA
    Multimedia Planning and Permitting Division                                          Office of Solid Waste
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    Protocol for Screening Level Ecological Risk Assessment
    Toxicological Profile H-26; Mercury	August 1999
    
    Information was not available on the fate of mercury in birds.
    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).  However, mercury levels in plant tissues increase as soil
    levels increase with 95% of the accumulation and retention in the root system (Beauford et al 1977;
    
    Cocking et al  1991). Mercury is reported to inhibit protein synthesis in plant leaves and may affect water-
    
    adsorbing and transporting mechanisms in plants (Adriano 1986).
    
    
    4.0    REFERENCES
    
    
    Adriano D.C.  1986. Trace elements in the terrestrial environment. Springer-Verlag. New York.
    
    ATSDR.  1993. Toxicological Profile for Mercury.  Agency for Toxic Substances and Disease Registry,
           Atlanta, GA.
    
    Beauford, W.  et al. 1977. "Uptake and distribution of mercury within higher plants."  Physiol. Plant
           39:261-265.
    
    Birge W.J., Black J.A, Westerman A.G, and Hudson J.E. 1979. The effect of mercury on reproduction of
           fish and amphibians. In: The biogeochemistry of mercury in the environment. Editor J.O.
           Nriagu. Elsevier/North Holland Biomedical Press.  New York.
    
    Callahan M, Slimak M, Gabel N, et al.  1979. Water-Related Environmental Fate of 129 Priority
           Pollutants. Vol 1 & 2.  Office of Water and Waste Management, U.S. Environmental Protection
           Agency, Washington, DC.  EPA-440/4-79-029a, EPA-440/4-79-029b. pp. 14-1 to 14-15.
    
    ClarksonT. 1989. "Mercury." J Am CoUToxicol 8:1291-1295.
    
    Cocking D.R., Hayes M.L., Rohrer M.J., Thomas R., and Ward D. 1991. "Compartmentalization of
           mercury in biotic components of terrestrial floodplain ecosystems adjacent to the south river at
           Wayneboro, Virginia."  Water, Air and Soil Pollution 57-58: 159-170.
    
    Das S.K., Sharma A, and Talukder G. 1982. "Effects of mercury on cellular systems  in mammals - A
           review." Nucleus (Calcutta) 25: 193-230.
    
    Eisler R.  1987. Mercury Hazards to Fish, Wildlife, and Invertebrates: A Synoptic Review.  U.S. Fish
           and Wildlife Service. Biological Report 85(1.10).
    
    Elhassani S.B.  1983. "The many faces of mercury poisoning." Journal of Toxicology 19: 875-906.
    
    EPA. 1984. Ambient Water Quality Criteria Document for Mercury. EPA 440/5-84-026. p.  10-11.
    U.S. EPA Region 6                                                             U.S. EPA
    Multimedia Planning and Permitting Division                                          Office of Solid Waste
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    Protocol for Screening Level Ecological Risk Assessment
    lexicological Profile H-26:  Mercury	August 1999
    
    EPA. 1985. Ambient Water Quality Criteria Document for Mercury.  Office of Water Regulations and
           Standards.  Washington D.C.  EPA 440/5-84-026.
    
    HSDB.  1997. Hazardous Substances Data Bank.
    
    Krabbenhoft D, Babiarz C. 1992. "The role of groundwater transport in aquatic mercury cycling." Water
           Resour Res 28(12):3119-3129. As cited in ATSDR 1993.
    
    Lee Y, Iverfeldt A.  1991.  "Measurement of methylmercury and mercury in run-off, lake and rain waters."
           Water Air Soil Pollut 56:309-321. As cited in ATSDR 1993.
    
    NRCC.  1979. "Effects of Mercury in the Canadian Environment." National research Council of Canada.
           NRCC No. 16739.  pp. 89, 101. As cited in HSDB 1997.
    
    Nielsen J, Andersen O. 1991.  "Methyl mercuric chloride toxicokinetics in mice. I:  Effects of strain, sex,
           route of administration and dose."  Pharmacol Toxicol 68:201-207. As cited in ATSDR 1993.
    
    Rosenblatt D.H., Miller T.A., Dacre J.C., MuU I.  And Cogley D.R.  1975.  Problem definition studies on
           potential environmental pollutants II. Physical, chemical, toxicological, and biological
           properties of 16 substances.  Technical Report 7509.  U.S. Army Medical Bioengineering
           Research and Development Laboratory. Fort Detrick, Frederick, Maryland.
    
    Rothstein A, Hayes A.  1964. "The turnover of mercury in rats exposed repeatedly to inhalation of vapor."
           Health Phys 10:1099-1113.
    
    Yoshida M, Satoh H, Kishimoto T, Yamamura Y. 1992. "Exposure to mercury via breast milk in
           suckling offspring of maternal guinea pigs exposed to mercury vapor after parturition." J Toxicol
           Environ Health 35:135-139. As cited in ATSDR 1993.
    U.S. EPA Region 6                                                             U.S. EPA
    Multimedia Planning and Permitting Division                                          Office of Solid Waste
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    Protocol for Screening Level Ecological Risk Assessment
    Toxicological Profile H-27;  Methanol	August 1999
                                             METHANOL
    1.0    SUMMARY
    
    Methanol is a highly water soluble hydrocarbon. It does not adsorb to organic carbon.  The primary
    removal process for methanol in soil and water is biodegradation. Aquatic, soil, and sediment communities
    can be exposed to methanol through direct contact. Upper-trophic-level receptors may be directly exposed
    through ingestion, inhalation, or dermal exposure.  Methanol does not bioconcentrate or move through
    food chains.
    
    The following is a profile of the fate of methanol in soil, surface water, and sediment; and the fate after
    uptake by ecological receptors.  Section 2 discusses the environmental fate and transport in soil, surface
    water, and sediment. Section 3 discusses the fate in ecological receptors.
    
    2.0    FATE IN SOIL, SURFACE WATER, AND SEDIMENT
    
    Based on biological screening studies, including soil microcosm studies, methanol undergoes
    biodegradation if released to the soil. Methanol is expected to be highly mobile in soil, based on its
    miscibility in water and low log K^,, value.  Evaporation from dry surfaces is also expected to occur, based
    on the high vapor pressure of methanol (Weber et al.  1981; Hansch and Leo 1985; HSDB 1997).
    
    Methanol is completely soluble in water. Methanol is significantly biodegradable in water, based on
    screening studies (HSDB 1997). Volatilization is expected to be a significant removal process (Lyman
    1982). Aquatic hydrolysis, oxidation, photolysis,  adsorption to sediment, and bioconcentration are not
    considered significant removal processes for methanol (HSDB 1997).
    
    3.0    FATE IN ECOLOGICAL RECEPTORS
    
    Methanol uptake across gill epithelia is the most significant exposure route.  However, based on its low
    bioconcentration factor for fish, methanol does not bioconcentrate  (Freitag et al. 1985; Bysshe 1982)
    (Hansch and Leo 1985).
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    Multimedia Planning and Permitting Division                                          Office of Solid Waste
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    Protocol for Screening Level Ecological Risk Assessment
    Toxicological Profile H-27:  Methanol	August 1999
    
    Mammals are exposed to methanol through ingestion, inhalation, and dermal contact.  Methanol is reported
    to readily absorb from the gastrointestinal and respiratory tracts (Gosselin et al. 1984), and rapidly
    distribute within tissues (Clayton and Clayton 1982). Following absorption, methanol is widely distributed
    in body tissue. Small amounts are excreted in the urine and expired air; however, methanol is mostly
    oxidized to formaldehyde and formic acid (Goodman and Gillman 1985).
    
    
    Information was not available on the fate of methanol in exposed birds or plants.
    
    
    4.0    REFERENCES
    Bysshe S.  1982. Bioconcentration factor in aquatic organisms.  In: Lyman W, Reehl W, Rosenblatt D,
           eds.  Handbook of Chemical Property Estimation Methods. McGraw-Hill Book Co., New York.
           pp 5-1 to 5-30.
    
    Clayton G, Clayton F, eds.  1982.  Patty's Industrial Hygiene and Toxicology.  3rded.  Vol2. John Wiley
           & Sons, New York.  pp. 4531-4534. As cited in HSDB 1997.
    
    Freitag D, Ballhorn L, Geyer H, Korte F. 1985. "Environmental hazard profile of organic chemicals: An
           experimental method for the assessment of the behavior of organic chemicals in the ecosphere by
           means of simple laboratory tests with 14C labeled chemicals." Chemosphere 14:1589-1616.
    
    Goodman L, Oilman A eds.  1985. The Pharmacological Basis of Therapeutics. 7th ed. Macmillan
           Publ, New York.  p. 381-382.
    
    Gosselin R, Smith R, Hodge H.  1984. Clinical toxicology of commercial products.  VolH. 5th ed.
           Williams and Wilkins, Baltimore, MD. p. HI-275.
    
    Hansch C, Leo A. 1985. Medchem Project Issue No. 26, Pomona College, Claremont, CA. As cited in
           HSDB 1997.
    
    HSDB.  1997.  Hazardous Substance Data Bank.
    
    Lyman W, Reehl W, Rosenblatt D, eds.. 1982. Handbook of Chemical Property Estimation Methods.
           McGraw Hill Book Company, New York.
    
    Weber R, Parker P, Bowser M.  1981. Vapor pressure distribution of selected organic chemicals. EPA
           600/2-81-021.  Industrial Environmental Research Laboratory, Cincinnati, OH. As cited in HSDB
           1997.
    U.S. EPA Region 6                                                             U.S. EPA
    Multimedia Planning and Permitting Division                                         Office of Solid Waste
    Center for Combustion Science and Engineering                                                      H-89
    

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    Protocol for Screening Level Ecological Risk Assessment
    Toxicological Profile H-28:  Nitropropane, 2-	August 1999
                                         NITROPROPANE, 2-
    1.0    SUMMARY
    
    2-nitropropane is a highly volatile, low molecular weight hydrocarbon. Generally, it does not adsorb to soil
    or sediment, and rapidly volatilizes from soil and surface water. Wildlife may be exposed to
    2-nitropropane through ingestion or inhalation. Due to its high water solubility, 2-nitropropane does not
    bioconcentrate in fish,  and does not bioaccumulate in wildlife.  2-nitropropane is rapidly metabolized and
    excreted by mammals.
    
    The following summarizes information on the fate of 2-nitropropane in soil, surface water and sediment,
    and its fate after uptake by ecological receptors.  Section 2 discusses the environmental fate and transport
    in soil, water and sediment.  Section 3 discusses the fate in ecological receptors.
    
    2.0    FATE IN SOIL, SURFACE WATER, AND SEDIMENT
    
    2-nitropropane rapidly volatilizes from soil, and also has the potential to leach in moist soils.
    2-nitropropane undergoes minimal degradation in soil (Freitag et al. 1988).
    
    2-nitropropane is highly soluble in water (Baker and Bollmeier 1981). It is expected to have a short
    half-life in surface water because of its propensity for rapid volatilization, based on its high vapor pressure
    (Dougan et al. 1976).  Adsorption of 2-nitropropane to suspended solids or sediment is not expected, based
    on its low KOC value (Lyman 1982).
    
    3.0    FATE IN ECOLOGICAL RECEPTORS
    
    2-nitropropane does not bioconcentrate in aquatic organisms (Baker and Bollmeier 1981; Freitag et al.
    1988). 2-nitropropane is readily absorbed by the gastrointestinal tract and the lungs, when inhaled
    Accumulation of 2-nitropropane in tissues of mammals is low because it is rapidly metabolized and
    eliminated after uptake (Nolan et al. 1982). 2-nitropropane may be excreted unchanged in expired air or as
    nitrite and nitrate in the urine (Browning 1965).
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    Multimedia Planning and Permitting Division                                          Office of Solid Waste
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    Protocol for Screening Level Ecological Risk Assessment
    Toxicological Profile H-28; Nitropropane, 2-	August 1999
    
    No information was available on the fate of 2-nitropropane in birds or plants.
    4.0    REFERENCES
    Baker B, Bollmeier A.  1981.  "Nitroparaffins." In: Kirk-Otmer Encyclopedia of Chemical Technology.
            3rd ed. John Wiley & Sons, New York.  15:969-987.
    
    Browning E. 1965. Toxicology and Metabolism of Industrial Solvents. Elsevier, New York. pp.
            285-288.
    
    Dougan J, et al.  1976.  Preliminary Scoring of Selected Organic Air Pollutants. ApdlCL EPA
            450/3-77-008d. pp.303. As cited in HSDB 1997.
    
    Freitag D, et al.  1988.  "Ecotoxicological Profile Analysis of Nitroparaffins According to Oecd Guidelines
            with C14-labelled Compounds." In: Tsca Set 8d Submissions to EPA for Nitromethane (Fiche
            No. ITS516767). As cited in HSDB 1997.
    
    HSDB.  1997. Hazardous Substance Data Bank.
    
    Lyman W.  1982.  "Adsorption Coefficient for Soils and Sediments." In: Lyman W, Reehl W, Rosenblatt
            D, eds. Handbook of Chemical Property Estimation Methods. McGraw-Hill Book Co., New
            York, pp 4-1 to 4-33.
    
    Nolan R, Unger A, Muller C.  1982. "Pharmacokinetics of Inhales [14c]-2-nitropropane in Male
            Sprague-dawley Rats." Ecotoxicol Environ Safety 6(4):388-397.
    U.S. EPA Region 6                                                             U.S. EPA
    Multimedia Planning and Permitting Division                                          Office of Solid Waste
    Center for Combustion Science and Engineering                                                      H-91
    

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    Protocol for Screening Level Ecological Risk Assessment
    Toxicological Profile H-29;  Polynuclear Aromatic Hydrocarbons (PAHS)     August 1999
                      POLYNUCLEAR AROMATIC HYDROCARBONS (PAHS)
    1.0    SUMMARY
    
    Polynuclear aromatic hydrocarbons (PAH) are a class of semi-volatile compounds that have a high affinity
    for soil and sediment particles.  PAHs have low water solubility. Low molecular weight PAHs volatilize
    and photolyze from soil and surface water, and may be biodegraded as well.  High molecular weight PAHs
    are resistant to volatilization, photolysis, and biodegradation.  PAHs can be bioconcentrated to high
    concentrations by some aquatic organisms. However, many aquatic organisms can metabolize PAHs. The
    main PAH exposure route for upper-trophic-level receptors is ingestion. However, wildlife can readily
    metabolize PAHs and eliminate the by-products. Therefore, food chain transfer and biomagnification are
    anticipated to be minimal.
    
    The following is a profile of the fate of PAHs in soil,  surface water and sediment; and the fate after uptake
    by ecological receptors.  The PAHs considered are benzo(a)anthracene, benzo(b)fluoranthene,
    benzo(k)fluoranthene, chrysene, dibenzo(a,h)anthracene, and indeno(l,2,3-cd)pyrene.  Section 2 discusses
    the environmental fate and transport in soil, surface water and sediment. Section 3 discusses the fate in
    ecological receptors.
    
    2.0    FATE IN SOIL, SURFACE WATER, AND SEDIMENT
    
    PAHs strongly adsorb to the soil; therefore, leaching to groundwater and volatilization are slow
    insignificant processes in most instances (HSDB 1997). However, the persistence of PAHs in soil is
    dependent upon the number of condensed rings that a PAH contains. The major source of degradation of
    PAHs in soil is microbial metabolism (ATSDR 1995). Volatilization and photolysis were determined to be
    important processes for the degradation of PAHs containing less than four aromatic rings, when analyzed
    from four surface soils amended with PAHs in sewage sludge. However, PAHs containing four or more
    aromatic rings showed insignificant abiotic losses  (Wild and Jones 1993).
    
    Within aquatic systems, PAHs are found sorbed to particles suspended in the water column or particles
    which have settled to the bottom. This is due to the low solubility and high affinity PAHs have for organic
    carbon. Studies have estimated that two-thirds of PAHs found in aquatic systems are in particle form and
    U.S. EPA Region 6                                                             U.S. EPA
    Multimedia Planning and Permitting Division                                         Office of Solid Waste
    Center for Combustion Science and Engineering                                                      H-92
    

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    Protocol for Screening Level Ecological Risk Assessment
    lexicological Profile H-29;  Polymiclear Aromatic Hydrocarbons (PAHS)     August 1999
    only one-third are in dissolved form (Eisler 1987). Low molecular weight PAHs (2 to 3 rings) studied in
    estuaries show that the primary removal processes are volatilization and biodegradation, while high
    molecular weight PAHs (4 or more rings) volatilize and adsorb to suspended sediments (Thomas 1982;
    Southworth et al. 1978; Southworth 1979).
    
    Photo-oxidation, chemical oxidation, and biodegradation by aquatic microorganisms are the primary
    degradation processes associated with PAHs in water (Neff 1979). The process of photo-oxidation varies
    widely among PAHs when considering the rate and extent of degradation.  Benzo(a)pyrene is the most
    resistant to photo-oxidation, while benzo(a)anthracene is the most sensitive (Neff 1979).  Microbial
    degradation of PAHs in water is very rapid under oxygenated conditions, but extremely slow under anoxic
    conditions (Neff 1979).
    
    3.0     FATE IN ECOLOGICAL RECEPTORS
    
    Sources of PAH accumulation in aquatic organisms include water, sediment, and food. Bioconcentration
    factors can range from low to very high, depending on the PAH and the receptor. Invertebrates and
    bottom-dwelling fish may accumulate PAHs through ingestion of sediment (Eisler 1987).
    
    Studies indicate that fish are capable of metabolizing PAHs by the mixed function oxidase (MFO) system
    in the liver. The breakdown products are then eliminated through the urine and feces. Half-lives ranging
    from 2 to 9 days have been reported for the elimination of PAHs in fish (Niimi 1987). Chrysene has a
    near-surface half-life computed for sunlight at latitude 40°N of 4.4 hours (Zepp and Schlotzhauer 1979).
    Assimilation of PAHs from contaminated food is readily achieved by fish and crustaceans; however, this
    process is limited for mollusks and polychaete worms (Eisler 1987). It is also noted that aquatic organisms
    such as phytoplankton, certain zooplankton, mussels,  scallops, and snails lack a metabolic detoxification
    enzyme system. Therefore, these organisms have potential for PAH accumulation (Malins 1977).
    
    PAHs can be introduced into mammals through ingestion, inhalation, and dermal exposure. Because PAHs
    are highly lipid soluble and can cross epithelial membranes, they are readily absorbed from the
    gastrointestinal tract and lung (HSDB 1997). PAHs are absorbed through the mucous lining of bronchi
    when inhaled (Bevan and Ulman 1991) and taken up by the gastrointestinal tract in fat-soluble compounds
    when ingested.  Passive diffusion is the process in which PAHs are distributed following percutaneous
    U.S. EPA Region 6                                                              U.S. EPA
    Multimedia Planning and Permitting Division                                          Office of Solid Waste
    Center for Combustion Science and Engineering                                                        H-93
    

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    Toxicological Profile H-29; Polynuclear Aromatic Hydrocarbons (PAHS)     August 1999
    absorption (Ng et al. 1991).  Once absorbed into the body, PAHs are distributed to the lymph fluid and
    then the blood stream.  Following oral or inhalation exposure, PAHs are widely distributed in animal tissue
    (Bartosek et al. 1984; Withey et al. 1991; Yamazaki and Kakiuchi 1989).
    
    PAHs have limited transfer across the placenta; therefore, PAH levels are generally lower in the fetus,
    when compared to maternal levels (Neubert and Tapken 1988; Withey et al. 1992). The major metabolism
    sites for PAHs are the liver and kidneys. Additional sites of metabolism include the adrenal glands, testes,
    thyroid, lungs, skin, sebaceous  glands, and placenta (Meditext 1997).  PAHs are primarily excreted
    through the urine and bile (Sevan and Weyand 1988; Grimmer et al. 1988; Petridou-Fischer et al. 1988;
    Weyand and Bevan 1986; Wolff et al. 1989).
    
    PAHs may be taken up by terrestrial plants from the soil or air depending on the concentration, solubility,
    and molecular weight of the PAHs.  Lower molecular weight PAHs are absorbed by plants more readily
    than higher molecular weight PAHs (USFWS  1987). Some plants are capable of producing
    benzo(b)fluoranthene (HSDB 1997). The partitioning of PAHs between vegetation and the atmosphere
    was found to be primarily dependent upon the  atmospheric gas-phase PAH concentration and the ambient
    temperature, when studied throughout the growing season under natural conditions (Simonich and Kites
    1994). Above-ground parts of vegetables have been found to contain more PAHs than underground parts,
    mainly attributable to airborne  deposition and  subsequent adsorption (USFWS 1987). Growth promoting
    effects were observed in higher plants, as  well as cultures of lower plants, when benzo(a)anthracene,
    indeno(l,2,3-cd)pyrene, and benzo(b)fluoranthene were tested in a series of soil and hydrocultures (Graf
    and Nowak 1968).
    
    Information was not available on the fate  of PAHs in exposed birds.
    
    4.0     REFERENCES
    ATSDR. 1995.  Toxicological Profile for Poly cyclic Aromatic Hydrocarbons. Agency for Toxic
            Substances and Disease Registry, U.S. Public Health Service.  August.
    Bartosek I, Guaitani A, Modica R, Fiume M, Urso R. 1984. "Comparative kinetics of oral
            benz(a)anthracene, chrysene and triphenylene in rats: Study with hydrocarbon mixtures."  Toxicol
            Lett 23:333-339.
    U.S. EPA Region 6                                                            U.S. EPA
    Multimedia Planning and Permitting Division                                         Office of Solid Waste
    Center for Combustion Science and Engineering                                                      H-94
    

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    Protocol for Screening Level Ecological Risk Assessment
    lexicological Profile H-29;  Polynuclear Aromatic Hydrocarbons (PAHS)     August 1999
    
    Bevan D, Ulman M. 1991.  "Examination of factors that may influence disposition of benzo(a)pyrene in
            vivo: Vehicles and asbestos." Cancer Lett 57(2): 173-180.
    
    Bevan D, Weyand E. 1988. "Compartmental analysis of the disposition of benzo(a)pyrene in rats."
            Carcinogenesis 9(11):2027-2032.
    
    EislerR. 1987. Polycyclic Aromatic Hydrocarbon Hazards to Fish, Wildlife, and Invertebrates: A
            Synoptic Review.  U.S. Fish and Wildlife Service, U.S. Department of the Interior.  Biological
            report 85(1.11). As cited in ATSDR 1995.
    
    Graf W, Nowak W. 1968. "Wachstumsforderung bei niederen und hoheren pfianzen durch kanzerogene
            polyzyklische aromate."  Arch Hyg Bakt 150:513-528.
    
    Grimmer G, Brune H, Dettbarn G, Heinrich U, Jacob J, Mohtashamipur E, Norpoth K, Pott F,
            Wenzel-Hartung R.  1988.  "Urinary and fecal excretion of chrysene and chrysene metabolites by
            rats after oral, intraperitoneal, intratracheal or intrapuhnonary application."  Arch Toxicol
            62(6):401-405.
    
    HSDB.  1997. Hazardous Substances Data Bank.
    
    Malins D.  1977. "Metabolism of aromatic hydrocarbons in marine organisms."  Ann NY Acad Sci
            298:482-496.
    
    Meditext.  1997. Medical Management Data Base. June.
    
    Neff J.  1979.  Polycyclic aromatic hydrocarbons in the aquatic environment. Sources, fates and
            biological effects. Applied Science Publishers, Ltd. London, England.
    
    Neubert D, Tapken S.  1988. "Transfer of benzo(a)pyrene into mouse embryos and fetuses." Arch
            Toxicol 62(2-3):236-239.
    
    Ng K, Chu I, Bronaugh R, Franklin C, Somers D. 1991. "Percutaneous absorption/metabolism of
            phenanthrene in the hairless guinea pig: Comparison of in vitro and in vivo results." Fundam Appl
            Toxicol 16(3):517-524.
    
    Niimi A. 1987. "Biological half-lifes of chemicals in fishes." Rev Environ Contain Toxicol 99:1-46.
    
    Petridou-Fischer J, Whaley S, Dahl A. 1988. "In vivo metabolism of nasally instilled benzo(a)pyrene in
            dogs and monkeys." Toxicology 48(1):31-40.
    
    Simonich S, Kites R.  1994.  "Importance of vegetation in removing polycyclic aromatic hydrocarbons
            from the atmosphere." Nature 370:49-51.
    
    Southworth G.  1979. "The role of volatilization on removing polycyclic aromatic hydrocarbons from
            aquatic environments." Bull Environ Contain Toxicol 21:507-514.
    U.S. EPA Region 6                                                              U.S. EPA
    Multimedia Planning and Permitting Division                                          Office of Solid Waste
    Center for Combustion Science and Engineering                                                       H-95
    

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    Protocol for Screening Level Ecological Risk Assessment
    lexicological Profile H-29;  Polynuclear Aromatic Hydrocarbons (PAHS)     August 1999
    
    Southworth G, Beauchamp J, Schmeider P.  1978. "Bioaccumulation potential of polycyclic aromatic
           hydrocarbons in Daphnia pulex." Water Research 12:973-977.
    
    Thomas R.  1982.  Volatilization from water.  In: Lyman W, Reehl W, Rosenblatt D, eds.  Handbook of
           Chemical Property Estimation Methods.  McGraw-Hill Book Company, New York, pp 15-1 to
           15-34.
    
    U.S. Fish and Wildlife Service (USFWS). 1987.  Polycyclic aromatic hydrocarbon hazards to fish,
           wildlife, and invertebrates: A synoptic review.  Biological Report 85 (1.11).  Washington D.C.
    
    Weyand E, Bevan D. 1986. "Benzo(a)pyrene disposition and metabolism in rats following intratracheal
           instillation." Cancer Res 46:5655-5661.
    
    Wild S, Jones K.  1993.  "Biological and abiotic losses of polynuclear aromatic hydrocarbons (PAHs) from
           soils freshly amended with sewage sludge." Environ Toxicol Chem 12:5-12.
    
    Withey J, Law F, Endrenyi L.  1991. "Pharmacokinetics and bioavailability of pyrene in the rat." J
           Toxicol Environ Health 32(4):429-447.
    
    Withey J, Shedden J, Law F, Abedini S.  1992. "Distribution to the fetus and major organs of the rat
           following inhalation exposure to pyrene." J Appl Toxicol 12(3):223-231.
    
    Wolff M, Herbert R, Marcus M, Rivera M, Landrigan P, Andrews L. 1989. "Polycyclic aromatic
           hydrocarbon (PAH) residues on skin in relation to air levels among roofers."  Arch Environ Health
           44(3): 157-163.
    
    Yamazaki H, Kakiuchi Y.  1989. "The uptake and distribution of benzo(a)pyrene in rat after continuous
           oral administration." Toxicol Environ Chem 24(I/2):95-104.
    
    Zepp R, Schlotzhauer P. 1979.  In: Jones P, Leber P, eds.  Polynuclear aromatic hydrocarbons.  Ann
           Arbor Science Publ., Ann Arbor MI. pp. 141-158. As cited in HSDB 1997.
    U.S. EPA Region 6                                                              U.S. EPA
    Multimedia Planning and Permitting Division                                          Office of Solid Waste
    Center for Combustion Science and Engineering                                                       H-96
    

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    Protocol for Screening Level Ecological Risk Assessment
    Toxicological Profile H-30;  Polychlorinated Biphenyls (PCBs)	August 1999
                              POLYCHLORINATED BIPHENYLS (PCBs)
    1.0     SUMMARY
    
    Polychlorinated biphenyls (PCB) are mixtures of different congeners of chlorobiphenyl. PCBs are a group
    of highly fat-soluble, semi-volatile compounds that readily bioaccumulate and biomagnify in ecological
    receptors, especially upper-trophic-level carnivores in aquatic food webs. In general, PCBs adsorb
    strongly to soil and sediment, and are soluble in fatty tissues. Volatilization and biodegradation of the
    lower chlorinated congeners also occur. The lexicological properties of individual PCBs are influenced
    primarily by: (1) lipophilicity, which is correlated with log K^, and (2) steric factors resulting from
    different patterns of chlorine substitution on the biphenyl molecule. In general, PCB isomers with high KOW
    values and high numbers of substituted chlorines in adjacent positions constitute the greatest environmental
    concern.  Biological responses to individual isomers or mixtures vary widely, even among closely related
    taxonomic species.
    
    The following is a profile of the fate of PCBs in soil, surface water, and sediment; and the fate after uptake
    by ecological receptors. Section 2 discusses the environmental fate and transport in soil, surface water, and
    sediment. Section 3 discusses the fate in ecological receptors.
    
    2.0    FATE IN SOIL, SURFACE WATER, AND SEDIMENT
    
    The environmental fate of PCBs in soil depends on the degree of chlorination of the molecule. In general,
    adsorption and the persistence of PCBs increases with an increase in the degree of chlorination (EPA
    1988). Mono-, di-, and trichlorinated biphenyls (Aroclors 1221 and 1232) biodegrade relatively rapidly.
    Tetrachlorinated biphenyls (Aroclors 1016 and 1242) biodegrade slowly, and higher chlorinated biphenyls
    (Aroclors 1248, 1254, and 1260) are resistant to biodegradation (HSDB 1997). Although biodegradation
    of higher chlorinated congeners may occur very slowly, no other degradation mechanisms have been shown
    to be significant in soil (HSDB 1997). Vapor loss of PCBs from soil surfaces appears to be an important
    mechanism with the rate of volatilization decreasing with increasing chlorination.  Although the
    volatilization rate may be low, the total loss by volatilization over time may be significant because of
    persistence and stability of PCBs (Sklarew and Girvin  1987).
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    Multimedia Planning and Permitting Division                                           Office of Solid Waste
    Center for Combustion Science and Engineering                                                       H-97
    

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    Protocol for Screening Level Ecological Risk Assessment
    lexicological Profile H-30;  Polychlorinated Biphenyls (PCBs)	August 1999
    In water, adsorption to sediments and organic matter is a major fate process for PCBs (EPA 1988;
    Callahan et al. 1979). Volatilization of dissolved PCBs is an important aquatic process. Strong PCB
    adsorption to sediment significantly decreases the rate of volatilization, with higher chlorinated PCBs
    having longer half-lives than the lower chlorinated PCBs (EPA 1988).
    
    3.0    FATE IN ECOLOGICAL RECEPTORS
    
    Diet is a major route of PCB uptake in many aquatic species (Eisler 1986). However, some species
    accumulate PCBs from the water column to a much larger extent than the diet, even when comparing
    closely-related species.  Based on its high log K^ value, receptors are expected to bioconcentrate and
    bioaccumulate PCBs to tissue levels much greater than the concentrations in water and sediment (Eisler
    1986). Due to their high lipophilicity, PCBs concentrate mostly in fatty tissues. For upper-trophic-level
    receptors, diet is the main exposure pathway for PCB exposure (Eisler 1986).  In aquatic food webs,
    evidence indicates that PCBs biomagnify in upper trophic levels, but not in lower trophic levels (Shaw and
    Cornell 1982).
    
    Among mammals, aquatic predators (e.g., mink, otters, seals, etc.) have been found to accumulate PCBs to
    significant levels. Lower chlorinated PCBs are eliminated more rapidly from lipids than higher chlorinated
    PCBs. Placental transfer of PCBs  occurs in mammals (Hidaka et al. 1983).
    
    The primary biochemical effect of PCBs is to induce hepatic mixed function oxidase systems, increasing an
    organism's capacity to biotransform or detoxify xenobiotic chemicals. PCBs also induce hepatic enzymes
    that metabolize naturally occurring steroidal hormones (Peakall 1975).  These hepatic microsomal enzyme
    systems are most likely correlated with observed adverse reproductive effects (Tanabe 1988).
    
    PCBs accumulate in bird tissues and eggs (Eisler 1986). Residues of PCBs in birds are affected by
    numerous biotic factors including fat content, tissue specificity, sex, and the developmental stage of an
    organism (Eisler 1986). Sexual differences in PCB bioaccumulation are pronounced due to the female's
    ability to pass a significant portion of the PCB burden to eggs (Lemmetyinen and Rantamaki 1980).
    
    Water snakes (Nerodia spp.) and turtles accumulate PCB levels similar to those of PCB residues in then-
    prey.  Aroclor 1260 accounted for  most of  the PCBs detected in water snakes (Sabourin et al. 1984;
    U.S. EPA Region 6                                                              U.S. EPA
    Multimedia Planning and Permitting Division                                           Office of Solid Waste
    Center for Combustion Science and Engineering                                                       H-98
    

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    Protocol for Screening Level Ecological Risk Assessment
    lexicological Profile H-30; Polychlorinated Biphenyls (PCBs)	August 1999
    
    Olafsson et al. 1983). These data suggest diet is an important route of PCS transfer in reptiles (McKim
    and Johnson 1983).
    
    
    Organic matter and clay content of soil influences the bioavailability of PCBs to plants (Strek and Weber
    1982). Uptake of PCBs from soils by plants has been documented, however, only very low amounts are
    typically accumulated (Iwata et al 1974, Iwata and Gunther 1976, Weber and Mrozek 1979).  Effects of
    PCBs on plants include reduced growth and chlorophyll content, and negative effects on photosynthesis
    (Strek and Weber 1982).
    
    
    Terrestrial and aquatic plants bioconcentrate PCBs (Sawhney and Hankin 1984). Aquatic plants also
    bioaccumulate PCBs from both the water column and sediments. Transfer of PCBs on microparticulate
    materials to phytoplankton is well documented, as is partitioning from aqueous solution into algal lipids
    (Rohrer et al. 1982).
    
    
    4.0    REFERENCES
    Callahan M, Slimak M, Gabel N, et al. 1979. Water-Related Environmental Fate of 129 Priority
           Pollutants.  Vol 1 & 2. Office of Water and Waste Management, U.S. Environmental Protection
           Agency, Washington, DC. EPA-440/4-79-029a, EPA-440/4-79-029b. pp. 36+.
    
    Eisler R. 1986.  Polychlorinated Biphenyl Hazards to Fish, Wildlife, and Invertebrates: A Synoptic
           Review.  U.S. Fish and Wildlife Service. Biological Reports 85(1.7).
    
    EPA.  1988.  Drinking Water Criteria Document for Polychlorinated Biphenyls (PCBs).
           ECAO-CIN-414. Environmental Criteria and Assessment Office, Cincinnati, OH.
    
    Hidaka H, Tanake S, Tatsukawa R. 1983. "DDT compounds and PCB isomers  and congeners in Weddel
           seals and their fate in the Antarctic marine ecosystem." Agric Biol Chem 47:2009-2017. As cited
           in Eisler 1986.
    
    HSDB.  1997. Hazardous Substance Data Bank.
    
    Iwata  Y. And Gunther F.A.  1976. "Translocation of the polychlorinated biphenyl Aroclor 1254 from soil
           into carrots under field conditions." Archives of Environmental Contamination and Toxicology. 4:
           44-59.
    
    Iwata  Y., Gunther F.A., and Westlake W.E.  1974. "Uptake of a PCB (Aroclor 12554) from soil by
           carrots under field conditions." Bulletin of Environmental Contamination and Toxicology. 11:523-
           528.
    U.S. EPA Region 6                                                             U.S. EPA
    Multimedia Planning and Permitting Division                                          Office of Solid Waste
    Center for Combustion Science and Engineering                                                      H-99
    

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    lexicological Profile H-30;  Polychlorinated Biphenyls (PCBs)	August 1999
    
    Lemmetyinen R, Rantamaki P.  1980.  "DDT and PCB residues in the arctic tern (Sterna paradisaed)
           nesting in the archipelago of southwestern Finland." Ann Zool Fennici 17:141-146.  As cited in
           Eisler 1986.
    
    McKim J, Johnson K.  1983.  "Polychlorinated biphenyls and p,p'-DDE in loggerhead and green
           postyearling Atlantic sea turtles." Bull Environ Contain Toxicol 31:53-60.
    
    Olafsson P, Bryan A, Bush B, Stone W.  1983.  "Snapping turtles - a biological screen for PCBs."
           Chemosphere 12:1525-1532. As cited in Eisler 1986.
    
    PeakallD.B.  1975.  "PCBs and their environmental effects." CRC Critical Reviews in Environmental
           Control.  5:469-508.
    
    Rohrer T, Forney J, Hartig J. 1982. "Organochlorine and heavy metal residues in standard fillets of coho
           and chinook salmon of the Great Lakes-1980." J Great Lakes Res 8:623-634.
    
    Sabourin T, Stickle W, Michot T, Villars C, Garton D, Mushinsky H.  1984.  "Organochlorine residue
           levels in Mississippi River water snakes in southern Louisiana."  Bull Environ Contain Toxicol
           32:460-468.
    
    Sawhney B, Hankin L.  1984. "Plant contamination by PCBs from amended soils." JFoodProt
           47:232-236.
    
    Shaw G, Council D. 1982. "Factors influencing polychlorinated biphenyls in organisms from an estuarine
           ecosystem," Aust J Mar Freshwater Res 33:1057-1010. As cited in Eilser 1986.
    
    Sklarew D, Girvin D. 1987.  Rev Environ Contain Toxicol 98:1-41. As cited in HSDB 1997.
    
    Strek H.J. and Weber J.B.  1982.  "Behavior of polychlorinated biphenyls (PCBs) in soils and plants."
           Environmental Pollution (Series A). 28: 291-312.
    
    Tanabe S. 1988. "PCB problems in the future: foresight from current knowledge." Environmental
           Pollution. 50:5-28.
    
    Weber J.B. and Mrozek E. 1979. "Polychlorinated biphenyls: absorption and translocation by plants and
           inactivation by activated carbon." Bulletin of Environmental Contamination and Toxicology.
           23:412-417.
    U.S. EPA Region 6                                                             U.S. EPA
    Multimedia Planning and Permitting Division                                          Office of Solid Waste
    Center for Combustion Science and Engineering                                                      H-100
    

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    Protocol for Screening Level Ecological Risk Assessment
    lexicological Profile H-31;  Pentachlorophenol	August 1999
                                      PENTACHLOROPHENOL
    1.0    SUMMARY
    
    Pentachlorophenol (PCP) has a strong affinity for soil, with sorption higher at lower pH and with increased
    organic content. Microorganisms readily metabolize PCP in soil, surface water, and sediment. Photolysis
    rapidly breaks down PCP in surface water. Ecological receptors will rapidly absorb PCP, but will also
    rapidly excrete it.  Therefore, the potential for bioconcentration and bioaccumulation is only moderate.
    PCP biomagnification has not been observed.
    
    The following is a profile of the fate of PCP in soil, surface water, and sediment, and the fate after uptake
    by ecological receptors. Section 2 discusses the environmental fate and transport in soil, water and
    sediment.  Section 3 discusses the fate in ecological receptors.
    
    2.0    FATE IN SOIL, SURFACE WATER, AND SEDIMENT
    
    PCP adsorbs strongly to soil, with adsorption higher in acidic conditions (Callahan et al. 1979). The
    amount of PCP adsorbed to soil at a given pH also increases with increasing organic content of the soil
    (Chang and Choi 1974). The half-life of PCP in soil ranges from weeks to months (Ide et al. 1972; Murthy
    1979; Rao and Davidson 1982).  Photolysis and hydrolysis do not appear to be significant processes of
    degradation in soil (Ball 1987). In certain soil environments, PCP may volatilize; however, in general,
    mobility of PCP in soil is limited (Arsenault 1976).
    
    Biodegradation is considered the major transformation mechanism for PCP in soil, with PCP metabolized
    rapidly by acclimated microorganisms (Kaufman 1978).  The main degradation products of PCP in soil are
    2,3,7,8-tetrachlorophenol and carbon dioxide (Knowlton and Huckins 1983).
    
    The fate of PCP in water and sediment is heavily dependent upon the pH of the water. At lower pH, more
    of the PCP dissociates and is available for degradation (Weiss et al. 1982). PCP also adsorbs to sediment
    more readily under acidic conditions, and is more mobile under neutral or alkaline conditions (Kuwatsuka
    and Igarashi 1975).
    U.S. EPA Region 6                                                              U.S. EPA
    Multimedia Planning and Permitting Division                                          Office of Solid Waste
    Center for Combustion Science and Engineering                                                      H-101
    

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    Protocol for Screening Level Ecological Risk Assessment
    Toxicological Profile H-31; Pentachlorophenol	August 1999
    In surface water, photolysis and biodegradation are the predominant transformation processes for PCP
    (ATSDR 1994). Photolysis occurs mainly at the water surface, with its impact decreasing with increasing
    depth (Callahan et al. 1979). The reported half-life for the photolysis of PCP is about 1 hour (Callahan et
    al. 1979). Biodegradation of PCP can occur under both aerobic and anaerobic conditions, with more rapid
    degradation under  aerobic conditions (Pignatello et al.  1983). The greatest biodegradation of PCP was
    observed in the top 0.5 to 1 cm layer of sediment.
    
    3.0    FATE IN ECOLOGICAL RECEPTORS
    
    The aquatic toxicity of PCP depends on water pH; at low pH, PCP is more lipophilic, with a high potential
    for accumulation.  At alkaline pH, PCP is more hydrophilic, with a decreased potential for bioconcentration
    (Eisler 1989).  Fish and bivalves may moderately bioconcentrate PCP (Makela et al. 1991).
    Accumulation of PCP in fish is rapid, and occurs primarily by direct uptake from water rather than through
    the food chain or diet. In fish, PCP residues are found in the liver, gill, muscle, and hepatopancreas. PCP
    is readily metabolized in the liver and hepatopancreas.  (Menzie 1978). Half-lives in tissues are less than
    24 hours (Eisler 1989).
    
    In mammals, PCP may be absorbed into the body through inhalation, diet or skin contact (Eisler 1989).
    The degree of accumulation is small, since PCP is  efficiently and rapidly excreted. The highest residuals
    are found in the liver and kidneys, likely reflecting that these organs are the principal organs for metabolism
    and excretion (Gasiewicz 1991). Small amounts of PCP have been shown to  cross the placenta (Shepard
    1986).
    
    Uptake into rice has been demonstrated in a 2-year study under flooded conditions. After a single
    application of radiolabeled PCP, 12.9% of the application was taken up by the plants within the first year,
    with the highest levels found in the roots (Eisler 1989).
    
    4.0    REFERENCES
    Arsenault R.  1976.  Pentachlorophenol and Contained Chlorinated Dibenzodioxins in the Environment.
            American Wood-Preservers Association, Alexandria, VA. pp. 122-147. As cited in ATSDR
            1994.
    U.S. EPA Region 6                                                             U.S. EPA
    Multimedia Planning and Permitting Division                                          Office of Solid Waste
    Center for Combustion Science and Engineering                                                      H-102
    

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    Protocol for Screening Level Ecological Risk Assessment
    Toxicological Profile H-31;  Pentachlorophenol	August 1999
    
    ATSDR. 1994.  Toxicological Profile for Pentachlorophenol. Agency for Toxic Substances and Disease
           Registry, Atlanta, GA.
    
    BallJ. 1987. Proc Ind Waste Conference.  41:347-351.  As cited in HSDB 1997.
    
    Callahan M, Slimak M, Gabel N, et al. 1979. Water-Related Environmental Fate of 129 Priority
           Pollutants. Vol 1 & 2. Office of Water and Waste Management, U.S. Environmental Protection
           Agency, Washington, DC. EPA-440/4-79-029a, EPA-440/4-79-029b.  pp. 87-1 to 87-13.
    
    Chang N, Choi J.  1974. "Studies on the adsorption of pentachlorophenol (PCP) in soil." Hanguk Touang
           Bilyo Hakkhoe Chi 7:197-220. As cited in ATSDR 1994.
    
    EislerR. 1989.  Pentachlorophenol Hazards to Fish, Wildlife, and Invertebrates: A Synoptic Review.
           US Fish and Wildlife Service. Biological Rep 85(1.17).
    
    GasiewiczT. 1991. Nitro compounds and related phenolic pesticides. In: Hayes W, Laws E, eds.
           Handbook of Pesticide Toxicology. Vol 3.  Academic Press, New York. pp. 1191-1269.
    
    HSDB.  1997. Hazardous Substances Data Bank.
    
    IdeA,etal.  1972.  AgricBiol Chem 36:1937-1944. As cited in HSDB 1997.
    
    Kaufman D. 1978. Degradation of pentachlorophenol in soil, and by soil organisms.  In: Rao K, ed.
           Pentachlorophenol: Chemistry, Pharmacology, and Environmental Toxicology. Plenum Press,
           New York. pp. 27-39.
    
    Knowlton M, Huckins J. 1983.  "Fate of Radiolabeled Sodium Pentachlorophenate in Littoral
           Microcessing." Bull Environ Contain Toxicol 30:206-213.
    
    Kuwatsuka S, Igarashi M.  1975. "Degradation of PCP in soil: H The relationship between the
           degradation."  Soil Sci Plant Nutr 21:405-414. As cited in ATSDR 1994.
    
    Makela T, Petanan T, Kukkonen J, et al. 1991.  "Accumulation and depuration of chlorinated phenolics in
           the freshwater mussel (Anodonta anatina L.)." Ecotoxicol Environ Safety 22:153-163. As cited in
           ATSDR 1994.
    
    Menzie C.  1978. Metabolism of Pesticides. U.S. Department of Interior, Fish and Wildlife Service.
           p. 221.
    
    MurthyB.  1979.  "Degradation of pentachlorophenol (PCP) in aerobic and anaerobic soil." J Environ Sci
           Health B 14:1-14.  As cited in HSDB 1997.
    
    Pignatello J, Martinson M, Steiert J, et al. 1983.  "Biodegradation and photolysis of pentachlorophenol in
           artificial freshwater streams." Appl Environ Microbiol 46:1024-1031.
    
    Rao P, Davidson J. 1982.  Retention and Transformation of Selected Pesticides and Phosphorus in
           Soil-Water Systems.  EPA 600/S3-82-060.  As cited in HSDB 1997.
    U.S. EPA Region 6                                                             U.S. EPA
    Multimedia Planning and Permitting Division                                          Office of Solid Waste
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    Protocol for Screening Level Ecological Risk Assessment
    lexicological Profile H-31;  Pentachlorophenol                               August 1999
    ShepardT. 1986. Catalog of Teratogenic Agents. 5th ed. Johns Hopkins University Press, Baltimore,
           MD. p. 443. As cited in HSDB 1997.
    
    Weiss U, et al. 1982. J Agric Food Chem 30:1191-1194.
    U.S. EPA Region 6                                                             U.S. EPA
    Multimedia Planning and Permitting Division                                         Office of Solid Waste
    Center for Combustion Science and Engineering                                                     H-104
    

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    Protocol for Screening Level Ecological Risk Assessment
    lexicological Profile H-32;  Thallium	August 1999
                                              THALLIUM
    1.0    SUMMARY
    
    In the environment, thallium exists in either the monovalent (thallous) or trivalent (thallic) form. Thallium is
    chemically reactive with air and moisture, undergoing oxidation. Thallium is relatively insoluble in water,
    although thallium compounds exhibit a wide range of solubilities. Thallium adsorbs to soil and sediment and
    is not transformed or biodegraded. In aquatic organisms, thallium is absorbed primarily from ingestion and
    thereafter bioconcentrates in the organism. In mammals, thallium is absorbed primarily from ingestion and is
    distributed to several organs and tissues, with the highest levels reported in the kidneys.  Thallium exposure
    in mammals causes cardiac, neurologic, reproductive and dermatological effects.  Thallium is taken up by
    plants and inhibits chlorophyll formation and seed germination.
    
    The following is a profile of the fate of thallium in soil, surface water and sediment; and the fate after uptake
    by ecological receptors.  Section 2 discusses the environmental fate and transport in soil, surface water and
    sediment.  Section 3 discusses the fate in ecological receptors.
    
    2.0    FATE IN SOIL, SURFACE WATER, AND SEDIMENT
    
    In soil, thallium exists in either the monovalent (thallous) or trivalent (thallic) form, with the monovalent form
    being more common and stable and, therefore, forming more numerous salts (Hampel 1968). Thallium is
    reactive with air and moisture, oxidizing slowly in air at 20° C and more rapidly with increasing temperatures
    (Standen 1967). Moisture increases the oxidation of thallium. Thallium adsorbs to soil and is not transformed
    or biodegraded (Callahan et al. 1979).
    
    Elemental thallium is relatively insoluble in water (Windholz 1976).  However, thallium compounds exhibit
    solubilities ranging from 220 mg/L to more than 700,000 mg/L (Standen 1967; Weast 1975).
    
    Thallium adsorbs to sediments and micaceous clays (Callahan et al. 1979; Frantz and Carlson 1987). Data
    regarding the transformation or biodegradation of thallium in water were not located.
    U.S. EPA Region 6                                                              U.S. EPA
    Multimedia Planning and Permitting Division                                          Office of Solid Waste
    Center for Combustion Science and Engineering                                                       H-105
    

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    Toxicological Profile H-32;  Thallium	August 1999
    3.0    ECOLOGICAL RECEPTORS
    The primary exposure route for aquatic organisms exposed to thallium is ingestion. Thallium bioconcentrates
    in aquatic organisms (Zitko and Carson 1975).  Toxic effects have been observed in numerous aquatic
    organisms including daphnia, fat-head minnow, sheepshead minnow, saltwater shrimp, atlantic salmon, bluegill
    sunfish, and others (USEPA 1980).
    
    Birds and mammals are exposed to thallium via ingestion of soil, water, and plant material (Lie et al. 1960).
    Following absorption, thallium is distributed to numerous organs including the skin, liver, and muscle, with
    the greatest amount found in the kidneys (Downs et al. 1960; Manzo et al. 1983). Thallium is excreted
    primarily in the urine, with some excretion in the feces (Lehman and Favari 1985).  Thallium is distributed
    from the maternal circulation to the fetus (Gibson et al. 1967; Gibson and Becker 1970).  Various effects and
    toxic responses have been reported. Tikhonova (1967) reported paralysis and pathological changes in the liver,
    kidneys, and stomach mucosa in rabbits chronically exposed to thallium.  Formigli et  al. (1986) reported
    testicular  toxicity  in rats  exposed  to thallium.   Grunfeld et al.  (1963) reported changes  in  the
    electrocardiographs of rabbits following oral exposure to thallium.
    
    Some levels of thallium occurs naturally in plants (Seiler 1988). Thallium is taken up by the roots of higher
    plants (Cataldo and Wildung 1983).  Thallium has been shown  to inhibit chlorophyll  formation and seed
    generation (OHM/TADS 1997).
    
    4.0     REFERENCES
    ATSDR. 1992. Toxicological Profile for Thallium. Agency for Toxic Substances and Disease Registry.
           July.
    Callahan M, Slimak M, Gabel N, et al. 1979.  Water-Related Environmental Fate of 129 Priority
           Pollutants. Voll.  EPA-440/4-79-029. Office of Water Planning and Standards, Washington,
           DC. pp. 18-1 to 18-8.
    Cataldo D, Wildung R.  1983. "The role of soil and plant metabolic processes in controlling trace element
           behavior and bioavailability to animals." Sci Total Environ 28:159-168.
    Downs, W.L., Scott J.K., Steadman L.T., Maynard E.A.  1960.  "Acute and Sub-acute Toxicity Studies of
           Thallium Compounds." American Industrial Hygiene Association Journal. 21:399-406.
    U.S. EPA Region 6                                                              U.S. EPA
    Multimedia Planning and Permitting Division                                          Office of Solid Waste
    Center for Combustion Science and Engineering                                                      H-106
    

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    Toxicological Profile H-32;  Thallium   	August 1999
    
    Formigli L., Scelsi R., Poggi P., Gregotti C., DiNucci A., Sabbioni E., Gottardi L., Manzo L. 1986.
            "Thallium-Induced Testicular Toxicity in the Rat." Env. Res. 40:531-539.
    
    Frantz G, Carlson R.  1987.  "Division S-2-soil chemistry: Effects of rubidium, cesium, and thallium on
            interlayer potassium release from transvaal vermiculite." Soil Sci Soc Am J 51:305-308.
    
    Grunfeld O, Battilana G., Aldana L., Hinostroza G., Larrea P.  1963.  "Electrocardiographic Changes in
            Experimental Thalh'um Poisoning." Am. Journal Vet Res. 24:1291-1296.
    
    Gibson I.E. and Becker B.A.  1970.  "Placenta! transfer, embryo toxicity and teratogenicity of thallium
            sulfate in normal and potassium-deficient rats."  Toxicol. Appl. Pharmacol. 16:120.  As cited in
            USEPA 1980.
    
    Gibson I.E. et al. 1967. "Placental transport and distribution of thallium-204 sulfate in newborn rats and
            mice." Toxicol. Appl. Pharmacol.  10: 408 (abst.). As cited in USEPA 1980.
    
    Hampel C.A.  (ed.).  1968.  The Encyclopedia of Chemical Elements.  Reinhold Publishers, New York. As
            cited in USEPA 1980.
    
    HSDB.  1997. Hazardous Substance Data Base
    
    Lehman P, Favari L. 1985.  "Acute thallium intoxication:  Kinetic study of the relative efficacy of several
            antidotal treatments in rats." Arch Toxicol 57:56-60.
    
    Lie R, Thomas R, Scott J.  1960. "The distribution and excretion of thallium-204 in the rat, with
            suggested rape's and a bioassay procedure." Health Phys 2:334-340.
    
    Manzo L, Scelsi R, Moglia A Poggi P, Alfonsi E, Pietra R, Mousty F, Sabbioni E. 1982. "Long-term
            toxicity of thallium in the rat". In: Chemical Toxicology and Clinical Chemistry of Metals.
            Academic Press, London, pp. 401-405.
    
    OHM/TADS.  1997. Oil and Hazardous Materials/Technical Assistance Data System. June.
    
    Seiler.  1988.  Handbook of the Toxicity of Inorganic Compounds, p. 678. As cited in HSDB 1997.
    
    Standen A. (ed.). 1967.  Kirk-Othmer Encyclopedia of Chemical Technology.  Interscience Publishers,
            New York.  As cited in USEPA 1980.
    
    Tikhonova T.S. 1967.  "Toxicity of thallium and its compounds in workers." Nov. Dannye Toksikol.
            Redk. Metal. JkhSoedin. Chem. Abstr. 71: 53248J, 1969.  As cited in USEPA 1980.
    
    U.S. Environmental Protection Agency (USEPA).  1980. Ambient Water Quality Criteria for Thallium.
            EPA 440/5-80-074.  October.
    
    Weast R.C. (ed.). 1975. Handbook of Chemistry and Physics.  56th ed. CRC Press.  Cleveland, Ohio.
            As cited in USEPA 1980.
    U.S. EPA Region 6                                                              U.S. EPA
    Multimedia Planning and Permitting Division                                          Office of Solid Waste
    Center for Combustion Science and Engineering                                                      H-107
    

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    lexicological Profile H-32;  Thallium	August 1999
    
    Windholz M. (ed).  1976.  The Merck Index. 9th Edition.  Merck and Co., Inc.  Rathway, New Jersey.
           As cited in USEPA 1980.
    
    Zitko V, Carson W, Carson W.  1975. "Thallium: Occurrence in the environment and toxicity to fish."
           Bull Environ Contam Toxicol 13:23-30. As cited in ATSDR 1992.
    U.S. EPA Region 6                                                             U.S. EPA
    Multimedia Planning and Permitting Division                                         Office of Solid Waste
    Center for Combustion Science and Engineering                                                     H-108
    

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    Protocol for Screening Level Ecological Risk Assessment
    Toxicological Profile H-33;  Vinyl Chloride	August 1999
                                          VINYL CHLORIDE
    1.0     SUMMARY
    
    Vinyl chloride is a low molecular weight organic compound that rapidly volatilizes after released to soil and
    surface water. Aquatic organisms may take up vinyl chloride, however it is rapidly depurated because it is
    highly water-soluble. Routes of exposure for wildlife include inhalation, ingestion, and dermal exposure.
    Bioaccumulation in terrestrial and aquatic organisms is not an important process in the environmental fate
    of vinyl chloride because of its high volatility and the rapid metabolism by higher-tropic-level receptors.
    
    The following is a profile of the fate of vinyl chloride in soil, surface water and sediment, and the fate after
    uptake by ecological receptors. Section 2 discusses the environmental fate and transport in soil, surface
    water, and sediment. Section 3 discusses the fate in ecological receptors.
    
    2.0     FATE IN SOIL, SURFACE WATER, AND SEDIMENT
    
    Vinyl chloride in dry soil has a very short half-life (less than 1 day) (Jury et al. 1984). Vinyl chloride has a
    high vapor pressure, indicating rapid volatilization from dry soil surfaces (Riddick et al. 1986; Verschueren
    1983). Vinyl chloride is also biodegraded and photolyzed in surface soil  (ATSDR 1995; Nelson and
    Jewell 1993).  Vinyl chloride does not adsorb to soil in significant amounts.
    
    Vinyl chloride in surface water has a half-life of a few  hours (Thomas 1982). An estimated half-life in
    fresh water for vinyl chloride of 2.5 hours was reported (Mabey et al. 1981).  Vinyl chloride is slightly
    soluble (Cowfer and Magistro 1983). However, vinyl  chloride released to surface water will quickly
    volatilize, negating other fate processes that might be significant based on physical and chemical
    parameters.
    
    3.0     FATE IN ECOLOGICAL RECEPTORS
    
    Vinyl chloride is not expected to significantly bioconcentrate in aquatic organisms because it has a very low
    log Kpw value. Bioconcentration and accumulation in aquatic carnivores is not expected because of the
    U.S. EPA Region 6                                                             U.S. EPA
    Multimedia Planning and Permitting Division                                          Office of Solid Waste
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    Protocol for Screening Level Ecological Risk Assessment
    Toxicological Profile H-33;  Vinyl Chloride	August 1999
    
    high volatility of vinyl chloride and the rapid metabolism of vinyl chloride by higher-tropic-level organisms
    (Freitag et al. 1985; Lu et al. 1977).
    
    
    In mammals, vinyl chloride may be absorbed by the body via inhalation (Bolt et al. 1977; Krajewski et al.
    1980; Withey 1976), ingestion (Feron et al. 1981; Watanabe et al.  1976; Withey 1976) and dermal contact
    (Hefner et al.  1975). It is rapidly absorbed and distributed throughout the tissues following uptake.
    Because of the rapid metabolism and excretion of vinyl chloride, storage within the body is limited.
    
    
    Information was not available on the fate of vinyl chloride in birds or plants.
    
    
    4.0    REFERENCES
    ATSDR. 1995. Toxicological Profile for Vinyl Chloride.  Agency for Toxic Substances and Disease
           Registry. August.
    
    Bolt H, Laib R, Kappus H, Buchter A. 1977. "Pharmacokinetics of vinyl chloride in the rat." Toxicology
           7:179-188.
    
    Cowfer J, Magistro A. 1983. Vinyl chloride. In: Kirk-Othmer Encyclopedia of Chemical Technology.
           Wiley Interscience, New York. 23:865-885.
    
    Feron V, Hendriksen C, Speek A, Til H, Spit B. 1981. "Lifespan oral toxicity of vinyl chloride in rats."
           FD Cosmet Toxicol 19:317-333.
    
    Freitag D, Ballhorn L, Geyer H, Korte F. 1985. "Environmental hazard profile of organic chemicals: An
           experimental method for the assessment of the behavior of organic chemicals in the ecosphere by
           means of simple laboratory tests with 14C labeled chemicals." Chemosphere 14:1589-1616.
    
    Hefner R, Watanabe P, Gehring P.  1975. "Percutaneous absorption of vinyl chloride."  Toxicol Appl
           Pharmacol 34:529-532.
    
    HSDB.  1997.  Hazardous Substance Data Bank.
    
    Jury W, Spencer W, Farmer W. 1984. "Behavior assessment model for trace organics in soil: IH.
           Application of screening model." J Environ Qual 13:573-579.
    
    Krajewski J, Dobecki M, Gromiec J.  1980. "Retention of vinyl chloride in the human lung."  Br J Ind
           Med 37:373-374.
    U.S. EPA Region 6                                                              U.S. EPA
    Multimedia Planning and Permitting Division                                          Office of Solid Waste
    Center for Combustion Science and Engineering                                                      H-l 10
    

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    Toxicological Profile H-33;  Vinyl Chloride	August 1999
    
    Lu P, Metcalf R, Plummer N, Mandel D.  1977. "The environmental fate of three carcinogens:
           Benzo-a-pyrene, benzidine, and vinyl chloride evaluated in lab model ecosystems." Arch Environ
           Contain Toxicol 6:129-142.
    
    Mabey W, Smith J, Podoll R, et al. 1981. Aquatic Fate Process Data for Organic Priority Pollutants.
           EPA 440/4-81-014. EPA Office of Water Regulations and Standards, Washington, DC. As cited
           in HSDB 1997.
    
    Nelson Y, Jewell W.  1993. "Vinyl chloride biodegradation with methanotrophic attached films."
           J Environ Eng 119(5):890-907.
    
    Riddick J, Hunger W, Sakano T. 1986. Organic solvents: Physical properties and methods of
           purification, techniques of chemistry.  Voin. 4th ed. John Wiley & Sons, New York.
           pp. 488-489. As cited in HSDB  1997.
    
    Thomas R.  1982.  Volatilization from water. In: Lyman W, Reehl W, Rosenblatt D, eds. Handbook of
           Chemical Property Estimation Methods. McGraw-Hill Book Company, New York. PP 15-1 TO
           15-34.
    
    Verschueren K. 1983. Handbook of Environmental Data on Organic Chemicals. 2nd ed.  Van Nostrand
           Reinhold Co., New York.  pp. 1185-1186.
    
    Watanabe P, McGowan G, Gehring P. 1976. "Fate of [14C]vinyl chloride after single oral administration
           in rats." Toxicol Appl Pharmacol 36:339-352. As cited in ATSDR 1995.
    
    Withey J. 1976. "Pharmacodynamics and uptake of vinyl chloride monomer administered by various
           routes to rats."  J Toxicol Environ Health 1:381-394.
    U.S. EPA Region 6                                                            U.S. EPA
    Multimedia Planning and Permitting Division                                         Office of Solid Waste
    Center for Combustion Science and Engineering                                                     H-l 11
    

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