United States
Environmental Protection
Agency
Office of Water (4305) EPA-823-R-00-002
Office of Solid Waste (5307W) February 2000
i&EPA
Appendix to
Bioaccumulation Testing
And Interpretation For
The Purpose Of Sediment
Quality Assessment
Status and Needs
Chemical-Specific
Summary Tables
-------
APPENDIX: CHEMICAL-SPECIFIC SUMMARY TABLES
BIOACCUMULATION TESTING AND INTERPRETATION
FOR THE PURPOSE OF
SEDIMENT QUALITY ASSESSMENT
STATUS AND NEEDS
February 2000
U.S. Environmental Protection Agency
Bioaccumulation Analysis Workgroup
Washington, DC 20460
-------
This document has been approved for publication by the U.S. Environmental Protection
Agency. Mention of trade names or commercial products does not constitute endorsement or
recommendation for use.
This document describes existing knowledge on the use of bioaccumulation data as part of
sediment quality assessments. It is not intended to serve as guidance or regulation. This
document cannot impose legally binding requirements on EPA, States, Indian tribes, or the
regulated community.
-------
The document is an appendix to Bioaccumulation Testing and Interpretation for the Purpose of
Sediment Quality Assessment: Status and Needs. It summarizes information on chemical
characteristics, including water solubilities, half-lives, and partition coefficients (log Kow and log
Koc); human health concerns; wildlife and aquatic organism partitioning factors; and food chain
multipliers. A brief profile of the chemical's toxicity, mode of action, and potential for
bioaccumulation is also included. Daily intake levels of concern for the protection of human health
were compiled, including estimated values for carcinogenic endpoints (slope factors) and
noncarcinogenic endpoints (reference doses) for the oral ingestion exposure pathway, and EPA's
carcinogenic classifications are provided. Factors affecting partitioning of the chemical in relation to
wildlife and aquatic organisms, food chain multipliers (biomagnification factors), toxic effects and
mode of action, and other information were compiled from various sources.
The data in the chemical summary tables will be useful in addressing the following issues pertaining
to bioaccumulation:
• What species are potentially available for testing?
• How should we account for differential partitioning ofbioaccumulative contaminants
among tissues?
• How can bioaccumulation methods be used to assess population-level effects?
• How can tissue-specific residue levels be coupled with chronic toxicity response data
to develop dose-response relationships for bioaccumulative contaminants?
m
-------
(EPA-823-R-00-002)
Errata
1) page 485: Replace paragraph under Human Health Section for Methylmercury with the following:
EPA is recommending that the Programs and Regions use 0.1 (jg/kg/day as an interim RfD for
methylmercury until the Agency has had an opportunity to review the work of the National Academy of
Science (NAS). NAS is performing an independent assessment of the Agency's reference dose (RfD) for
methylmercury (EPA 1999).
[U.S. EPA. 1999. Memo: Transmittal of Interim Agency Guidance on the Use of Methylmercury
Reference Dose in Making Risk Management Decisions. From: Peter D. Robertson Acting Deputy
Administrator, To: Assistant Administrators, General Counsel, Inspector General, Chief Financial
Officer, Associate Administrators, Regional Administrators and Staff Office Directors (April 19, 1999)].
2) pages 7, 23, 35, 45, 61: Add to Human Health: Oral slope factor: 2.0 per mg/kg/d based on environmental
mixtures of PCBs in aquatic organisms (EPA 1996)
[U.S. EPA. 1996. Cancer Dose-Response Assessment for Application to Environmental Mixtures.
EPA/600/P-96/001F. Washington, DC].
3) The table below provides the latest World Health Organization (WHO ) toxic equivalent factors (
TEFs) for dioxins, furans, and coplanar PCBs. They are more recent than those cited in this document.
Congener
2,3,7,8-TCDD
,2,3,7,8-PeCDD
,2,3,4,7,8-HxCDD
,2,3,6,7,8-HxCDD
,2,3,7,8,9-HxCDD
,2,3,4,6,7,8,-HpCDD
OCDD
2,3,7,8-TCDF
1,2,3,7,8-PeCDF
2,3,4,7,8-PeCDF
,2,3,4,7,8-HxCDF
,2,3,6,7,8-HxCDF
,2,3,7,8,9-HxCDF
2,3,4,6,7,8-HxCDF
,2,3,4,6,7,8-HpCDF
,2,3,4,7,8,9-HpCDF
OCDF
3,4,4',5-TCB(81)
3,3',4,4'-TCB(77)
3,3',4,4',5-PeCB(126)
3,3',4,4',5,5'-HxCB(169)
2,3,3',4,4'-PeCB(105)
2,3,4,4',5-PeCB(114)
2,3',4,4',5-PeCB(118)
2',3,4,4',5-PeCB(123)
2,3,3 ',4,4',5-HxCB(156)
2,3,3 ',4,4',5-HxCB(157)
2,3',4,4',5,5'-HxCB(167)
2,3,3',4,4',5,5'-HpCB(189)
Toxic Equivalent Factor (TEF)
1
1
0.1
0.1
0.1
0.01
0.0001
0.1
0.05
0.5
0.1
0.1
0.1
0.1
0.01
0.01
0.0001
0.0001
0.0001
0.1
0.01
0.0001
0.0005
0.0001
0.0001
0.0005
0.0005
0.00001
0.0001
Van den Berg, et. al. 1998. Toxic Equivalency Factors (TEFs) for PCBs, PCDDs, PCDFs for Humans and
Wildlife. Environ. Health Perspect. 106(12):775-792.
-------
APPENDIX
Chemical-Specific Summary Tables
-------
-------
CONTENTS
Chemical Page
Acenaphthene 1
Aroclor 1016 7
Aroclor 1242 23
Aroclor 1248 35
Aroclor 1254 45
Aroclor 1260 61
Arsenic 71
Benzo(a)anthracene 83
Benzo(a)pyrene 89
Benzo(b)fluoranthene 109
Benzo(g,h,i)perylene 113
Benzo(k)fluoranthene 119
Cadmium 123
Chlordane 163
Chlorpyrifos 179
Chromium (hexavalent) 193
Chrysene 103
Copper 209
1,2,3,4,6,7,8-HeptaCDD 231
1,2,3,4,7,8-HexaCDD 241
1,2,3,6,7,8-HexaCDD 249
1,2,3,7,8-PentaCDD 259
2,3,7,8-TCDD 269
p,p'-DDD 317
p,p -DDE 327
p,p'-DDT 351
Diazinon 369
Dicofol 377
Dieldrin 381
Chemical Page
Disulfoton 399
1,2,3,4,7,8-HexaCDF 405
1,2,3,7,8-PentaCDF 412
2,3,4,7,8-PentaCDF 421
2,3,7,8-TCDF 431
Fluoranthene 443
Heptachlor 455
Lead 465
Methylmercury 485
Nickel 525
Oxyfluorfen 533
PCB 28 536
PCB 77 547
PCB 81 561
PCB 105 571
PCB 118 585
PCB 126 599
PCB 156 609
PCB 169 621
Pentachlorophenol 631
Phenanthrene 649
Pyrene 659
Selenium 667
Silver 685
Tributyltin 693
Terbufos 745
Total PCBs 751
Toxaphene 787
Zinc 801
-------
-------
BIOACCUMULATION SUMMARY ACENAPHTHENE
Chemical Category: POLYNUCLEAR AROMATIC HYDROCARBON (low molecular weight)
Chemical Name (Common Synonyms): ACENAPHTHENE CASRN: 83-32-9
Chemical Characteristics
Solubility in Water: Insoluble [1] Half-Life: No data [1,2]
Log Kow: 3.92 [3] Log Koc: 3.85 L/kg organic carbon
Human Health
Oral RfD: 6 x 10"2 mg/kg/day [4] Confidence: Low uncertainty factor = 3000
Critical Effect: Hepatotoxicity
Oral Slope Factor: No data [4] Carcinogenic Classification: -
Wildlife
Partitioning Factors: Partitioning factors for acenaphthene in wildlife were not found in the literature.
Food Chain Multipliers: Food chain multipliers for acenaphthene in wildlife were not found in the
literature.
Aquatic Organisms
Partitioning Factors: The water quality criterion tissue level (WQCTL) for acenaphthene, which is
calculated by multiplying the water quality chronic value (710 |ig/L) by the BCF (389.05), is 276,222
Hg/kg [5].
Food Chain Multipliers: Food chain multipliers for acenaphthene in aquatic organisms were not found
in the literature.
Toxicity/Bioaccumulation Assessment Profile
Most polynuclear aromatic hydrocarbons (PAHs) occur in sediment as complex mixtures. The toxicities
of individual PAHs are additive and increase with increasing Kow, whereas the bioavailabilities of PAHs
decrease as a function of their Kows. The 10-day LCSOs for Eohaustorius estuarius and Leptocheirus
plumulosus in water were 374 |ig/L and 678 |ig/L, respectively [6]. Both amphipod species were exposed
to acenaphthene-spiked sediments with total organic carbon ranging from 0.82 percent to 4.21 percent.
-------
BIOACCUMULATION SUMMARY ACENAPHTHENE
The 10-day LCSOs ranged from 1,630 to 4,330 |ig/g for E. estuarius and from 7,730 |ig/g to >23,500 |ig/g
for L. plumulosus.
Bioaccumulation of low-molecular-weight PAHs including acenaphthene from sediments by
Rhepoxynius abronius (amphipod) and Armandia brevis (polychaete) was similar; however, a large
difference in tissue concentration between these two species was measured for high-molecular-weight
PAHs [12]. Meador et al. [12] concluded that the low-molecular-weight PAHs were available to both
species from interstitial water, while sediment ingestion was a much more important uptake route for the
high-molecular-weight PAHs. The authors also indicated that bioavailability of the high-molecular
weight-PAHs to amphipods was significantly reduced due to their partitioning to dissolved organic
carbon.
-------
Summary of Biological Effects Tissue Concentrations for Acenaphthene
Species:
Taxa
Invertebrates
Nereis succinea,
Polychaete worm
Corbicula fluminea,
Asiatic clam
Concentration, Units in1:
Sediment
umol/g
0.00003
0.001
0.0004
DDL
DDL
Water
umol/L
<0.003
<0.003
Toxicity: Ability to Accumulate2: Source:
Tissue (Sample Type) Log Log
umol/g Effects BCF BAF BSAF Reference Comments3
DDL4 [7] F
DDL
DDL
0.025
DDL
<0.0005 [8] F
<0.0007
Mytilus edulis,
Blue mussel
-0.35
[9]
Crassostrea
virginica,
Eastern oyster
-0.03
[9]
Macoma balthica, 0.00003
Baltic macoma 0.001
0.0004
BDL
BDL
BDL
[7]
Mercenaria
mercenaria,
Northern quahoŁ
-0.44
-0.09
[9]
Mya arenaria,
Softshell
0.09
[9]
-------
Summary of Biological Effects Tissue Concentrations for Acenaphthene
Species:
Taxa
Decapoda
Concentration, Units in1: Toxicity:
Sediment Water Tissue (Sample Type)
umol/g umol/L umol/g Effects
0.034
0.041
0.675
0.001
0.017
0.027
Ability to Accumulate2: Source:
Log Log
BCF BAF BSAF Reference Comments3
[10] F
Homarus
americanus,
American lobster
-0.89
[9]
Fishes
Fundiiliis spp.,
Killifish
-0.33
[9]
Poecilia reticulata,
Guppy
0.14-0.15
0.047
0.027
0.047
0.051
[11]
Lepomis sp.,
Sunfish
0.034
0.041
0.675
0.058
0.038
0.092
[10]
Tautogolabrus
adspersus, Tautog
-1.22
[9]
1 Concentration units based on wet weight unless otherwise noted.
2 BCF = bioconcentration factor, BAF = bioaccumulation factor, BSAF = biota-sediment accumulation factor.
3 L = laboratory study, spiked sediment, single chemical; F = field study, multiple chemical exposure; other unusual study conditions or observations noted.
4 BDL = below detection limit.
-------
BIOACCUMULATION SUMMARY ACENAPHTHENE
References
1. Merck index, 10th ed., 1983, p. 5. (Cited in: USEPA. 1995. Hazardous Substances Data Bank
(HSDB). National Library of Medicine online (TOXNET). U.S. Environmental Protection Agency,
Office of Health and Environmental Assessment, Environmental Criteria and Assessment Office,
Cincinnati, OH. September.)
2. USEPA. 1989. Chemical fate rate constants for SARA section 313 chemicals and Superfund Health
Evaluation Manual chemicals. Prepared by Chemical Hazard Assessment Division, Syracuse
Research Corporation, for U.S. Environmental Protection Agency, Office of Toxic Substances,
Exposure Evaluation Division, Washington, DC, and Environmental Criteria and Assessment Office,
Cincinnati, OH. August 11.
3. Karickhoff, S.W., and J.M. Long. 1995. Internal report on summary of measured, calculated and
recommended log Kow values. Draft. Prepared by U.S. Environmental Protection Agency, Office of
Research and Development, Environmental Research Laboratory-Athens, for E. Southerland, Office
of Water, Office of Science and Technology, Standards and Applied Science Division, Washington,
DC. April 10.
4. USEPA. 1995. Integrated Risk Information System (IRIS). National Library of Medicine online
(TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental
Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. September.
5. Neff, J.M. 1995. Water quality criterion tissue level approach for establishing tissue residue criteria
for chemicals. Report to U.S. Environmental Protection Agency.
6. Swartz, R.C. 1991. Acenaphthene and phenanthrene files. Memorandum to David J. Hansen. June
26, 1991.
7. Foster, G.D., and D.A. Wright. 1988. Unsubstituted polynuclear aromatic hydrocarbons in
sediments, clams, and clam worms from Chesapeake Bay. Mar. Pollut. Bull. 19:459-465.
8. Harrington, J.M., and D.B. Crane. 1994. Presence of target compounds from creosote impregnated
timber in water and tissue of the asiatic clam (Corbicula flumined) near Ryer Island Ferry,
Sacramento River Delta. Report by California Department of Fish and Game Water Pollution Control
Laboratory, Rancho Cordova, CA.
9. NOAA. 1991. The potential for biological effects ofsediment-sorb ed contaminants tested in the
National Status and Trends Program. NOAA Technical Memorandum NOS OMA 52. National
Oceanic and Atmospheric Administration, Office of Oceanography and Marine Assessment,
Rockville, MD.
10. Burkhard, L.P., and B.R. Sheedy. 1995. Evaluation of screening procedures for bioconcentratable
organic chemicals in effluents and sediments. Environ. Toxicol. Chem. 14:697-711.
11. Schoor, W.P., D.E. WiUiams, and N. Takahashi. 1991. The induction of cytochrome P-450-IA1 in
juvenile fish by creosote-contaminated sediment. Arch. Environ. Contam. Toxicol. 20:497-504.
5
-------
BIOACCUMULATION SUMMARY ACENAPHTHENE
12. Meador, J.P., E. Casillas, C.A. Sloan, and U. Varanasi. 1995. Comparative bioaccumulation of
polycyclic aromatic hydrocarbons from sediments by two infaunal invertebrates. Mar. Ecol Prog.
Ser. 123: 107-124.
-------
BIOACCUMULATION SUMMARY AROCLOR 1016
Chemical Category: POLYCHLORINATED BIPHENYLS
Chemical Name (Common Synonyms): Aroclor 1016 CASRN: 1336-36-3
Chemical Characteristics
Solubility in Water: 225-250 ng/L at 25°C [1] Half-Life: No data [2,3]
Log Kow: 5.6 [4] Log Koc: No data [4]
Human Health
Oral RfD: 7 x 10'5 mg/kg-day [5] Confidence: Medium [5]
Critical Effect: PCBs have been shown to cause reproductive failure, birth defects, lesions, tumors,
liver disorders, and death among sensitive species. Their toxicity is further enhanced by their ability
to bioaccumulate and to biomagnify within the food chain due to extremely high lipophilicity [2].
Oral Slope Factor: No data [5] Carcinogenic Classification: Unknown [5]
Wildlife
Partitioning Factors: No partitioning factors for Aroclor 1016 were identified for wildlife.
Food Chain Multipliers: For PCBs as a class the most toxic congeners have been shown to be
selectively accumulated from organisms at one trophic level to the next [6]. At least three studies have
concluded that PCBs have the potential to biomagnify in food webs based on aquatic organisms and
predators that feed primarily on aquatic organisms [7,8,9]. The results from Biddinger and Gloss [7] and
USAGE [9] generally agreed that highly water-insoluble compounds (including PCBs) have the potential
to biomagnify in these types of food webs. Thomann's [10] model also indicated that highly water-
insoluble compounds (log Kow values 5 to 7) showed the greatest potential to biomagnify. A
biomagnification factor of 32 was determined for total PCBs from alewife to herring gull eggs in Lake
Ontario [11]. No specific food chain multipliers were identified for Aroclor 1016.
Aquatic Organisms
Partitioning Factors: No partitioning factors for Aroclor 1016 were identified for aquatic organisms.
Food Chain Multipliers: Polychlorinated biphenyls as a class have been demonstrated to biomagnify
through the food web. Oliver and Niimi [12], studying accumulation of PCBs in various organisms in
the Lake Ontario food web, reported concentrations of total PCBs in phytoplankton, zooplankton, and
several species of fish. Their data indicated a progressive increase in tissue PCB concentrations moving
-------
BIOACCUMULATION SUMMARY AROCLOR 1016
from organisms lower in the food web to top aquatic predators. In a study of PCB accumulation in lake
trout (Salvelinus namaycusK) of Lake Ontario, Rasmussen et al. [13] reported that each trophic level
contributed about a 3.5-fold biomagnification factor to the PCB concentrations in the trout. No specific
food chain multipliers were identified for Aroclor 1016.
Toxicity/Bioaccumulation Assessment Profile
PCBs are a group (209 congeners/isomers) of organic chemicals, based on various substitutions of
chlorine atoms on a basic biphenyl molecule. These manufactured chemicals have been widely used in
various processes and products because of the extreme stability of many isomers, particularly those with
five or more chlorines [14]. A common use of PCBs was as dielectric fluids in capacitors and
transformers. In the United States, Aroclor is the most familiar registered trademark of commercial PCB
formulations. Generally, the first two digits in the Aroclor designation indicate that the mixture contains
biphenyls, and the last two digits give the weight percent of chlorine in the mixture. The exception to this
code is Aroclor 1016, which contains mono- through hexachlorinated homologs with an average chlorine
content of 41 percent [4].
As a result of their stability and their general hydrophobic nature, PCBs released to the environment have
dispersed widely throughout the ecosystem [14]. PCBs are among the most stable organic compounds
known, and chemical degradation rates in the environment are thought to be slow. As a result of their
highly lipophilic nature and low water solubility, PCBs are generally found at low concentrations in water
and at relatively high concentrations in sediment [15]. Individual PCB congeners have different physical
and chemical properties based on the degree of chlorination and position of chlorine substitution,
although differences with degree of chlorination are more significant [15]. Solubilities and octanol-water
partition coefficients for PCB congeners range over several orders of magnitude [16]. Octanol-water
partition coefficients, which are often used as estimators of the potential for bioconcentration, are highest
for the most chlorinated PCB congeners.
Dispersion of PCBs in the aquatic environment is a function of their solubility [15] while PCB mobility
within and sorption to sediment are a function of chlorine substitution pattern and degree of chlorination
[17]. The concentration of PCB s in sediments is a function of the physical characteristics of the sediment,
such as grain size [18,19] and total organic carbon content [18,19,20,21]. Fine sediments typically
contain higher concentrations of PCBs than coarser sediments because of more surface area [15]. Mobility
of PCBs in sediment is generally quite low for the higher chlorinated biphenyls [17]. Therefore, it is
common for the lower chlorinated PCBs to have a greater dispersion from the original point source [15].
Limited mobility and high rates of sedimentation could prevent some PCB congeners in the sediment
from reaching the overlying water via diffusion [17].
The persistence of PCBs in the environment is a result of their general resistance to degradation [16]. The
rate of degradation of PCB congeners by bacteria decreases with increasing degree of chlorination [22];
other structural characteristics of the individual PCBs can affect susceptibility to microbial degradation
to a lesser extent [16]. Photochemical degradation, via reductive dechlorination, is also known to occur
in aquatic environments; the higher chlorinated PCBs appear to be most susceptible to this process [21].
Toxicity of PCB congeners is dependent on the degree of chlorination as well as the position of chlorine
substitution. Lesser chlorinated congeners are more readily absorbed, but are metabolized more rapidly
8
-------
BIOACCUMULATION SUMMARY
AROCLOR 1016
than higher chlorinated congeners [23]. PCB congeners with no chlorine substituted in the ortho (2 and
2') positions but with four or more chlorine atoms at the meta (3 and 3') and para (4 and 4') positions can
assume a planar conformation that can interact with the same receptor as the highly toxic 2,3,7,8-
tetrachlorodibenzo-p-dioxin (TCDD) [24]. Examples of these more toxic, coplanar congeners are
3,3',4,4'-tetrachlorobiphenyl (PCB 77), 3,3',4,4',5-pentachlorobiphenyl (PCB 126), and 3,3',4,4'5,5'-
hexachlorobiphenyl (PCB 169). A method that has been proposed to estimate the relative toxicity of
mixtures is to use toxic equivalency factors (TEFs) [25]. With this method, relative potencies for
individual congeners are calculated by expressing their potency in relation to 2,3,7,8-TCDD. The
following TEFs have been recommended [25,26]:
Congener Class
3,3',4,4',5-PentaCB
3,3',4,4',5,5'-HexaCB
3,3',4,4'-TetraCB
Monoortho coplanar PCBs
Diortho coplanar PCBs
Recommended TEF
0.1
0.05
0.01
0.001
0.00002
Due to the toxicity, high Kow values, and highly persistent nature of many PCBs, they possess a high
potential to bioaccumulate and exert reproductive effects in higher-trophic-level organisms. Aquatic
organisms have a strong tendency to accumulate PCBs from water and food sources. The log
bioconcentration factor for fish is approximately 4.70 [27]. This factor represents the ratio of
concentration in tissue to the ambient water concentration. Aquatic organisms living in association with
PCB-contaminated sediments generally have tissue concentrations equal to or greater than the
concentration of PCB in the sediment [27]. Once taken up by an organism, PCBs partition primarily into
lipid compartments [15]. Thus, differences in PCB concentration between species and between different
tissues within the same species may reflect differences in lipid content [15]. PCB concentrations in
polychaetes and fish have been strongly correlated to their lipid content [28]. Elimination of PCBs from
organisms is related to the characteristics of the specific PCB congeners present. It has been shown that
uptake and depuration rates in mussels are high for lower-chlorinated PCBs and much lower for higher-
chlorinated congeners [29, 30]. In some species, tissue concentrations of PCBs in females can be reduced
during gametogenesis because of PCB transfer to the more lipophilic eggs. Therefore, the transferred
PCBs are eliminated from the female during spawning [31,32]. Fish and other aquatic organisms
biotransform PCBs more slowly than other species, and they appear less able to metabolize, or excrete,
the higher chlorinated PCB congeners [31]. Consequently, fish and other aquatic organisms may
accumulate more of the higher chlorinated PCB congeners than is found in the environment [16].
The acute toxicity of PCBs appears to be relatively low, but results from chronic toxicity tests indicate
that PCB toxicity is directly related to the duration of exposure [1]. Toxic responses have been noted to
occur at concentrations of 0.03 and 0.014 |ig/L in marine and freshwater environments, respectively [1].
The LC50 for grass shrimp exposed to PCBs in marine waters for 4 days was 6.1 to 7.8 ug/L [1 ]. Chronic
toxicity of PCBs presents a serious environmental concern because of their resistance to degradation [33],
although the acute toxicity of PCBs is relatively low compared to that of other chlorinated hydrocarbons.
Sediment contaminated with PCBs has been shown to elicit toxic responses at relatively low
-------
BIOACCUMULATION SUMMARY AROCLOR 1016
concentrations. Sediment bioassays and benthic community studies suggest that chronic effects generally
occur in sediment at total PCB concentrations exceeding 370 |ig/kg [34].
A number of field and laboratory studies provide evidence of chronic sublethal effects on aquatic
organisms at low tissue concentrations [16]. Field and Dexter [16] suggest that a number of marine and
freshwater fish species have experienced chronic toxicity at PCB tissue concentrations of less than 1.0
mg/kg and as low as 0.1 mg/kg. Spies et al. [35] reported an inverse relationship between PCB
concentrations in starry flounder eggs in San Francisco Bay and reproductive success, with an effective
PCB concentration in the ovaries of less than 0.2 mg/kg. Monod [36] also reported a significant
correlation between PCB concentrations in eggs and total egg mortality in Lake Geneva char. PCBs have
also been shown to cause induction of the mixed function oxidase (MFO) system in aquatic animals, with
MFO induction by PCBs at tissue concentrations within the range of environmental exposures [16].
10
-------
Summary of Biological Effects Tissue Concentrations for Aroclor 1016
Species: Concentration, Units in1:
Taxa Sediment Water
Invertebrates
Crassostrea
virginica, Oyster
Limiiliis polyphemus,
Horseshoe Crab
Fishes
Lagodon
rhomboides, Pinfish
Tissue (Sample Type)
4 mg/kg
(whole body)4
32 mg/kg
(whole body)4
95 mg/kg
(whole body)4
11. 2 mg/kg
(whole body)4
3 1.9 mg/kg
(whole body)4
11. 2 mg/kg
(whole body)4
38 mg/kg (muscle)4
30 mg/kg (muscle)4
72 mg/kg
(muscle and skin)4
Toxicity: Ability to Accumulate2:
Log Log
Effects BCF BAF BSAF
Growth,
ED10
Growth, NA
Growth, NA
Growth, NA
Growth, NA
Mortality, NA
Mortality,
ED50
Mortality,
ED50
Mortality,
ED50
Source:
Reference
[38]
[38]
[37]
[37]
[37]
[38]
[38]
[38]
Comments3
L; reduction in shell
growth
L; reduction in shell
growth
L; reduction in shell
growth
L; delayed molting;
less than 50%
molted after 96 days
starting with
T2-stage crabs
L; delayed molting;
less than 50%
molted after 96 days
starting with
Tl -stage crabs
L; less than 50%
mortality starting
with T2-stage crabs
L; 50% mortality
L; 50% mortality
L; 50% mortality
-------
Summary of Biological Effects Tissue Concentrations for Aroclor 1016
Species: Concentration, Units in1:
Taxa Sediment Water Tissue (Sample Type)
48 mg/kg
(muscle and skin)4
205 mg/kg
(whole body)4
106 mg/kg
(whole body)4
38 mg/kg (muscle)4
72 mg/kg
(muscle and skin)4
205 mg/kg
(whole body)4
30 mg/kg (muscle)4
48 mg/kg
(muscle and skin)4
106 mg/kg
(whole body)4
38 mg/kg (muscle)4
72 mg/kg
(muscle and skin)4
Toxicity:
Effects
Mortality,
ED50
Mortality,
ED50
Behavior,
LOED
Behavior,
LOED
Behavior,
LOED
Cellular,
LOED
Cellular,
LOED
Cellular,
LOED
Morphology,
LOED
Morphology,
LOED
Morphology,
LOED
Ability to Accumulate2: Source:
Log Log
BCF BAF BSAF Reference
[38]
[38]
[38]
[38]
[38]
[38]
[38]
[38]
[38]
[38]
[38]
Comments3
L; 50% mortality
L; 50% mortality
L; erratic
swimming, stopped
feeding, loss of
equilibrium
L; erratic
swimming, stopped
feeding, loss of
equilibrium
L; erratic
swimming, stopped
feeding, loss of
equilibrium
L; liver and
pancreatic cell
alterations
L; liver and
pancreatic cell
alterations
L; liver and
pancreatic cell
alterations
L; darkened
coloration
L; darkened
coloration
L; darkened
coloration
-------
Summary of Biological Effects Tissue Concentrations for Aroclor 1016
Species: Concentration, Units in1:
Taxa Sediment Water Tissue (Sample Type)
205 mg/kg
(whole body)4
140 mg/kg (muscle)4
30 mg/kg (muscle)4
180 mg/kg
(muscle and skin)4
48 mg/kg
(muscle and skin)4
2.2 mg/kg
(whole body)4
620 mg/kg
(whole body)4
106 mg/kg (whole
body)4
65 mg/kg
(whole body)4
23 mg/kg (muscle)4
Toxicity: Ability to Accumulate2:
Log Log
Effects BCF BAF BSAF
Mortality,
LOED
Mortality,
LOED
Mortality,
LOED
Mortality,
LOED
Mortality,
LOED
Mortality,
LOED
Mortality,
LOED
Mortality, NA
Cellular,
NOED
Cellular,
NOED
Source:
Reference
[38]
[38]
[38]
[38]
[38]
[38]
[38]
[38]
[38]
[38]
Comments3
L; statistically
significant increase
in mortality
L; statistically
significant increase
in mortality
L; statistically
significant increase
in mortality
L; statistically
significant increase
in mortality
L; 5% mortality in
96 hours
L; statistically
significant increase
in mortality
L; statistically
significant increase
in mortality
L; 18% mortality in
96 hours
L; no incidence of
pathology (liver and
pancreatic
alterations)
L; no incidence of
pathology (liver and
pancreatic
alterations)
-------
Summary of Biological Effects Tissue Concentrations for Aroclor 1016
Species: Concentration, Units in1:
Taxa Sediment Water Tissue (Sample Type)
49 mg/kg
(muscle and skin)4
111 mg/kg
(whole body)4
63 mg/kg (muscle)4
23 mg/kg (muscle)4
76 mg/kg
(muscle and skin)4
49 mg/kg
(muscle and skin)4
21 mg/kg
(whole body)4
170 mg/kg
(whole body)4
111 mg/kg
(whole body)4
Toxicity: Ability to Accumulate2:
Log Log
Effects BCF BAF BSAF
Cellular,
NOED
Mortality,
NOED
Mortality,
NOED
Mortality,
NOED
Mortality,
NOED
Mortality,
NOED
Mortality,
NOED
Mortality,
NOED
Physiological,
NOED
Source:
Reference
[38]
[38]
[38]
[38]
[38]
[38]
[38]
[38]
[38]
Comments3
L; no incidence of
pathology (liver and
pancreatic
alterations)
L; no statistically
significant increase
in mortality
L; no statistically
significant increase
in mortality
L; no statistically
significant increase
in mortality
L; no statistically
significant increase
in mortality
L; no mortality in
96 hours
L; no statistically
significant increase
in mortality
L; no statistically
significant increase
in mortality
L; no reduced
ability to survive
osmotic stress after
exposure
-------
Summary of Biological Effects Tissue Concentrations for Aroclor 1016
Species: Concentration, Units in1:
Taxa Sediment Water Tissue (Sample Type)
23 mg/kg (muscle)4
49 mg/kg
(muscle and skin)4
111 mg/kg
(whole body)4
1.1 mg/kg
(whole body)4
22 mg/kg
(whole body)4
44 mg/kg
(whole body)4
3.8 mg/kg
(whole body)4
42 mg/kg
(whole body)4
1,100 mg/kg
(whole body)4
1,1 00 mg/kg
(whole body)4
200 mg/kg
(whole body)4
Toxicity: Ability to Accumulate2:
Log Log
Effects BCF BAF BSAF
Physiological,
NOED
Physiological,
NOED
Mortality,
LOED
Mortality, NA
Mortality, NA
Mortality,
LOED
Mortality, NA
Behavior,
LOED
Morphology,
LOED
Mortality,
LOED
Mortality,
LOED
Source:
Reference
[38]
[38]
[38]
[38]
[38]
[38]
[38]
[38]
[39]
[39]
[39]
Comments3
L; no reduced
ability to survive
osmotic stress after
exposure
L; no reduced
ability to survive
osmotic stress after
exposure
L; 33% mortality in
96 hours
L; 38% mortality in
96 hours
L; 93% mortality in
96 hours
L; 8% mortality in
96 hours
L; 43% mortality in
96 hours
L; uncoordinated
swimming,
cessation of feeding
L; darkened body
coloration, body
lesions
L; lethal to 86% of
fry in 28 days
L; 88% juvenile
mortality in 28 days
-------
Summary of Biological Effects Tissue Concentrations for Aroclor 1016
Species: Concentration, Units in1:
Taxa Sediment Water Tissue (Sample Type)
l,100mg/kg
(whole body)4
4.2 mg/kg
(whole body)4
17 mg/kg
(whole body)4
66 mg/kg
(whole body)4
0.81 mg/kg (whole
body)4
4.9 mg/kg
(whole body)4
22 mg/kg
(whole body)4
38 mg/kg
(whole body)4
Toxicity: Ability to Accumulate2:
Log Log
Effects BCF BAF BSAF
Development,
NOED
Development,
NOED
Development,
NOED
Mortality,
NOED
Mortality,
NOED
Mortality,
NOED
Mortality,
NOED
Mortality,
NOED
Source:
Reference
[39]
[39]
[39]
[39]
[39]
[39]
[39]
[39]
Comments3
L; no effect on
fertilization success,
survival of embryos
to hatching, and
survival of fry two
weeks after
hatching
L; no effect on
fertilization success,
survival of embryos
to hatching, and
survival of fry two
weeks after
hatching
L; no effect on
fertilization success,
survival of embryos
to hatching, and
survival of fry two
weeks after
hatching
L; no effect on fry
mortality in 28 days
L; no effect on fry
mortality in 28 days
L; no effect on fry
mortality in 28 days
L; no effect on fry
mortality in 28 days
L; no effect on fry
mortality in 28 days
-------
Summary of Biological Effects Tissue Concentrations for Aroclor 1016
Species: Concentration, Units in1:
Taxa Sediment Water Tissue (Sample Type)
5.9 mg/kg
(whole body)4
26 mg/kg
(whole body)4
57 mg/kg
(whole body)4
2.3 mg/kg
(whole body)4
8.9 mg/kg
(whole body)4
1 1 mg/kg
(whole body)4
79 mg/kg
(whole body)4
230 mg/kg
(whole body)4
10 mg/kg
(whole body)4
54 mg/kg
(whole body)4
220 mg/kg
(whole body)4
Toxicity:
Effects
Mortality,
NOED
Mortality,
NOED
Mortality,
NOED
Mortality,
NOED
Mortality,
NOED
Mortality,
NOED
Mortality,
NOED
Mortality,
NOED
Mortality,
NOED
Mortality,
NOED
Mortality,
NOED
Ability to Accumulate2: Source:
Log Log
BCF BAF BSAF Reference
[39]
[39]
[39]
[39]
[39]
[39]
[39]
[39]
[39]
[39]
[39]
Comments3
L; no effect on fry
mortality in 28 days
L; no effect on fry
mortality in 28 days
L; no effect on
juvenile mortality in
28 days
L; no effect on
juvenile mortality in
28 days
L; no effect on
juvenile mortality in
28 days
L; no effect on
juvenile mortality in
28 days
L; no effect on
juvenile mortality in
28 days
L; no effect on
juvenile mortality in
28 days
L; no effect on
juvenile mortality in
28 days
L; no effect on
juvenile mortality in
28 days
L; no effect on adult
mortality in 28 days
-------
Summary of Biological Effects Tissue Concentrations for Aroclor 1016
Species: Concentration, Units in1:
Taxa Sediment Water Tissue (Sample
0.84 mg/kg
(whole body)4
1.5 mg/kg
(whole body)4
12 mg/kg
(whole body)4
46 mg/kg
(whole body)4
100 mg/kg
(whole body)4
5.4 mg/kg
(whole body)4
22 mg/kg
(whole body)4
110 mg/kg
(whole body)4
Toxicity: Ability to Accumulate2:
Log Log
Type) Effects BCF BAF BSAF
Mortality,
NOED
Mortality,
NOED
Mortality,
NOED
Mortality,
NOED
Mortality,
NOED
Mortality,
NOED
Mortality,
NOED
Source:
Reference Comments3
[39] L; no effect on adult
mortality in 28 days
[39] L; no effect on adult
mortality in 28 days
[39] L; no effect on adult
mortality in 28 days
[39] L; no effect on adult
mortality in 28 days
[39] L; no effect on adult
mortality in 28 days
[39] L; no effect on adult
mortality in 28 days
[39] L; no effect on adult
mortality in 28 days
[39]
1 Concentration units based on wet weight unless otherwise noted.
2 BCF = bioconcentration factor, BAF = bioaccumulation factor, BSAF = biota-sediment accumulation factor.
3 L = laboratory study, spiked sediment, single chemical; F = field study, multiple chemical exposure; other unusual study conditions or observations noted.
4 This entry was excerpted directly from the Environmental Residue-Effects Database (ERED, www.wes.army.mil/el/ered, U.S. Army Corps of Engineers and U.S.
Environmental Protection Agency). The original publication was not reviewed, and the reader is strongly urged to consult the publication to confirm the
information presented here.
-------
BIOACCUMULATION SUMMARY AROCLOR 1016
References
1. USEPA. 1980. Ambient water quality criteria document: Poly chlorinated biphenyls. EPA
440/5-80-068. (Cited in USEPA. 1996. Hazardous Substances Data Bank (HSDB). National
Library of Medicine online (TOXNET). U.S. Environmental Protection Agency, Office of Health
and Environmental Assessment, Environmental Criteria and Assessment Office, Cinncinati, OH.
February.)
2. Eisler, R. 1986. Poly chlorinated biphenyl hazards to fish, wildlife, and invertebrates: A synoptic
review. U.S. Fish Wild. Serv. Biol. Rep. 85(1.7).
3. MacKay, D., W.Y. Shiu, and K.C. Ma. 1992. Illustrated handbook of physical-chemical
properties and environmental fate for organic chemicals. Vol. I, Monoaromatic hydrocarbons,
chlorobenzenes, and PCBs. Lewis Publishers, Boca Raton, FL.
4. Agency for Toxic Substances and Disease Registry. 1993. Toxicological profile for
poly chlorinated biphenyls. Prepared by Syracuse Research Corporation. Prepared for U.S.
Department of Health and Human Services, Public Health Service. April 1993.
5. USEPA. 1995. Integrated Risk Information System (IRIS). National Library of Medicine online
(TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental
Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. September.
6. Jones, P.O., J.P. Giesy, T.J. Kubiak, D.A. Verbrugge, J.C. Newstead, J.P. Ludwig, D.E. Tillit,
R. Crawford, N. De Galan, and G.T. Ankley. 1993. Biomagnification of bioassay-derived 2, 3,
7, 8-tetrachlorodibenzo-p-dioxin equivalents. Chemosphere 26:1203-1212.
7. Biddinger, G.R., and S.P. Gloss. 1984. The importance of trophic transfer in the
bioaccumulation of chemical contaminants in aquatic ecosystems. Residue Rev. 91:103-145.
8. Kay, S.H. 1984. Potential for biomagnification of contaminants within marine and freshwater
food webs. Technical Report D-84-7. U.S. Army Corps of Engineers, Waterways Experiment
Station, Vicksburg, MS.
9. USAGE. 1995. Trophic transfer and biomagnification potential of contaminants in aquatic
ecosystems. Environmental Effects of Dredging, Technical Notes EEDP-01-33. U.S. Army
Corps of Engineers, Waterways Experiment Station, Vicksburg, MS.
10. Thomann, R.V. 1989. Bioaccumulation model of organic chemical distribution in aquatic food
chains. Environ. Sci. Technol. 23:699.
11. Hoffman, D.J., C.P. Rice, and T.J. Kubiak. 1996. PCBs and dioxins in birds. In Environmental
contaminants in wildlife, ed. W.N. Beyer, G.H. Heinz, and A.W. Redmon-Horwood, pp. 165-207.
Lewis Publishers, Boca Raton, FL.
19
-------
BIOACCUMULATION SUMMARY AROCLOR 1016
12. Oliver, E.G., and AJ. Niimi. 1988. Trophodynamic analysis of polychlorinated biphenyl
congeners and other chlorinated hydrocarbons in the Lake Ontario ecosystem. Environ. Set
Technol. 22:388-397.
13. Rasmussen, J.B., DJ. Rowan, D.R.S. Lean, and J.H. Carey. 1990. Food chain structure in
Ontario lakes determines PCB levels in lake trout (Salvelinus namaycush) and other pelagic fish.
Can. J. Fish. Aquat. Sci. 47:2030-2038.
14. Rand, G.M., P.O. Wells, and L.S. McCarty. 1995. Chapter 1. Introduction to aquatic toxicology.
In Fundamentals of aquatic toxicology: Effects, environmental fate, and risk assessment, ed. G.
M. Rand, pp. 3-67. Taylor and Francis, Washington, DC.
15. Phillips, DJ.H. 1986. Use of organisms to quantify PCB s in marine and estuarine environments.
In PCBs and the environment, ed. J.S. Waid, pp.127-182. CRC Press, Inc., Boca Raton, FL.
16. Field, L.J., and R.N. Dexter. 1998. A discussion of PCB target levels in aquatic sediments.
Unpublished document. January 11, 1988.
17. Fisher, J.B., R.L. Petty, and W. Lick. 1983. Release of polychlorinated biphenyls from
contaminated lake sediments: Flux and apparent diffusivities of four individual PCBs. Environ.
Pollut. 5B: 121-132.
18. Pavlou, S.P., and R.N. Dexter. 1979. Distribution of polychlorinated biphenyls (PCB) in
estuarine ecosystems: Testing the concept of equilibrium partitioning in the marine environment.
Environ. Sci. Technol. 13:65-71.
19. Lynch, T.R., and H.E. Johnson. 1982. Availability of hexachlorobiphenyl isomer to benthic
amphipods from experimentally contaminated sediments. In Aquatic Toxicology and Hazard
Assessment: Fifth Conference, ASTM STP 766, ed. J.G. Pearson, R.B. Foster, and W.E. Bishop,
pp. 273-287. American Society of Testing and Materials, Philadelphia, PA.
20. Chou, S.F.J., and R.A. Griffin. 1986. Solubility and soil mobility of polychlorinated biphenyls.
In PCBs and the environment, ed. J. S. Waid, Vol. 1, pp. 101-120. CRC Press, Inc., Boca Raton,
FL.
21. Sawhney, B.L. 1986. Chemistry and properties of PCBs in relation to environmental effects.
In PCBs and the environment, ed. J.S. Waid, pp. 47-65. CRC Press, Inc., Boca Raton, FL.
22. Furukawa, K. 1986. Modification of PCBs by bacteria and other microorganisms. In PCBs and
the environment, ed. J. S. Waid, Vol. 2, pp. 89-100. CRC Press, Inc., Boca Raton, FL.
23. Bolger, M. 1993. Overview of PCB toxicology. Proceedings of the U.S. Environmental
Protection Agency's National Technical Workshop "PCBs in Fish Tissue," EPA/823-R-93-
003.U.S. Environmental Protection Agency, Office of Water, Washington, DC, May 10-11,
1993, pp. 37-53.
20
-------
BIOACCUMULATION SUMMARY AROCLOR 1016
24. Erickson, M.D. 1993. Introduction to PCBs and analytical methods. EPA/823-R-93-003.
Proceedings of the U.S. Environmental Protection Agency's National Technical Workshop
"PCBs in Fish Tissue," U.S. Environmental Protection Agency, Office of Water, Washington,
DC, May 10-11, pp. 3-9.
25. Safe, S. 1990. Polychlorinated biphenyls (PCBs), dibenzo-p-dioxins (PCDDs), dibenzofurans
(PCDFs), and related compounds: Environmental and mechanistic considerations which support
the development of toxic equivalency factors (TEFs). Critical Reviews in Toxicology 21(1):51-
26. USEPA. 1991. Workshop report on toxicity equivalency factors for poly chlorinated bipheny I
congeners. EPA/625/3-91/020. U.S. Environmental Protection Agency. (Eastern Research
Group, Inc., Arlington, MA.)
27. Neff, J.M. 1984. Bioaccumulation of organic micropollutants from sediments and suspended
particulates by aquatic animals. Fres. Z. Anal. Chem. 319:132-136.
28. Shaw, G. R., and D. W. Connell. 1982. Factors influencing concentrations of polychlorinated
biphenyls in organisms from an estuarine ecosystem. Aust. J. Mar. Freshw. Res. 33:1057-1070.
29. Tanabe, S., R. Tatsukawa, and DJ.H. Phillips. 1987. Mussels as bioindicators of PCB pollution:
A case study on uptake and release of PCB isomers and congeners in green-lipped mussels
(Perna viridis) in Hong Kong waters. Environ. Pollut. 47:41-62.
30. Pruell, R. J., J. L. Lake, W. R. Davis, and J. G. Quinn. 1986. Uptake and depuration of organic
contaminants by blue mussels (Mytilus edulis) exposed to environmentally contaminated
sediments. Mar. Biol. 91:497-508.
31. Lech, J.J., and R.E. Peterson. 1983. Biotransformation and persistence of polychlorinated
biphenyls (PCBs) in fish. In PCBs: Human and environmental hazards, ed. F.M. D'ltri and M.A.
Kamrin, pp. 187-201. Ann Arbor Science Publishers, Inc., Ann Arbor, MI.
32. Stout, V.F. 1986. What is happening to PCBs? Elements of effective environmental monitoring
as illustrated by an analysis of PCB trends in terrestrial and aquatic organisms. In PCBs and the
environment, ed. J.S. Waid. CRC Press, Inc., Boca Raton, FL.
33. Mearns, A.J., M. Malta, G. Shigenaka, D. MacDonald, M. Buchman, H. Harris, J. Golas, and G.
Lauenstein. 1991. Contaminant trends in the Southern California Bight: Inventory and
assessment. Technical Memorandum NOAA ORCA 62. National Oceanic and Atmospheric
Administration. Seattle, WA.
34. 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. NOAA Tech. Memo. NOS
OMA 52. National Oceanic and Atmospheric Administration, Seattle, WA.
21
-------
BIOACCUMULATION SUMMARY AROCLOR 1016
35. Spies, R. B., D. W. Rice, Jr., P. A. Montagna, and R. R. Ireland. 1985. Reproductive success,
xenobiotic contaminants and hepatic mixed-function oxidase (MFO) activity in Platichthys
stellatus populations from San Francisco Bay. Mar. Environ. Res. 17:117-121.
36. Monod, G. 1985. Egg mortality of Lake Geneva char (Salvelinus alpinus) contaminated by PCB
and DDT derivatives. Bull. Environ. Contain. Toxicol. 35:531-536.
37. Neff, J. M., and C.S. Giam. 1977. Effects of Aroclor 1016 and Halowax 1099 to juvenile
horsehoe crabs Limulus polyphemus. Reference Not Available.
38. Hansen, D.J., P.R. Parrish, and J. Forester. 1974. Aroclor 1016: Toxicity to and uptake by
estuarine animals. Environ. Res. 7:363-373.
39. Hansen, D.J., S.C. Schimmel, and J. Forester. 1975. Effects of Aroclor 1016 on embryos, fry,
juveniles, and adults of sheepshead minnows (Cyprinodon variegatus). Trans. Amer. Fish. Soc.
104:584-588.
22
-------
BIOACCUMULATION SUMMARY AROCLOR 1242
Chemical Category: POLYCHLORINATED BIPHENYLS
Chemical Name (Common Synonyms): Aroclor 1242 CASRN: 53469-21-9
Chemical Characteristics
Solubility in Water: 240 ng/L at 25°C [1] Half-Life: No data [2,3]
Log Kow: 5.6 [4] Log Koc: No data [4]
Human Health
Oral RfD: No data [5] Confidence: —
Critical Effect: PCBs have been shown to cause reproductive failure, birth defects, lesions, tumors,
liver disorders, and death among sensitive species. Their toxicity is further enhanced by their ability
to bioaccumulate and to biomagnify within the food chain due to extremely high lipophilicity [2].
Oral Slope Factor: No data [5] Carcinogenic Classification: A2 [5]
Wildlife
Partitioning Factors: No partitioning factors for Aroclor 1242 were identified for wildlife.
Food Chain Multipliers: For PCBs as a class the most toxic congeners have been shown to be
selectively accumulated from organisms at one trophic level to the next [6]. At least three studies have
concluded that PCBs have the potential to biomagnify in food webs based on aquatic organisms and
predators that feed primarily on aquatic organisms [7,8,9]. The results from Biddinger and Gloss [7] and
USAGE [9] generally agreed that highly water-insoluble compounds (including PCBs) have the potential
to biomagnify in these types of food webs. Thomann's [10] model also indicated that highly water-
insoluble compounds (log Kow values 5 to 7) showed the greatest potential to biomagnify. A
biomagnification factor of 32 was determined for total PCBs from alewife to herring gull eggs in Lake
Ontario [11]. No specific food chain multipliers were identified for Aroclor 1242.
Aquatic Organisms
Partitioning Factors: No partitioning factors for Aroclor 1242 were identified for aquatic
organisms.
Food Chain Multipliers: Polychlorinated biphenyls as a class have been demonstrated to biomagnify
through the food web. Oliver and Niimi [12], studying accumulation of PCBs in various organisms in
the Lake Ontario food web, reported concentrations of total PCBs in phytoplankton, zooplankton, and
several species of fish. Their data indicated a progressive increase in tissue PCB concentrations moving
23
-------
BIOACCUMULATION SUMMARY AROCLOR 1242
from organisms lower in the food web to top aquatic predators. In a study of PCB accumulation in lake
trout (Salvelinus namaycush) of Lake Ontario, Rasmussen et al. [13] reported that each trophic level
contributed about a 3.5-fold biomagnification factor to the PCB concentrations in the trout. No specific
food chain multipliers were identified for Aroclor 1242.
Toxicity/Bioaccumulation Assessment Profile
PCBs are a group (209 congeners/isomers) of organic chemicals, based on various substitutions of
chlorine atoms on a basic biphenyl molecule. These manufactured chemicals have been widely used in
various processes and products because of the extreme stability of many isomers, particularly those with
five or more chlorines [14]. A common use of PCBs was as dielectric fluids in capacitors and
transformers. In the United States, Aroclor is the most familiar registered trademark of commercial PCB
formulations. Generally, the first two digits in the Aroclor designation indicate that the mixture contains
biphenyls, and the last two digits give the weight percent of chlorine in the mixture (e.g., Aroclor 1242
contains biphenyls with approximately 42 percent chlorine).
As a result of their stability and their general hydrophobic nature, PCBs released to the environment have
dispersed widely throughout the ecosystem [14]. PCBs are among the most stable organic compounds
known, and chemical degradation rates in the environment are thought to be slow. As a result of their
highly lipophilic nature and low water solubility, PCBs are generally found at low concentrations in water
and at relatively high concentrations in sediment [15]. Individual PCB congeners have different physical
and chemical properties based on the degree of chlorination and position of chlorine substitution,
although differences with degree of chlorination are more significant [15]. Solubilities and octanol-water
partition coefficients for PCB congeners range over several orders of magnitude [16]. Octanol-water
partition coefficients, which are often used as estimators of the potential for bioconcentration, are highest
for the most chlorinated PCB congeners.
Dispersion of PCBs in the aquatic environment is a function of their solubility [15] while PCB mobility
within and sorption to sediment are a function of chlorine substitution pattern and degree of chlorination
[17]. The concentration of PCB s in sediments is a function of the physical characteristics of the sediment,
such as grain size [18,19] and total organic carbon content [18,19,20,21]. Fine sediments typically
contain higher concentrations of PCBs than coarser sediments because of more surface area [15]. Mobility
of PCBs in sediment is generally quite low for the higher chlorinated biphenyls [17]. Therefore, it is
common for the lower chlorinated PCBs to have a greater dispersion from the original point source [15].
Limited mobility and high rates of sedimentation could prevent some PCB congeners in the sediment
from reaching the overlying water via diffusion [17].
The persistence of PCBs in the environment is a result of their general resistance to degradation [16]. The
rate of degradation of PCB congeners by bacteria decreases with increasing degree of chlorination [22];
other structural characteristics of the individual PCBs can affect susceptibility to microbial degradation
to a lesser extent [16]. Photochemical degradation, via reductive dechlorination, is also known to occur
in aquatic environments; the higher chlorinated PCBs appear to be most susceptible to this process [21].
Toxicity of PCB congeners is dependent on the degree of chlorination as well as the position of chlorine
substitution. Lesser chlorinated congeners are more readily absorbed, but are metabolized more rapidly
than higher chlorinated congeners [23]. PCB congeners with no chlorine substituted in the ortho (2 and
24
-------
BIOACCUMULATION SUMMARY
AROCLOR 1242
2') positions but with four or more chlorine atoms at the meta (3 and 3') and para (4 and 4') positions
can assume a planar conformation that can interact with the same receptor as the highly toxic 2,3,7,8-
tetrachlorodibenzo-p-dioxin (TCDD) [24]. Examples of these more toxic, coplanar congeners are
3,3',4,4'-tetrachlorobiphenyl (PCB 77), 3,3',4,4',5-pentachlorobiphenyl (PCB 126), and 3,3',4,4',5,5'-
hexachlorobiphenyl (PCB 169). A method that has been proposed to estimate the relative toxicity of
mixtures is to use toxic equivalency factors (TEFs) [25]. With this method, relative potencies for
individual congeners are calculated by expressing their potency in relation to 2,3,7,8-TCDD. The
following TEFs have been recommended [25,26]:
Congener Class
3,3',4,4',5-PentaCB
3,3',4,4',5,5'-HexaCB
3,3'4,4'-TetraCB
Monoortho coplanar PCBs
Diortho coplanar PCBs
Recommended TEF
0.1
0.05
0.01
0.001
0.00002
Due to the toxicity, high Kow values, and highly persistent nature of many PCBs, they possess a high
potential to bioaccumulate and exert reproductive effects in higher-trophic-level organisms. Aquatic
organisms have a strong tendency to accumulate PCBs from water and food sources. The log
bioconcentration factor for fish is approximately 4.70 [27]. This factor represents the ratio of
concentration in tissue to the ambient water concentration. Aquatic organisms living in association with
PCB-contaminated sediments generally have tissue concentrations equal to or greater than the
concentration of PCB in the sediment [27]. Once taken up by an organism, PCBs partition primarily into
lipid compartments [15]. Thus, differences in PCB concentration between species and between different
tissues within the same species may reflect differences in lipid content [15]. PCB concentrations in
polychaetes and fish have been strongly correlated to their lipid content [28]. Elimination of PCBs from
organisms is related to the characteristics of the specific PCB congeners present. It has been shown that
uptake and depuration rates in mussels are high for lower-chlorinated PCBs and much lower for higher-
chlorinated congeners [29, 30]. In some species, tissue concentrations of PCBs in females can be reduced
during gametogenesis because of PCB transfer to the more lipophilic eggs. Therefore, the transferred
PCBs are eliminated from the female during spawning [31,32]. Fish and other aquatic organisms
biotransform PCBs more slowly than other species, and they appear less able to metabolize, or excrete,
the higher chlorinated PCB congeners [31]. Consequently, fish and other aquatic organisms may
accumulate more of the higher chlorinated PCB congeners than is found in the environment [16].
The acute toxicity of PCBs appears to be relatively low, but results from chronic toxicity tests indicate
that PCB toxicity is directly related to the duration of exposure [1]. Toxic responses have been noted to
occur at concentrations of 0.03 and 0.014 ug/L in marine and freshwater environments, respectively [1].
The LC50 for grass shrimp exposed to PCBs in marine waters for 4 days was 6.1 to 7.8 |ig/L [1 ]. Chronic
toxicity of PCBs presents a serious environmental concern because of their resistance to degradation [33],
although the acute toxicity of PCBs is relatively low compared to that of other chlorinated hydrocarbons.
Sediment contaminated with PCBs has been shown to elicit toxic responses at relatively low
concentrations. Sediment bioassays and benthic community studies suggest that chronic effects generally
occur in sediment at total PCB concentrations exceeding 370 |ig/kg [34].
25
-------
BIOACCUMULATION SUMMARY AROCLOR 1242
A number of field and laboratory studies provide evidence of chronic sublethal effects on aquatic
organisms at low tissue concentrations [16]. Field and Dexter [16] suggest that a number of marine and
freshwater fish species have experienced chronic toxicity at PCB tissue concentrations of less than 1.0
mg/kg and as low as 0.1 mg/kg. Spies et al. [35] reported an inverse relationship between PCB
concentrations in starry flounder eggs in San Francisco Bay and reproductive success, with an effective
PCB concentration in the ovaries of less than 0.2 mg/kg. Monod [36] also reported a significant
correlation between PCB concentrations in eggs and total egg mortality in Lake Geneva char. PCBs have
also been shown to cause induction of the mixed function oxidase (MFO) system in aquatic animals, with
MFO induction by PCBs at tissue concentrations within the range of environmental exposures [16].
26
-------
Summary of Biological Effects Tissue Concentrations for Aroclor 1242
Species: Concentration, Units in1:
Taxa Sediment Water
Invertebrates
Hyalella azteca,
Amphipod -
freshwater
Fishes
Oncorhynchus
mykiss;
Rainbow trout
Salmo salar,
Atlantic salmon
Ictalurus punctatus,
Channel catfish
Tissue (Sample Type)
30 mg/kg
(whole body)4
1.3 mg/kg
(whole body)4
0.54 mg/kg (eggs)4
3.8 mg/kg (brain)4
14.6 mg/kg (kidney)4
11. 9 mg/kg
(muscle and skin)4
14.3 mg/kg
(whole body)4
3.8 mg/kg (brain)4
Toxicity:
Effects
Mortality,
NOED
Mortality,
LOED
Mortality,
ED75
Growth,
LOED
Growth,
LOED
Growth,
LOED
Growth,
LOED
Morphology;
LOED
Ability to Accumulate2: Source:
Log Log
BCF BAF BSAF Reference
[38]
[39]
[40]
[41]
[41]
[41]
[41]
[41]
Comments3
L; radiolabeled
compounds;
Exp_conc = 3-100
L; 10% mortality
L; estimated wet
weight; eggs
obtained from
hatchery stock. 41
|ig/g lipid
L; 40% reduction in
mean weight
L; 40% reduction in
mean weight
L; 40% reduction in
mean weight
L; 40% reduction in
mean weight
L; increased size of
liver
-------
Summary of Biological Effects Tissue Concentrations for Aroclor 1242
Species:
Taxa
Concentration, Units in1: Toxicity: Ability to Accumulate2:
Sediment Water Tissue (Sample Type) Effects
Log Log
BCF BAF BSAF
Source:
Reference Comments3
14.6 mg/kg (kidney)4 Morphology;
LOED
11.9 mg/kg Morphology;
(muscle and skin)4 LOED
14.3 mg/kg
(whole body)4
11.9 mg/kg
(muscle and skin)4
11.4 mg/kg
(muscle and skin)4
Morphology;
LOED
1.16 mg/kg (blood)4 Cellular,
NOED
3.8 mg/kg (brain)4 Cellular,
NOED
14.6 mg/kg (kidney)4 Cellular,
NOED
11.7 mg/kg (kidney)4 Cellular,
NOED
Cellular,
NOED
Cellular,
NOED
[41] L; increased size of
liver
[41] L; increased size of
liver
[41] L; increased size of
liver
[41] L; no effect on
histopathology of
liver, brain, kidney
[41] L; no effect on
histopathology of
liver, brain, kidney
[41] L; no effect on
histopathology of
liver, brain, kidney
[41] L; no effect on
histopathology of
liver, brain, kidney
[41] L; no effect on
histopathology of
liver, brain, kidney
[41] L; no effect on
histopathology of
liver, brain, kidney
-------
Summary of Biological Effects Tissue Concentrations for Aroclor 1242
Species: Concentration, Units in1:
Taxa Sediment Water Tissue (Sample Type)
8.23 mg/kg (ovary)4
5.76 mg/kg (testis)4
14.3 mg/kg
(whole body)4
10.9 mg/kg
(whole body)4
1.1 6 mg/kg (blood)4
3.8 mg/kg (brain)4
14.6 mg/kg (kidney)4
1 1 .7 mg/kg (kidney)4
11. 9 mg/kg
(muscle and skin)4
1 1 .4 mg/kg
(muscle and skin)4
Toxicity: Ability to Accumulate2:
Log Log
Effects BCF BAF BSAF
Cellular, NOED
Cellular,
NOED
Cellular,
NOED
Cellular,
NOED
Mortality,
NOED
Mortality,
NOED
Mortality,
NOED
Mortality,
NOED
Mortality,
NOED
Mortality,
NOED
Source:
Reference
[41]
[41]
[41]
[41]
[41]
[41]
[41]
[41]
[41]
[41]
Comments3
L; no effect on
histopathology of
liver, brain, kidney
L; no effect on
histopathology of
liver, brain, kidney
L; no effect on
histopathology of
liver, brain, kidney
L; no effect on
histopathology of
liver, brain, kidney
L; no effect on
mortality
L; no effect on
mortality
L; no effect on
mortality
L; no effect on
mortality
L; no effect on
mortality
L; no effect on
mortality
-------
Summary of Biological Effects Tissue Concentrations for Aroclor 1242
Species:
Taxa
Concentration, Units in1:
Sediment Water Tissue (Sample Type)
8.23 mg/kg (ovary)4
5.76 mg/kg (testis)4
14.3 mg/kg
(whole body)4
10.9 mg/kg
(whole body)4
Toxicity:
Effects
Mortality,
NOED
Mortality,
NOED
Mortality,
NOED
Mortality,
NOED
Ability to Accumulate2: Source:
Log Log
BCF BAF BSAF Reference
[41]
[41]
[41]
[41]
Comments3
L; no effect
mortality
L; no effect
mortality
L; no effect
mortality
L; no effect
mortality
on
on
on
on
Concentration units based on wet weight unless otherwise noted.
BCF = bioconcentration factor, BAF = bioaccumulation factor, BSAF = biota-sediment accumulation factor.
L = laboratory study, spiked sediment, single chemical; F = field study, multiple chemical exposure; other unusual study conditions or observations noted.
This entry was excerpted directly from the Environmental Residue-Effects Database (ERED, www.wes.army.mil/el/ered, U.S. Army Corps of Engineers and U.S.
Environmental Protection Agency). The original publication was not reviewed, and the reader is strongly urged to consult the publication to confirm the information
presented here.
-------
BIOACCUMULATION SUMMARY AROCLOR 1242
References
1. USEPA. 1980. Ambient water quality criteria document: Poly chlorinated biphenyls. EPA
440/5-80-068. (Cited in USEPA. 1996. Hazardous Substances Data Bank (HSDB). National
Library of Medicine online (TOXNET). U.S. Environmental Protection Agency, Office of Health
and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH.
February.)
2. Eisler, R. 1986. Poly chlorinated biphenyl hazards to fish, wildlife, and invertebrates: A synoptic
review. U.S. Fish Wildl. Serv. Biol. Rep. 85(1.7).
3. MacKay, D., W.Y. Shiu, and K.C. Ma. 1992. Illustrated handbook of physical-chemical
properties and environmental fate for organic chemicals. Vol. I, Monoaromatic hydrocarbons,
chlorobenzenes, and PCBs. Lewis Publishers, Boca Raton, FL.
4. Agency for Toxic Substances and Disease Registry. 1993. Toxicological profile for
poly chlorinated biphenyls. Prepared by Syracuse Research Corporation. Prepared for U.S.
Department of Health and Human Services, Public Health Service. April 1993.
5. USEPA. 1995. Integrated Risk Information System (IRIS). National Library of Medicine online
(TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental
Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. September.
6. Jones, P.O., J.P. Giesy, T.J. Kubiak, D.A. Verbrugge, J.C. Newstead, J.P. Ludwig, D.E. Tillit,
R. Crawford, N. De Galan, and G.T. Ankley. 1993. Biomagnification of bioassay-derived 2, 3,
7, 8-tetrachlorodibenzo-p-dioxin equivalents. Chemosphere 26:1203-1212.
7. Biddinger, G.R., and S.P. Gloss. 1984. The importance of trophic transfer in the
bioaccumulation of chemical contaminants in aquatic ecosystems. Residue Rev. 91:103-145.
8. Kay, S.H. 1984. Potential for biomagnification of contaminants within marine and freshwater
food webs. Technical Report D-84-7. U.S. Army Corps of Engineers, Waterways Experiment
Station, Vicksburg, MS.
9. USAGE. 1995. Trophic transfer and biomagnification potential of contaminants in aquatic
ecosystems. Environmental Effects of Dredging, Technical Notes EEDP-01-33. U.S. Army
Corps of Engineers, Waterways Experiment Station, Vicksburg, MS.
10. Thomann, R.V. 1989. Bioaccumulation model of organic chemical distribution in aquatic food
chains. Environ. Sci. Technol. 23:699.
11. Hoffman, D.J., C.P. Rice, and T.J. Kubiak. 1996. PCBs and dioxins in birds. In Environmental
contaminants in wildlife, ed. W.N. Beyer, G.H. Heinz, and A.W. Redmon-Horwood, pp. 165-207.
Lewis Publishers, Boca Raton, FL.
31
-------
BIOACCUMULATION SUMMARY AROCLOR 1242
12. Oliver, E.G., and AJ. Niimi. 1988. Trophodynamic analysis of polychlorinated biphenyl
congeners and other chlorinated hydrocarbons in the Lake Ontario ecosystem. Environ. Set
Technol. 22:388-397.
13. Rasmussen, J.B., DJ. Rowan, D.R.S. Lean, and J.H. Carey. 1990. Food chain structure in
Ontario lakes determines PCB levels in lake trout (Salvelinus namaycush) and other pelagic fish.
Can. J. Fish. Aquat. Sci. 47:2030-2038.
14. Rand, G.M., P.O. Wells, and L.S. McCarty. 1995. Chapter 1. Introduction to aquatic toxicology.
In Fundamentals of aquatic toxicology: Effects, environmental fate, and risk assessment, ed. G.
M. Rand, pp. 3-67. Taylor and Francis, Washington, DC.
15. Phillips, DJ.H. 1986. Use of organisms to quantify PCB s in marine and estuarine environments.
In PCBs and the environment, ed. J.S. Waid, pp.127-182. CRC Press, Inc., Boca Raton, FL.
16. Field, L.J., and R.N. Dexter. 1998. A discussion of PCB target levels in aquatic sediments.
Unpublished document. January 11, 1988.
17. Fisher, J.B., R.L. Petty, and W. Lick. 1983. Release of polychlorinated biphenyls from
contaminated lake sediments: Flux and apparent diffusivities of four individual PCBs. Environ.
Pollut. 5B: 121-132.
18. Pavlou, S.P., and R.N. Dexter. 1979. Distribution of polychlorinated biphenyls (PCB) in
estuarine ecosystems: Testing the concept of equilibrium partitioning in the marine environment.
Environ. Sci. Technol. 13:65-71.
19. Lynch, T.R., and H.E. Johnson. 1982. Availability of hexachlorobiphenyl isomer to benthic
amphipods from experimentally contaminated sediments. In Aquatic Toxicology and Hazard
Assessment: Fifth Conference, ASTM STP 766, ed. J.G. Pearson, R.B. Foster, and W.E. Bishop,
pp. 273-287. American Society of Testing and Materials, Philadelphia, PA.
20. Chou, S.F.J., and R.A. Griffin. 1986. Solubility and soil mobility of polychlorinated biphenyls.
In PCBs and the environment, ed. J. S. Waid, Vol. 1, pp. 101-120. CRC Press, Inc., Boca Raton,
FL.
21. Sawhney, B.L. 1986. Chemistry and properties of PCBs in relation to environmental effects.
In PCBs and the environment, ed. J.S. Waid, pp. 47-65. CRC Press, Inc., Boca Raton, FL.
22. Furukawa, K. 1986. Modification of PCBs by bacteria and other microorganisms. In PCBs and
the environment, ed. J. S. Waid, Vol. 2, pp. 89-100. CRC Press, Inc., Boca Raton, FL.
23. Bolger, M. 1993. Overview of PCB toxicology. Proceedings of the U.S. Environmental
Protection Agency's National Technical Workshop "PCBs in Fish Tissue," EPA/823-R-93-003.
U.S. Environmental Protection Agency, Office of Water, Washington, DC, May 10-11, 1993,
pp. 37-53.
32
-------
BIOACCUMULATION SUMMARY AROCLOR 1242
24. Erickson, M.D. 1993. Introduction to PCBs and analytical methods. Proceedings of the U.S.
Environmental Protection Agency's National Technical Workshop "PCBs in Fish Tissue,"
EPA/823-R-93-003. U.S. Environmental Protection Agency, Office of Water, Washington, DC,
May 10-11, 1993, pp. 3-9.
25. Safe, S. 1990. Polychlorinated biphenyls (PCBs), dibenzo-p-dioxins (PCDDs), dibenzofurans
(PCDFs), and related compounds: Environmental and mechanistic considerations which support
the development of toxic equivalency factors (TEFs). Crit. Rev. Toxicol 21(l):51-88.
26. USEPA. 1991. Workshop report on toxicity equivalency factors for poly chlorinated bipheny I
congeners. EPA/625/3-91/020. U.S. Environmental Protection Agency. (Eastern Research
Group, Inc., Arlington, MA.)
27. Neff, J.M. 1984. Bioaccumulation of organic micropollutants from sediments and suspended
particulates by aquatic animals. Fres. Z. Anal. Chem. 319:132-136.
28. Shaw, G.R., and D. W. Connell. 1982. Factors influencing concentrations of polychlorinated
biphenyls in organisms from an estuarine ecosystem. Aust. J. Mar. Freshw. Res. 33:1057-1070.
29. Tanabe, S., R. Tatsukawa, and DJ.H. Phillips. 1987. Mussels as bioindicators of PCB pollution:
A case study on uptake and release of PCB isomers and congeners in green-lipped mussels
(Perna viridis) in Hong Kong waters. Environ. Pollut. 47:41-62.
30. Pruell, R. J., J. L. Lake, W. R. Davis, and J. G. Quinn. 1986. Uptake and depuration of organic
contaminants by blue mussels (Mytilus edulis) exposed to environmentally contaminated
sediments. Mar. Biol. 91:497-508.
31. Lech, J.J., and R.E. Peterson. 1983. Biotransformation and persistence of polychlorinated
biphenyls (PCBs) in fish. In PCBs: Human and environmental hazards, ed. P.M. D'ltri and M.A.
Kamrin, pp. 187-201. Ann Arbor Science Publishers, Inc., Ann Arbor, MI.
32. Stout, V.F. 1986. What is happening to PCBs? Elements of effective environmental monitoring
as illustrated by an analysis of PCB trends in terrestrial and aquatic organisms. In PCBs and the
environment, ed. J.S. Waid. CRC Press, Inc., Boca Raton, FL.
33. Mearns, A.J., M. Malta, G. Shigenaka, D. MacDonald, M. Buchman, H. Harris, J. Golas, and G.
Lauenstein. 1991. Contaminant trends in the Southern California Bight: Inventory and
assessment. Technical Memorandum NOAA ORCA 62. National Oceanic and Atmospheric
Administration. Seattle, WA.
34. 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. NOAA Tech. Memo. NOS
OMA 52. National Oceanic and Atmospheric Administration, Seattle, WA.
35. Spies, R. B., D. W. Rice, Jr., P. A. Montagna, and R. R. Ireland. 1985. Reproductive success,
xenobiotic contaminants and hepatic mixed-function oxidase (MFO) activity in Platichthys
stellatus populations from San Francisco Bay. Mar. Environ. Res. 17:117-121.
33
-------
BIOACCUMULATION SUMMARY AROCLOR 1242
36. Monod, G. 1985. Egg mortality of Lake Geneva char (Salvelinus alpinus) contaminated by PCB
and DDT derivatives. Bull Environ. Contain. Toxicol. 35:531-536.
37. Toxscan, Inc. 1990. Technical evaluation of environmental impact potential for propose d ocean
disposal of dredged material from Berth 256 Fire Station 111 in Los Angeles Harbor. Toxscan,
Inc., Marine Bioassay Laboratories Division, Watsonville, CA. Prepared for the Port of Los
Angeles, San Pedro, CA.
38. Borgmann, U., N.P. Norwood, and K.M. Ralph. 1990. Chronic toxicity and bioaccumulation of
2,5,2',5'- and 3,4,3',4'-tetrachlorobiphenyl and Aroclor 1242 in the amphipod Hyalella azteca.
Arch. Environ. Contain. Toxicol., 19:558-564
39. Hogan, J.W., and J.L. Brauhn. 1975. Abnormal rainbow trout fry from eggs containing high
residues of a PCB (Aroclor 1242). Progress. Fish Cult. 37 (4):229-230
40. Zitko, V., and R.L. Saunders. 1979. Effect of PCBs and other organochlorine compounds on the
hatchability of Atlantic salmon (Salmo solar) eggs. Bull. Environm. Contain. Toxicol 21:
125-130.
41. Hansen, L.G., W.B. Wiekhorst, and J. Simon. 1976. Effects of dietary Aroclor 1242 on channel
catfish (Ictalurus punctatus) and the selective accumulation of PCB components. /. Fish. Res.
Bd. Can. 33:1343-1352.
34
-------
BIOACCUMULATION SUMMARY AROCLOR 1248
Chemical Category: POLYCHLORINATED BIPHENYLS
Chemical Name (Common Synonyms): Aroclor 1248 CASRN: 12672-29-6
Chemical Characteristics
Solubility in Water: 54 ng/Lat 25°C [1] Half-Life: No data [2,3]
Log Kow: 6.2 [4] Log Koc: No data [4]
Human Health
Oral RfD: Inadequate data to calculate [5] Confidence: —
Critical Effect: PCBs have been shown to cause reproductive failure, birth defects, lesions, tumors, liver
disorders, and death among sensitive species. Their toxicity is further enhanced by their ability to
bioaccumulate and to biomagnify within the food chain due to extremely high lipophilicity [2]. —
Oral Slope Factor: No data [5] Carcinogenic Classification: A2 [5]
Wildlife
Partitioning Factors: No partitioning factors for Aroclor 1248 were identified for wildlife.
Food Chain Multipliers: For PCBs as a class the most toxic congeners have been shown to be
selectively accumulated from organisms at one trophic level to the next [6]. At least three studies have
concluded that PCBs have the potential to biomagnify in food webs based on aquatic organisms and
predators that feed primarily on aquatic organisms [7,8,9]. The results from Biddinger and Gloss [7] and
USAGE [9] generally agreed that highly water-insoluble compounds (including PCBs) have the potential
to biomagnify in these types of food webs. Thomann's [10] model also indicated that highly water-
insoluble compounds (log Kow values 5 to 7) showed the greatest potential to biomagnify. A
biomagnification factor of 32 was determined for total PCBs from alewife to herring gull eggs in Lake
Ontario [11]. No specific food chain multipliers were identified for Aroclor 1248.
Aquatic Organisms
Partitioning Factors: No partitioning factors for Aroclor 1248 were identified for aquatic organisms.
Food Chain Multipliers: Polychlorinated biphenyls as a class have been demonstrated to biomagnify
through the food web. Oliver and Niimi [12], studying accumulation of PCBs in various organisms in
the Lake Ontario food web, reported concentrations of total PCBs in phytoplankton, zooplankton, and
several species of fish. Their data indicated a progressive increase in tissue PCB concentrations moving
from organisms lower in the food web to top aquatic predators. In a study of PCB accumulation in lake
35
-------
BIOACCUMULATION SUMMARY AROCLOR 1248
trout (Salvelinus namaycush) of Lake Ontario, Rasmussen et al. [13] reported that each trophic level
contributed about a 3.5-fold biomagnification factor to the PCB concentrations in the trout. No specific
food chain multipliers were identified for Aroclor 1248.
Toxicity/Bioaccumulation Assessment Profile
PCBs are a group (209 congeners/isomers) of organic chemicals, based on various substitutions of
chlorine atoms on a basic biphenyl molecule. These manufactured chemicals have been widely used in
various processes and products because of the extreme stability of many isomers, particularly those with
five or more chlorines [14]. A common use of PCBs was as dielectric fluids in capacitors and
transformers. In the United States, Aroclor is the most familiar registered trademark of commercial PCB
formulations. Generally, the first two digits in the Aroclor designation indicate that the mixture contains
biphenyls, and the last two digits give the weight percent of chlorine in the mixture (e.g., Aroclor 1260
contains biphenyls with approximately 60 percent chlorine).
As a result of their stability and their general hydrophobic nature, PCBs released to the environment have
dispersed widely throughout the ecosystem [14]. PCBs are among the most stable organic compounds
known, and chemical degradation rates in the environment are thought to be slow. As a result of their
highly lipophilic nature and low water solubility, PCBs are generally found at low concentrations in water
and at relatively high concentrations in sediment [15]. Individual PCB congeners have different physical
and chemical properties based on the degree of chlorination and position of chlorine substitution,
although differences with degree of chlorination are more significant [15]. Solubilities and octanol-water
partition coefficients for PCB congeners range over several orders of magnitude [16]. Octanol-water
partition coefficients, which are often used as estimators of the potential for bioconcentration, are highest
for the most chlorinated PCB congeners.
Dispersion of PCBs in the aquatic environment is a function of their solubility [15] while PCB mobility
within and sorption to sediment are a function of chlorine substitution pattern and degree of chlorination
[17]. The concentration of PCB s in sediments is a function of the physical characteristics of the sediment,
such as grain size [18,19] and total organic carbon content [18,19,20,21]. Fine sediments typically
contain higher concentrations of PCBs than coarser sediments because of more surface area [15]. Mobility
of PCBs in sediment is generally quite low for the higher chlorinated biphenyls [17]. Therefore, it is
common for the lower chlorinated PCBs to have a greater dispersion from the original point source [15].
Limited mobility and high rates of sedimentation could prevent some PCB congeners in the sediment
from reaching the overlying water via diffusion [17].
The persistence of PCBs in the environment is a result of their general resistance to degradation [16]. The
rate of degradation of PCB congeners by bacteria decreases with increasing degree of chlorination [22];
other structural characteristics of the individual PCBs can affect susceptibility to microbial degradation
to a lesser extent [16]. Photochemical degradation, via reductive dechlorination, is also known to occur
in aquatic environments; the higher chlorinated PCBs appear to be most susceptible to this process [21].
Toxicity of PCB congeners is dependent on the degree of chlorination as well as the position of chlorine
substitution. Lesser chlorinated congeners are more readily absorbed, but are metabolized more rapidly
than higher chlorinated congeners [23]. PCB congeners with no chlorine substituted in the ortho (2 and
2') positions but with four or more chlorine atoms at the meta (3 and 3') and para (4 and 4') positions can
36
-------
BIOACCUMULATION SUMMARY
AROCLOR 1248
assume a planar conformation that can interact with the same receptor as the highly toxic 2,3,7,8-
tetrachlorodibenzo-p-dioxin (TCDD) [24]. Examples of these more toxic, coplanar congeners are
3,3',4,4'-tetrachlorobiphenyl (PCB 77), 3,3',4,4',5-pentachlorobiphenyl (PCB 126), and 3,3',4,4',5,5'-
hexachlorobiphenyl (PCB 169). A method that has been proposed to estimate the relative toxicity of
mixtures is to use toxic equivalency factors (TEFs) [25]. With this method, relative potencies for
individual congeners are calculated by expressing their potency in relation to 2,3,7,8-TCDD. The
following TEFs have been recommended [25,26]:
Congener Class
3,3',4,4',5-PentaCB
3,3',4,4',5,5'-HexaCB
3,3'4,4'-TetraCB
Monoortho coplanar PCBs
Diortho coplanar PCBs
Recommended TEF
0.1
0.05
0.01
0.001
0.00002
Due to the toxicity, high Kow values, and highly persistent nature of many PCBs, they possess a high
potential to bioaccumulate and exert reproductive effects in higher-trophic-level organisms. Aquatic
organisms have a strong tendency to accumulate PCBs from water and food sources. The
bioconcentration factor for fish is approximately 50,000 [27]. This factor represents the ratio of
concentration in tissue to the ambient water concentration. Aquatic organisms living in association with
PCB-contaminated sediments generally have tissue concentrations equal to or greater than the
concentration of PCB in the sediment [27]. Once taken up by an organism, PCBs partition primarily into
lipid compartments [15]. Thus, differences in PCB concentration between species and between different
tissues within the same species may reflect differences in lipid content [15]. PCB concentrations in
polychaetes and fish have been strongly correlated to their lipid content [28]. Elimination of PCBs from
organisms is related to the characteristics of the specific PCB congeners present. It has been shown that
uptake and depuration rates in mussels are high for lower-chlorinated PCBs and much lower for higher-
chlorinated congeners [29, 30]. In some species, tissue concentrations of PCBs in females can be reduced
during gametogenesis because of PCB transfer to the more lipophilic eggs. Therefore, the transferred
PCBs are eliminated from the female during spawning [31,32]. Fish and other aquatic organisms
biotransform PCBs more slowly than other species, and they appear less able to metabolize, or excrete,
the higher chlorinated PCB congeners [31]. Consequently, fish and other aquatic organisms may
accumulate more of the higher chlorinated PCB congeners than is found in the environment [16].
The acute toxicity of PCBs appears to be relatively low, but results from chronic toxicity tests indicate
that PCB toxicity is directly related to the duration of exposure [1]. Toxic responses have been noted to
occur at concentrations of 0.03 and 0.014 |ig/L in marine and freshwater environments, respectively [1].
The LC50 for grass shrimp exposed to PCBs in marine waters for 4 days was 6.1 to 7.8 ug/L [1 ]. Chronic
toxicity of PCBs presents a serious environmental concern because of their resistance to degradation [33],
although the acute toxicity of PCBs is relatively low compared to that of other chlorinated hydrocarbons.
Sediment contaminated with PCBs has been shown to elicit toxic responses at relatively low
concentrations. Sediment bioassays and benthic community studies suggest that chronic effects generally
occur in sediment at total PCB concentrations exceeding 370 ug/kg [34].
37
-------
BIOACCUMULATION SUMMARY AROCLOR 1248
A number of field and laboratory studies provide evidence of chronic sublethal effects on aquatic
organisms at low tissue concentrations [16]. Field and Dexter [16] suggest that a number of marine and
freshwater fish species have experienced chronic toxicity at PCB tissue concentrations of less than 1.0
mg/kg and as low as 0.1 mg/kg. Spies et al. [35] reported an inverse relationship between PCB
concentrations in starry flounder eggs in San Francisco Bay and reproductive success, with an effective
PCB concentration in the ovaries of less than 0.2 mg/kg. Monod [36] also reported a significant
correlation between PCB concentrations in eggs and total egg mortality in Lake Geneva char. PCBs have
also been shown to cause induction of the mixed function oxidase (MFO) system in aquatic animals, with
MFO induction by PCBs at tissue concentrations within the range of environmental exposures [16].
38
-------
Summary of Biological Effects Tissue Concentrations for Aroclor 1248
Species:
Taxa
Concentration, Units in:
Toxicity:
Ability to Accumulate:
Log Log
Sediment Water Tissue (Sample Type) Effects BCF BAF BSAF
Source:
Reference Comments
Invertebrates
[NO DATA FOUND]
Fishes
[NO DATA FOUND]
Wildlife
[NO DATA FOUND]
-------
BIOACCUMULATION SUMMARY AROCLOR 1248
References
1. USEPA. 1980. Ambient water quality criteria document: Poly chlorinated biphenyls. EPA
440/5-80-068. (Cited in USEPA. 1996. Hazardous Substances Data Bank (HSDB). National
Library of Medicine online (TOXNET). U.S. Environmental Protection Agency, Office of Health
and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH.
February.)
2. Eisler, R. 1986. Polychlorinated biphenyl hazards to fish, wildlife, and invertebrates: A synoptic
review. U.S. Fish Wildl. Serv. Biol. Rep. 85(1.7).
3. MacKay, D., W.Y. Shiu, and K.C. Ma. 1992. Illustrated handbook of physical-chemical
properties and environmental fate for organic chemicals. Vol. I, Monoaromatic hydrocarbons,
chlorobenzenes, andPCBs. Lewis Publishers, Boca Raton, FL.
4. Agency for Toxic Substances and Disease Registry. 1993. Toxicological profile for
polychlorinated biphenyls. Prepared by Syracuse Research Corporation. Prepared for U.S.
Department of Health and Human Services, Public Health Service. April 1993.
5. USEPA. 1995. Integrated Risk Information System (IRIS). National Library of Medicine online
(TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental
Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. September.
6. Jones, P.O., J.P. Giesy, T.J. Kubiak, D.A. Verbrugge, J.C. Newstead, J.P. Ludwig, D.E. Tillit, R.
Crawford, N. De Galan, and G.T. Ankley. 1993. Biomagnification of bioassay-derived 2, 3, 7,
8-tetrachlorodibenzo-p-dioxin equivalents. Chemosphere 26:1203-1212.
7. Biddinger, G.R., and S.P. Gloss. 1984. The importance of trophic transfer in the bioaccumulation
of chemical contaminants in aquatic ecosystems. Residue Rev. 91:103-145.
8. Kay, S.H. 1984. Potential for biomagnification of contaminants within marine and freshwater
food webs. Technical Report D-84-7. U.S. Army Corps of Engineers, Waterways Experiment
Station, Vicksburg, MS.
9. USAGE. 1995. Trophic transfer and biomagnification potential of contaminants in aquatic
ecosystems. Environmental Effects of Dredging, Technical Notes EEDP-01-33. U.S. Army Corps
of Engineers, Waterways Experiment Station, Vicksburg, MS.
10. Thomann, R.V. 1989. Bioaccumulation model of organic chemical distribution in aquatic food
chains. Environ. Sci. Technol. 23:699.
11. Hoffman, D.J., C.P. Rice, and T.J. Kubiak. 1996. PCBs and dioxins in birds. In Environmental
contaminants in wildlife, ed. W.N. Beyer, G.H. Heinz, and A.W. Redmon-Horwood, pp. 165-207.
Lewis Publishers, Boca Raton, FL.
40
-------
BIOACCUMULATION SUMMARY AROCLOR 1248
12. Oliver, E.G., and AJ. Niimi. 1988. Trophodynamic analysis of polychlorinated biphenyl
congeners and other chlorinated hydrocarbons in the Lake Ontario ecosystem. Environ. Sci.
Technol 22:388-397.
13. Rasmussen, J.B., DJ. Rowan, D.R.S. Lean, and J.H. Carey. 1990. Food chain structure in
Ontario lakes determines PCB levels in lake trout (Salvelinus namaycush) and other pelagic fish.
Can. J. Fish. Aquat. Sci. 47:2030-2038.
14. Rand, G.M., P.G. Wells, and L.S. McCarty. 1995. Chapter 1. Introduction to aquatic toxicology.
In Fundamentals of aquatic toxicology: Effects, environmental fate, and risk assessment, ed.
G.M. Rand, pp. 3-67. Taylor and Francis, Washington, DC.
15. Phillips, D.J.H. 1986. Use of organisms to quantify PCBs in marine and estuarine environments.
In PCBs and the environment, ed. J.S. Waid, pp. 127-182. CRC Press, Inc., Boca Raton, FL.
16. Field, L.J. and R.N. Dexter. 1998. A discussion of PCB target levels in aquatic sediments.
Unpublished document. January 11, 1988.
17. Fisher, J.B., R.L. Petty, and W. Lick. 1983. Release of polychlorinated biphenyls from
contaminated lake sediments: Flux and apparent diffusivities of four individual PCBs. Environ.
Pollut. 5B: 121-132.
18. Pavlou, S.P., and R.N. Dexter. 1979. Distribution of polychlorinated biphenyls (PCB) in
estuarine ecosystems: Testing the concept of equilibrium partitioning in the marine environment.
Environ. Sci. Technol. 13:65-71.
19. Lynch, T.R., and H.E. Johnson. 1982. Availability of hexachlorobiphenyl isomer to benthic
amphipods from experimentally contaminated sediments. In Aquatic Toxicology and Hazard
Assessment: Fifth Conference, ASTM STP 766, ed. J.G. Pearson, R.B. Foster, and W.E. Bishop,
pp. 273-287. American Society of Testing and Materials, Philadelphia, PA.
20. Chou, S.F.J., and R.A. Griffin. 1986. Solubility and soil mobility of polychlorinated biphenyls.
In PCBs and the environment, ed. J. S. Waid, Vol. 1, pp. 101-120. CRC Press, Inc., Boca Raton,
FL.
21. Sawhney, B.L. 1986. Chemistry and properties of PCBs in relation to environmental effects. In
PCBs and the environment, ed. J.S. Waid, pp. 47-65. CRC Press, Inc., Boca Raton, FL.
22. Furukawa, K. 1986. Modification of PCBs by bacteria and other microorganisms. In PCBs and
the environment, ed. J. S. Waid, Vol. 2, pp. 89-100. CRC Press, Inc., Boca Raton, FL.
41
-------
BIOACCUMULATION SUMMARY AROCLOR 1248
23. Bolger, M. 1993. Overview of PCB toxicology. Proceedings of the U.S. Environmental
Protection Agency's National Technical Workshop "PCBs in Fish Tissue," EPA/823-R-93-003.
U.S. Environmental Protection Agency, Office of Water, Washington, DC, May 10-11, 1993, pp.
37-53.
24. Erickson, M.D. 1993. Introduction to PCBs and analytical methods. Proceedings of the U.S.
Environmental Protection Agency's National Technical Workshop "PCBs in Fish Tissue,"
EPA/823-R-93-003. U.S. Environmental Protection Agency, Office of Water, Washington, DC,
May 10-11, 1993, pp. 3-9.
25. Safe, S. 1990. Polychlorinated biphenyls (PCBs), dibenzo-p-dioxins (PCDDs), dibenzofurans
(PCDFs), and related compounds: Environmental and mechanistic considerations which support
the development of toxic equivalency factors (TEFs). Crit. Rev. Toxicol. 21(l):51-88.
26. USEPA. 1991. Workshop report on toxicity equivalency factors for poly chlorinated bipheny I
congeners. EPA/625/3-91/020. U.S. Environmental Protection Agency. (Eastern Research
Group, Inc., Arlington, MA.)
27. Neff, J.M. 1984. Bioaccumulation of organic micropollutants from sediments and suspended
particulates by aquatic animals. Fres. Z. Anal Chem. 319:132-136.
28. Shaw, G.R., and D.W. Connell. 1982. Factors influencing concentrations of polychlorinated
biphenyls in organisms from an estuarine ecosystem. Aust. J. Mar. Freshw. Res. 33:1057-1070.
29. Tanabe, S., R. Tatsukawa, and D.J.H. Phillips. 1987. Mussels as bioindicators of PCB pollution:
A case study on uptake and release of PCB isomers and congeners in green-lipped mussels (Perna
viridis) in Hong Kong waters. Environ. Pollut. 47:41-62.
30. Pruell, R.J., J.L. Lake, W.R. Davis, and J.G. Quinn.. 1986. Uptake and depuration of organic
contaminants by blue mussels (Mytilus edulis) exposed to environmentally contaminated
sediments. Mar. Biol. 91:497-508.
31. Lech, J.J., and R.E. Peterson. 1983. Biotransformation and persistence of polychlorinated
biphenyls (PCBs) in fish. In PCBs: Human and environmental hazards, ed. P.M. D'ltri and M.A.
Kamrin, pp. 187-201. Ann Arbor Science Publishers, Inc., Ann Arbor, MI.
32. Stout, V.F. 1986. What is happening to PCBs? Elements of effective environmental monitoring
as illustrated by an analysis of PCB trends in terrestrial and aquatic organisms. In PCBs and the
environment, ed. J.S. Waid. CRC Press, Inc., Boca Raton, FL.
33. Mearns, A.J., M. Malta, G. Shigenaka, D. MacDonald, M. Buchman, H. Harris, J. Golas, and G.
Lauenstein. 1991. Contaminant trends in the Southern California Bight: Inventory and
assessment. Technical Memorandum NOAA ORCA 62. National Oceanic and Atmospheric
Administration. Seattle, WA.
42
-------
BIOACCUMULATION SUMMARY AROCLOR 1248
34. 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. NOAA Tech. Memo. NOS
OMA 52. National Oceanic and Atmospheric Administration, Seattle, WA.
35. Spies, R.B., D.W. Rice, Jr., P.A. Montagna, and R.R. Ireland. 1985. Reproductive success,
xenobiotic contaminants and hepatic mixed-function oxidase (MFO) activity in Platichthys
stellatus populations from San Francisco Bay. Mar. Environ. Res. 17:117-121.
36. Monod, G. 1985. Egg mortality of Lake Geneva char (Salvelinus alpinus) contaminated by PCB
and DDT derivatives. Bull. Environ. Contain. Toxicol. 35:531-536.
43
-------
44
-------
BIOACCUMULATION SUMMARY AROCLOR 1254
Chemical Category: POLYCHLORINATED BIPHENYLS
Chemical Name (Common Synonyms): Aroclor 1254 CASRN: 11097-69-1
Chemical Characteristics
Solubility in Water: 12 |ig/L at 25°C[1] Half-Life: No data [2,3]
LogKow: — LogKoc: —
Human Health
Oral RfD: 2 x 10"5 mg/kg-day [4] Confidence: Medium; uncertainty factor = 300
Critical Effect: Ocular exudate, inflamed and prominent Meibomian glands, distorted growth of
fingernails and toenails; decreased antibody (IgG and IgM) response to sheep erythrocyte
Oral Slope Factor: No data [4] Carcinogenic Classification: A2 [4]
Wildlife
Partitioning Factors: No partitioning factors for Aroclor 1254 were identified for wildlife.
Food Chain Multipliers: For PCBs as a class, the most toxic congeners have been shown to be
selectively accumulated from organisms at one trophic level to the next [5]. At least three studies have
concluded that PCBs have the potential to biomagnify in food webs based on aquatic organisms and
predators that feed primarily on aquatic organisms [6,7,8]. The results from Biddinger and Gloss [6] and
USAGE [8] generally agreed that highly water-insoluble compounds (including PCBs) have the potential
to biomagnify in these types of food webs. Thomann's [9] model also indicated that highly water-
insoluble compounds (log Kow values 5 to 7) showed the greatest potential to biomagnify. A
biomagnification factor of 28 was calculated by [10] for transfer of total PCBs from fish to bald eagle
eggs. Similarly, a biomagnification factor of 32 was determined for total PCBs from alewife to herring
gull eggs in Lake Ontario [11]. No specific foot chain multipliers were identified for Aroclor 1254.
Aquatic Organisms
Partitioning Factors: BSAFs for Dover sole were approximately 0.96 for muscle and 1.14 for liver.
Invertebrates collected from New Bedford, MA, and Long Island Sound, NY, had BSAFs ranging from
3.2 to 4.8. These data are presented in the attached summary table.
Food Chain Multipliers: Polychlorinated biphenyls as a class have been demonstrated to biomagnify
through the food web. Oliver and Niimi [12], studying accumulation of PCBs in various organisms in
the Lake Ontario food web, reported concentrations of total PCBs in phytoplankton, zooplankton, and
45
-------
BIOACCUMULATION SUMMARY AROCLOR 1254
several species of fish. Their data indicated a progressive increase in tissue PCB concentrations moving
from organisms lower in the food web to top aquatic predators. In a study of PCB accumulation in lake
trout (Salvelinus namaycush) of Lake Ontario, Rasmussen et al. [13] reported that each trophic level
contributed about a 3.5-fold biomagnification factor to the PCB concentrations in the trout. No specific
biomagnification data were identified for Aroclor 1254.
Toxicity/Bioaccumulation Assessment Profile
PCBs are among the most stable organic compounds known, and rates of chemical degradation in the
environment are thought to be slow. Highly lipophilic, PCBs are generally found at low concentrations
in water and at relatively high concentrations in sediment [14]. PCBs are a class of 209 discrete chemical
compounds called congeners, in which one to ten chlorine atoms are attached to biphenyl. PCBs were
commonly produced as complex mixtures of congeners for a variety of uses, including dielectric fluids
in capacitors and transformers. In the United States, Aroclor is the most familiar requested trademark of
commercial PCB formulations. The first two digits in the Aroclor designation (12) indicate that the
mixture contains biphenyls, and the last two digits give the weight percent of chlorine in the mixture (e.g.,
Aroclor 1254 contains biphenyls with approximately 54 percent chlorine).
Individual PCB congeners have different physical and chemical properties based on the degree of
chlorination and position of chlorine substitution, although differences in the degree of chlorination affect
partitioning more significantly, but toxicity is more dependent on position [15]. Octanol-water partition
coefficients, which are often used as estimators of the potential for bioconcentration, are highest for PCB
congeners with the highest degree of chlorination. Solubilities and octanol-water partition coefficients
range over several orders of magnitude. Due to their higher water solubility, lower-chlorinated PCBs
might show greater dispersion from a point source, whereas the higher-chlorinated compounds might
remain in the sediments closer to the source [15]. The mobility of PCBs in sediment is also a function
of the chlorine substitution pattern and degree of chlorination and is generally quite low, particularly for
the higher-chlorinated biphenyls [16]. Therefore, high rates of sedimentation could prevent PCBs in the
sediment from reaching the overlying water via diffusion [16].
PCB concentrations in sediment are affected by physical characteristics of the sediment such as grain size
and total organic carbon content [17,18]. Fine sediments typically contain higher concentrations of PCBs
than coarser sediments [15]. Sorption to sediments is a function of total organic carbon content [19,20].
Toxicity of PCB congeners is dependent on the degree of chlorination as well as the isomer. Lesser
chlorinated congeners are more readily absorbed, but are metabolized more rapidly than higher
chlorinated congeners [21]. PCB congeners with no chlorine substituted in the ortho (2 and 2') positions
but with four or more chlorine atoms at the meta (3 and 3') and para (4 and 4') positions can assume a
planar conformation that can interact with the same receptor as the highly toxic 2,3,7,8-
tetrachlorodibenzo-p-dioxin (TCDD) [22]. Examples of these more toxic, coplanar congeners are
3,3',4,4'-tetrachlorobiphenyl (PCB 77), 3,3',4,4',5-pentachlorobiphenyl (PCB 126), and 3,3',4,4',5,5'-
hexachlorobiphenyl (PCB 169). A method that has been proposed to estimate the relative toxicity of
mixtures is to use toxic equivalency factors (TEFs) [23]. With this method, relative potencies for
individual congeners are calculated by expressing their potency in relation to 2,3,7,8-TCDD. The
following TEFs have been recommended [23,24]:
46
-------
BIOACCUMULATION SUMMARY
AROCLOR 1254
Congener Class
3,3',4,4',5-TCB
3,3',4,4',5,5'-HCB
3,3',4,4'-TeCB
Monoortho coplanar PCBs
Diortho coplanar PCBs
Recommended TEF
0.1
0.05
0.01
0.001
0.00002
Due to the toxicity, high Kow values, and highly persistent nature of many PCBs, they possess a high
potential to bioaccumulate and exert reproductive effects in higher-trophic-level organisms. Aquatic
organisms have a strong tendency to accumulate PCBs from water and food sources. The
bioconcentration factor for fish is approximately 50,000 [25]. This factor represents the ratio of
concentration in tissue to the ambient water concentration. PCB concentrations in tissues of aquatic
organisms will generally be greater than, or equal to, sediment concentrations [26]. PCB concentrations
in fish have been strongly correlated to their lipid content. Elimination of PCBs from organisms is related
to the characteristics of the specific PCB congeners present. It has been shown that uptake and depuration
rates in mussels are high for lower-chlorinated PCBs and much lower for higher-chlorinated congeners
[27,28]. Elimination of PCBs from the body can occur during egg production and spawning in females
of some species [29,30]. There is a limited capacity for fish and other aquatic organisms to biotransform
or metabolize PCBs.
Sediment contaminated with PCBs has been shown to elicit toxic responses at relatively low
concentrations. Sediment bioassays and benthic community studies suggest that chronic effects generally
occur in sediment at total PCB concentrations exceeding 370 |ig/kg [31]. The LC50 for grass shrimp
exposed to PCBs in marine waters for 4 days was 6.1 to 7.8 |ig/L [1]. Chronic toxicity of PCBs presents
a serious environmental concern because of their resistance to degradation [32], although the acute
toxicity of PCBs is relatively low compared to that of other chlorinated hydrocarbons. Toxic responses
have been noted to occur at concentrations of 0.03 and 0.014 |ig/L in marine and freshwater
environments, respectively [1].
47
-------
Summary of Biological Effects Tissue Concentrations for Aroclor 1254
Species:
Taxa
Concentration, Units in1:
Toxicity:
Ability to Accumulate2:
Log Log
Sediment Water Tissue (Sample Type) Effects BCF BAF BSAF
Source:
Reference Comments3
Nephtys incisa,
Polychaete worm
New Bedford:
3,070-7,180 ng/g
(TOC: 4.16-4.67%)
3.22
n = 3
[38]
F; New Bedford,
MA; Long Island
Sound, NY
AF =
Long Island:
40.3-48.3 ng/g
(TOC: 2.39-2.62%)
4.29
n = 3
[Organism],
[Sediment] (ng/
Crassostrea
virginica, Oyster
425 mg/kg
(whole body)4
425 mg/kg
(whole body)4
101 mg/kg
(whole body)4
Cellular,
LOED
Growth,
LOED
Cellular,
NOED
101 mg/kg
(whole body)4
425 mg/kg
(whole body)4
101 mg/kg
(whole body)4
Growth,
NOED
Mortality,
NOED
Mortality,
NOED
[49] L; atrophy of
digestive
diverticulata
[49] L; reduced growth
[49] L; no effect on
histopathology of
digestive
diverticulata
[49] L; no effect on
growth
[49] L; no effect on
mortality
[49] L; no effect on
mortality
Crassostrea
virginica, Oyster
33 mg/kg
(whole body)4
8.1 mg/kg
(whole body)4
Growth, NA
Growth, NA
[46] L; 41 % reduction in
rate of shell growth
[46] L; 19% reduction in
rate of shell growth
-------
Summary of Biological Effects Tissue Concentrations for Aroclor 1254
Species:
Taxa
Yoldia limatula,
Bivalve
Concentration, Units in1: Toxicity:
Sediment Water Tissue (Sample Type) Effects
33 mg/kg Mortality,
(whole body)4 NOED
8.1 mg/kg Mortality,
(whole body)4 NOED
New
Bedford:
3,070-7,180
ng/g
(TOC: 4.16-
4.67%)
Long Island:
40.3-48.3
ng/g
(TOC: 2.39-
2.62%)
Ability to Accumulate2: Source:
Log Log
BCF BAF BSAF Reference Comments3
[46] L; no effect on
survival in 96 hours
[46] L; no effect on
survival in 96 hours
4.07 [38] F; New Bedford,
n = 3 MA; Long Island
Sound, NY
4.79
n = 3
Macoma nasuta,
Clam
Concentrations at
Stations:
[39] L; standard bioassay
with field collected
sediments with
multiple
contaminants.
-------
Summary of Biological Effects Tissue Concentrations for Aroclor 1254
Species: Concentration, Units in1:
Taxa Sediment Water
<20 |ig/kg
dw
<20 |ig/kg
dw
<20 |ig/kg
dw
<20 |ig/kg
dw
Daphnia magna,
Cladoceran
GammarM^
pseudolimnaeus,
Amphipod
Gammarus tigrinus,
Amphipod
Penaeiis diioramm,
Pink shrimp
Palaemonetes
kadiakensis,
Grass shrimp
Tissue (Sample Type)
21.4 |ig/kg,
(variance = 9.8, n=5)
35.2* ng/kg,
(variance = 27.2, n=5)
20 |ig/kg,
(variance = 0, n=5)
27.8* |ig/kg,
(variance = 20.7, n=5)
* statistically significant
increase
10.4 mg/kg
(whole body)4
7.8 mg/kg
(whole body)4
4.64 mg/kg
(whole body)4
3.9 mg/kg
(whole body)4
3.2 mg/kg
(whole body)4
Toxicity: Ability to Accumulate2:
Log Log
Effects BCF BAF BSAF
100% survival
100% survival
100% survival
100% survival
Mortality,
NOED
Mortality,
NOED
Behavior,
NOED
Mortality,
ED 100
Mortality,
NOED
Source:
Reference Comments3
Tissue burdens and
toxicity were
determined in
separate aquaria
after 20 and 10
days, respectively.
[52] L; radiolabeled
compound
[52] L; radiolabeled
compound
[51] L; radiolabeled
compound
[46] L; 100% mortality
after 48 hours
[52] L; radiolabeled
compound
-------
Summary of Biological Effects Tissue Concentrations for Aroclor 1254
Species: Concentration, Units in1:
Taxa Sediment Water
Orconectes nais,
Crayfish
Callinectes sapidiis,
Blue crab
Culex tarsalis,
Mosquito
Chaoboms
punctipennis, Midge
Corydalus cornutus,
Midge
Pteronarcys dorsata,
Giant black stonefly
Tissue (Sample Type)
0.04 mg/kg
(whole body)4
16 mg/kg
(whole body)4
33 mg/kg
(whole body)4
1.3 mg/kg
(whole body)4
33 mg/kg
(whole body)4
0.14 mg/kg
(whole body)4
23 mg/kg
(whole body)4
5.4 mg/kg
(whole body)4
1.2 mg/kg
(whole body)4
1.02 mg/kg
(whole body)4
1 .4 mg/kg
(whole body)4
Toxicity: Ability to Accumulate2:
Log Log
Effects BCF BAF BSAF
Mortality,
NOED
Mortality, NA
Behavior,
NOED
Mortality,
NOED
Mortality,
NOED
Mortality,
NOED
Mortality,
NOED
Mortality,
NOED
Mortality,
NOED
Mortality,
NOED
Mortality,
NOED
Source:
Reference
[52]
[46]
[46]
[46]
[46]
[46]
[46]
[52]
[52]
[52]
[52]
Comments3
L; radiolabeled
compound
L; lethal to 18 of 25
fish in 20 days
L; no effect on
sense of equilibrium
or behavior
L; no effect on
survival in 48 hours
L; no effect on
survival in 20 days
L; no effect on
survival in 48 hours
L; no effect on
survival in 20 days
L; radiolabeled
compound
L; radiolabeled
compound
L; radiolabeled
compound
L; radiolabeled
compound
-------
Summary of Biological Effects Tissue Concentrations for Aroclor 1254
Species:
Taxa
Acheta domesticus,
House cricket
Fishes
Oncorhynchus
kisutch,
Coho salmon
Oncorhynchus
mykiss,
Rainbow trout
Concentration, Units in1: Toxicity: Ability to Accumulate2:
Log Log
Sediment Water Tissue (Sample Type) Effects BCF BAF BSAF
Soil:
1,000 ppm 148.6ppm Signficant
mortality (LC50
2,000 ppm 143. 9 ppm =1,200 ppm)
0.37 mg/kg (liver) Mortality,
ED10
0.15 mg/kg Development,
(whole body)4 LOED
0.5 mg/kg (liver) Physiological,
LOED
0.2 mg/kg Physiological,
(whole body)4 LOED
Source:
Reference Comments3
[37] L; 14-d soil
bioassay; despite
high mortality no
significant
differences were
seen in growth rate
or food
consumption
between surviving
crickets and control
crickets.
[48] L; 10% mortality of
smolts
[48] L; reduced ability of
smolts to adapt to
seawater
[48] L; delayed increase
in plasma thyroxine
(T4) prior to
smoltification by 30
days
[50] L; increased
ethoxyresorufm o-
deethylase (EROD)
activity
-------
Summary of Biological Effects Tissue Concentrations for Aroclor 1254
Species:
Taxa
Oncorhynchus
mykiss,
Rainbow trout
Oncorhynchus
mykiss,
Rainbow trout
Pimephales
promelas,
Fathead minnow
Concentration, Units in1:
Sediment Water Tissue (Sample Type)
0.2 mg/kg
(whole body)4
Muscle or liver = 300
H8/k8
0.82|ig/gdw 5.25-1 1.6 n-g/g
14-27 |ig/g 13.7-47.2 |ig/g
dw
Toxicity: Ability to Accumulate2:
Log Log
Effects BCF BAF BSAF
Physiological,
LOED
Elevated hepatic
MFO (EROD)
activity after 70
days
No effect
Reproduction
inhibited.
Frequency and
fecundity 5-30%
of control
values.
Source:
Reference Comments3
[50] L; increased
ethoxyresorufin o-
deethylase (EROD)
activity
[40] L
[41] L; organism survival
and weight
unaffected by PCB
concentration.
Increased lipid
concentrations were
seen with increased
reproductive effects.
Measurement
endpoints for effects
not well-defined.
Pleuronectes
americanus,
Winter flounder
Eggs = 7.1 |ig/kg
Reduced growth
in length and
weight
[42]
-------
Summary of Biological Effects Tissue Concentrations for Aroclor 1254
Species:
Taxa
Microstomus
pacificus,
Dover sole
Concentration, Units in1:
Sediment Water
2.y ng/kg,
dw (median
TOC - 7.6%)
Toxicity:
Tissue (Sample Type) Effects
Muscle =1.1* |ig/kg,
dw (236 %lipids)
T iwr —190* no/Vo
Ability to Accumulate2:
Log Log
BCF BAF BSAF
0.96
1 4
Source:
Reference Comments3
[43] BSAFs are lipid and
TOC normalized
values reported in
(24.8% lipids)
*median concentration
text.
Salvelinus fontinalis,
Brook trout
39mg/kg (fillet)
Physiological,
LOED
[44] L; 7 doses over 18-
day period; effect at
only exposure dose;
hepatic enzyme
induction
Cypriniis carpio,
Common carp
0.1 mg/kg
(whole body)4
Physiological,
LOED
[50] L;increased
ethoxyresorufin o-
deethylase (EROD)
activity
Lagodon
rhomboides, Pinfish
17 mg/kg
(whole body)4
3.8 mg/kg
(whole body)4
0.98 mg/kg
(whole body)4
Mortality,
NOED
Mortality,
NOED
Mortality,
NOED
[46] L; no effect on
survival in 48 hours
[46] L; no effect on
survival in 48 hours
[46] L; no effect on
survival in 48 hours
Ictalums punctatus,
Channel catfish
100 mg/kg
(whole body)4
Physiological,
NOED
[47] L; no effect on
neurotransmitters
-------
Summary of Biological Effects Tissue Concentrations for Aroclor 1254
Species:
Taxa
Platycephalus
bassensis,
Sand flathead
Concentration, Units in1:
Sediment Water Tissue (Sample Type)
10 mg/kg
(whole body)4
100 mg/kg
(whole body)4
10 mg/kg
(whole body)4
Toxicity: Ability to Accumulate2:
Log Log
Effects BCF BAF BSAF
Physiological,
ED50
Physiological,
LOED
Physiological,
NOED
Source:
Reference Comments3
[45] L; 50% increase in
activity of uridine
diphosphoglucuro-
nosyltransferase
[45] L; induction (3x) of
ethoxyresorufin o-
deethylase (EROD)
activity
[45] L; no induction of
ethoxyresorufin o-
deethylase (EROD)
activity
Concentration units based on wet weight unless otherwise noted.
BCF = bioconcentration factor, BAF = bioaccumulation factor, BSAF = biota-sediment accumulation factor.
L = laboratory study, spiked sediment, single chemical; F = field study, multiple chemical exposure; other unusual study conditions or observations noted.
This entry was excerpted directly from the Environmental Residue-Effects Database (ERED, www.wes.army.mil/el/ered, U.S. Army Corps of Engineers and U.S.
Environmental Protection Agency). The original publication was not reviewed, and the reader is strongly urged to consult the publication to confirm the information
presented here.
-------
BIOACCUMULATION SUMMARY AROCLOR 1254
References
1. USEPA. 1980. Ambient water quality criteria document: Polychlorinated biphenyls. EPA 440/5-
80-068. (Cited in USEPA. 1996. Hazardous Substances Data Bank (HSDB). National Library
of Medicine online (TOXNET). U.S. Environmental Protection Agency, Office of Health and
Environmental Assessment, Environmental Criteria and Assessment Office, Cinncinati, OH.
February.)
2. Eisler, R. 1986. Polychlorinated biphenyl hazards to fish, wildlife, and invertebrates: A synoptic
review. U.S. Fish Wildl. Serv. Biol. Rep. 85(1.7).
3. MacKay, D., W.Y. Shiu, and K.C. Ma. 1992. Illustrated handbook of physical-chemical
properties and environmental fate for organic chemicals. Vol. I, Monoaromatic hydrocarbons,
chlorobenzenes, andPCBs. Lewis Publishers, Boca Raton, FL.
4. Agency for Toxic Substances and Disease Registry. 1993. Toxicological profile for
Polychlorinated biphenyls. Prepared by Syracuse Research Corporation. Prepared for U.S.
Department of Health and Human Services, Public Health Service. April 1993.
5. USEPA. 1995. Integrated Risk Information System (IRIS). National Library of Medicine online
(TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental
Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. September.
6. Jones, P.O., J.P. Giesy, T.J. Kubiak, D.A. Verbrugge, J.C. Newstead, J.P. Ludwig, D.E. Tillit, R.
Crawford, N. De Galan, and G.T. Ankley. 1993. Biomagnification of bioassay-derived 2, 3, 7,
8-tetrachlorodibenzo-p-dioxin equivalents. Chemosphere 26:1203-1212.
7. Biddinger, G.R., and S.P. Gloss. 1984. The importance of trophic transfer in the bioaccumulation
of chemical contaminants in aquatic ecosystems. Residue Rev. 91:103-145.
8. Kay, S.H. 1984. Potential for biomagnification of contaminants within marine and freshwater
food webs. Technical Report D-84-7. U.S. Army Corps of Engineers, Waterways Experiment
Station, Vicksburg, MS.
9. USAGE. 1995. Trophic transfer and biomagnification potential of contaminants in aquatic
ecosystems. Environmental Effects of Dredging, Technical Notes EEDP-01-33. U.S. Army Corps
of Engineers, Waterways Experiment Station, Vicksburg, MS.
10. Thomann, R.V. 1989. Bioaccumulation model of organic chemical distribution in aquatic food
chains. Environ. Sci. Technol. 23:699.
11. Hoffman, D.J., C.P. Rice, and T.J. Kubiak. 1996. PCBs and dioxins in birds. In Environmental
contaminants in wildlife, ed. W.N. Beyer, G.H. Heinz, and A.W. Redmon-Horwood, pp. 165-207.
Lewis Publishers, Boca Raton, FL.
56
-------
BIOACCUMULATION SUMMARY AROCLOR 1254
12. Oliver, E.G., and AJ. Niimi. 1988. Trophodynamic analysis of polychlorinated biphenyl
congeners and other chlorinated hydrocarbons in the Lake Ontario ecosystem. Environ. Set
Technol. 22:388-397.
13. Rasmussen, J.B., DJ. Rowan, D.R.S. Lean, and J.H. Carey. 1990. Food chain structure in
Ontario lakes determines PCB levels in lake trout (Salvelinus namaycush) and other pelagic fish.
Can. J. Fish. Aquat. Sci. 47:2030-2038.
14. Rand, G.M., P.O. Wells, and L.S. McCarty. 1995. Chapter 1. Introduction to aquatic toxicology.
In Fundamentals of aquatic toxicology: Effects, environmental fate, and risk assessment, ed. G.
M. Rand, pp. 3-67. Taylor and Francis, Washington, DC.
15. Phillips, D.J.H. 1986. Use of organisms to quantify PCBs in marine and estuarine environments.
In PCBs and the environment, ed. J.S. Waid, pp. 127-182. CRC Press, Inc., Boca Raton, FL.
16. Field, LJ. and R.N. Dexter. 1998. A discussion of PCB target levels in aquatic sediments.
Unpublished document. January 11, 1988.
17. Fisher, J.B., R.L. Petty, and W. Lick. 1983. Release of polychlorinated biphenyls from
contaminated lake sediments: Flux and apparent diffusivities of four individual PCBs. Environ.
Pollut. 5B: 121-132.
18. Pavlou, S.P., and R.N. Dexter. 1979. Distribution of polychlorinated biphenyls (PCB) in
estuarine ecosystems: Testing the concept of equilibrium partitioning in the marine environment.
Environ. Sci. Technol. 13:65-71.
19. Lynch, T.R., and H.E. Johnson. 1982. Availability of hexachlorobiphenyl isomer to benthic
amphipods from experimentally contaminated sediments. In Aquatic Toxicology and Hazard
Assessment: Fifth Conference, ASTM STP 766, ed. J.G. Pearson, R.B. Foster, and W.E. Bishop,
pp. 273-287. American Society of Testing and Materials, Philadelphia, PA.
20. Chou, S.F.J., and R.A. Griffin. 1986. Solubility and soil mobility of polychlorinated biphenyls.
In PCBs and the environment, ed. J. S. Waid, Vol. 1, pp. 101-120. CRC Press, Inc., Boca Raton,
FL.
21. Sawhney, B.L. 1986. Chemistry and properties of PCBs in relation to environmental effects. In
PCBs and the environment, ed. J.S. Waid, pp. 47-65. CRC Press, Inc., Boca Raton, FL.
22. Furukawa, K. 1986. Modification of PCBs by bacteria and other microorganisms. In PCBs and
the environment, ed. J. S. Waid, Vol. 2, pp. 89-100. CRC Press, Inc., Boca Raton, FL.
23. Bolger, M. 1993. Overview of PCB toxicology. Proceedings of the U.S. Environmental
Protection Agency's National Technical Workshop "PCBs in Fish Tissue," EPA/823-R-93-003.
U.S. Environmental Protection Agency, Office of Water, Washington, DC, May 10-11, 1993, pp.
37-53.
57
-------
BIOACCUMULATION SUMMARY AROCLOR 1254
24. Erickson, M.D. 1993. Introduction to PCBs and analytical methods. Proceedings of the U.S.
Environmental Protection Agency's National Technical Workshop "PCBs in Fish Tissue"
EPA/823-R-93-003. U.S. Environmental Protection Agency, Office of Water, Washington, DC,
May 10-11, 1993, pp. 3-9.
25. Safe, S. 1990. Polychlorinated biphenyls (PCBs), dibenzo-p-dioxins (PCDDs), dibenzofurans
(PCDFs), and related compounds: Environmental and mechanistic considerations which support
the development of toxic equivalency factors (TEFs). Critical Reviews in Toxicology 21(l):51-88.
26. USEPA. 1991. Workshop report on toxicity equivalency factors for poly chlorinated biphenyl
congeners. EPA/625/3-91/020. U.S. Environmental Protection Agency. (Eastern Research Group,
Inc., Arlington, MA.)
27. Neff, J.M. 1984. Bioaccumulation of organic micropollutants from sediments and suspended
particulates by aquatic animals. Fres. Z. Anal. Chem. 319:132-136.
28. Shaw, G.R., and D. W. Connell. 1982. Factors influencing concentrations of polychlorinated
biphenyls in organisms from an estuarine ecosystem. Aust. J. Mar. Freshw. Res. 33:1057-1070.
29. Tanabe, S., R. Tatsukawa, and DJ.H. Phillips. 1987. Mussels as bioindicators of PCB pollution:
A case study on uptake and release of PCB isomers and congeners in green-lipped mussels (Perna
viridis) in Hong Kong waters. Environ. Pollut. 47:41-62.
30. Pruell, R. J., J. L. Lake, W. R. Davis, and J. G. Quinn.. 1986. Uptake and depuration of organic
contaminants by blue mussels (Mytilus edulis) exposed to environmentally contaminated
sediments. Mar. Biol. 91:497-508.
31. Lech, J.J., and R.E. Peterson. 1983. Biotransformation and persistence of polychlorinated
biphenyls (PCBs) in fish. In PCBs: Human and environmental hazards, ed. P.M. D'ltri and M.A.
Kamrin, pp. 187-201. Ann Arbor Science Publishers, Inc., Ann Arbor, MI.
32. Stout, V.F. 1986. What is happening to PCBs? Elements of effective environmental monitoring
as illustrated by an analysis of PCB trends in terrestrial and aquatic organisms. In PCBs and the
Environment, ed. J.S. Waid. CRC Press, Inc., Boca Raton, FL.
33. Mearns, A.J., M. Malta, G. Shigenaka, D. MacDonald, M. Buchman, H. Harris, J. Golas, and G.
Lauenstein. 1991. Contaminant trends in the Southern California Bight: Inventory and
assessment. Technical Memorandum NOAA ORCA 62. National Oceanic and Atmospheric
Administration. Seattle, WA.
34. 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. NOAA Tech. Memo. NOS OMA
52. National Oceanic and Atmospheric Administration, Seattle, WA.
35. Spies, R. B., D. W. Rice, Jr., P. A. Montagna, and R. R. Ireland. 1985. Reproductive success,
xenobiotic contaminants and hepatic mixed-function oxidase (MFO) activity in Platichthys
stellatus populations from San Francisco Bay. Mar. Environ. Res. 17:117-121.
58
-------
BIOACCUMULATION SUMMARY AROCLOR 1254
36. Monod, G. 1985. Egg mortality of Lake Geneva char (Salvelinus alpinus) contaminated by PCB
and DDT derivatives. Bull Environ. Contain. Toxicol. 35:531-536.
37. Paine, J.M., MJ. McKee, and E. Ryan. 1993. Toxicity and bioaccumulation of soil PCBs in
crickets: Comparison of laboratory and field studies. Environ. Toxicol. Chem. 12:2097-2103.
38. Lake, J.L., N.I. Rubinstein, H. Lee, C.A. Lake, J. Heltshe, and S. Pavignano. 1990. Equilibrium
partitioning and bioaccumulation of sediment-associated contaminants by infaunal organisms.
Environ. Toxicol. Chem. 9:1095-1106.
39. Toxscan, Inc. 1990. Technical evaluation of environmental impact potential for proposed ocean
disposal of dredged material from Berth 256 Fire Station 111 in Los Angeles Harbor. Toxscan,
Inc., Marine Bioassay Laboratories Division, Watsonville, CA. Prepared for the Port of Los
Angeles, San Pedro, CA.
40. Melancon, M.J., K.A. Turnquist, and J.J. Lech. 1989. Relation of hepatic monooxygenase activity
to tissue PCBs in rainbow trout (Salmo gairdneri} injected with [14C] PCBs. Environ. Toxicol.
Chem. 8:777-782.
41. Dillon, T.M., and R.M. Engler. 1988. Relationship between PCB tissue residues and reproductive
success of fathead minnows. Environmental effects of Dredging Technical Notes. EEDD-01-13,
April 1988. U.S. Army Engineer Waterways Experiment Station.
42. Black, D.E., O.K. Phelps, and R.L. Lapan. 1988. The effect of inherited contamination on eggs
in larval winter flounder, Pseudopleuronectes americanus. Mar. Environ. Res. 25:45-62.
43. Young, D.R., AJ. Mearns, and R.W. Gossett. 1991. Bioaccumulation of p,p -DDE and PCB
1254 by a flatfish bioindicator from highly contaminated sediment of southern California. In
Organic substances and sediments in water - Biological, ed. R.A. Baker, Vol. 3, pp. 159-169.
Lewis Publishers, Inc., Chelsea, MI.
44. Addison, R.F., M.E. Zinck, and D.E. Willis. 1978. Induction of hepatic mixed function oxidase
(mfo) enzymes in trout (Salvelinus fontinalis) by feeding Aroclor 1254 or 3-methylcholanthrene.
Comp. Biochem. Physiol. 61c:323-325.
45. Brumley, C.M., V.S. Haritos, J.T. Ahokas, and D.A. Holdway. 1995. Validation of biomarkers
of marine pollution exposure in sand flathead using aroclor 1254. Aquat. Toxicol. 31:249.262.
46. Duke, T.W., J.I. Lowe, and AJ. Wilson, Jr. 1970. A polychlorinated biphenyl (Aroclor 1254) in
the water, sediment, and biota of Escambia Bay, Florida. Bull. Environ. Contam. Toxicol. 5:171-
180.
47. Fingerman, S., and E.G. Short, Jr. 1983. Changes in neurotransmitter levels in channel catfish after
exposure to benzo(a)pyrene, naphthalene, and Aroclor 1254. Bull. Environ. Contam. Toxicol.
30:147-151.
59
-------
BIOACCUMULATION SUMMARY AROCLOR 1254
48. Folmar, L.C., W.W. Dickhoff, W.S. Zaugg and H.O. Hodgins. 1982. The effects of Aroclor 1254
and No. 2 fuel oil on smoltification and sea-water adaptation of coho salmon (Oncorhynchus
kisutch). Aquat. Toxicol 2:291-299.
49. Lowe, J.I., P.R. Parrish, J.M. Patrick, Jr., and J. Forester. 1972. Effects of the polychlorinated
biphenyl Aroclor 1254 on the American oyster Crassostrea virginica. Mar. Biol. 17:209-214.
50. Melancon, M.J., and J.J. Lech. 1983. Dose-effect relationship for induction of hepatic
monooxygenase activity in rainbow trout and carp by Aroclor 1254. Aquat. Toxicol. 4:51-61.
51. Pinkney, A.E., G.V. Poje, R.M. Sansur, C.C. Lee, and J.M. O'Connor. 1985. Uptake and retention
of 14C-Aroclor 1254 in the amphipod, Gammarus tigrinus, fed contaminated fungus, Fusarium
oxysporum. Arch. Environ. Contain. Toxicol. 14: 59-64.
52. Sanders, H.O., and Chandler, J.H. 1972. Biological magnification of a polychlorinated biphenyl
(Aroclor 1254) from water by aquatic invertebrates. Bull. Environ. Contain. Toxicol.
60
-------
BIOACCUMULATION SUMMARY AROCLOR 1260
Chemical Category: POLYCHLORINATED BIPHENYLS
Chemical Name (Common Synonyms): Aroclor 1260 CASRN: 11096-82-5
Chemical Characteristics
Solubility in Water: 0.027 mg/L at 25°C [1] Half-Life: No data [2,3]
Log Kow: 6.8 [4] Log Koc: No data [4]
Human Health
OralRfD: No data [5] Confidence: —
Critical Effect: PCBs have been shown to cause reproductive failure, birth defects, lesions, tumors,
liver disorders, and death among sensitive species. Their toxicity is further enhanced by their ability
to bioaccumulate and to biomagnify within the food chain due to extremely high lipophilicity [2].
Oral Slope Factor: No data [5] Carcinogenic Classification: A2 [5]
Wildlife
Partitioning Factors: No partitioning factors for Aroclor 1260 were identified for wildlife.
Food Chain Multipliers: For PCBs as a class the most toxic congeners have been shown to be
selectively accumulated from organisms at one trophic level to the next [6]. At least three studies have
concluded that PCBs have the potential to biomagnify in food webs based on aquatic organisms and
predators that feed primarily on aquatic organisms [7,8,9]. The results from Biddinger and Gloss [7] and
USAGE [9] generally agreed that highly water-insoluble compounds (including PCBs) have the potential
to biomagnify in these types of food webs. Thomann's [10] model also indicated that highly water-
insoluble compounds (log Kow values 5 to 7) showed the greatest potential to biomagnify. A
biomagnification factor of 32 was determined for total PCBs from alewife to herring gull eggs in Lake
Ontario [11] No specific food chain multipliers were identified for Aroclor 1260.
Aquatic Organisms
Partitioning Factors: No partitioning factors for Aroclor 1260 were identified for aquatic organisms.
Food Chain Multipliers: Polychlorinated biphenyls as a class have been demonstrated to biomagnify
through the food web. Oliver and Niimi [12], studying accumulation of PCBs in various organisms in
the Lake Ontario food web, reported concentrations of total PCBs in phytoplankton, zooplankton, and
several species of fish. Their data indicated a progressive increase in tissue PCB concentrations moving
61
-------
BIOACCUMULATION SUMMARY AROCLOR 1260
from organisms lower in the food web to top aquatic predators. In a study of PCB accumulation in lake
trout (Salvelinus namaycush) of Lake Ontario, Rasmussen et al. [13] reported that each trophic level
contributed about a 3.5-fold biomagnification factor to the PCB concentrations in the trout. No specific
food chain multipliers were identified for Aroclor 1260.
Toxicity/Bioaccumulation Assessment Profile
PCBs are a group (209 congeners/isomers) of organic chemicals, based on various substitutions of
chlorine atoms on a basic biphenyl molecule. These manufactured chemicals have been widely used in
various processes and products because of the extreme stability of many isomers, particularly those with
five or more chlorines [14]. A common use of PCBs was as dielectric fluids in capacitors and
transformers. In the United States, Aroclor is the most familiar registered trademark of commercial PCB
formulations. Generally, the first two digits in the Aroclor designation indicate that the mixture contains
biphenyls, and the last two digits give the weight percent of chlorine in the mixture (e.g., Aroclor 1260
contains biphenyls with approximately 60 percent chlorine).
As a result of their stability and their general hydrophobic nature, PCBs released to the environment have
dispersed widely throughout the ecosystem [14]. PCBs are among the most stable organic compounds
known, and chemical degradation rates in the environment are thought to be slow. As a result of their
highly lipophilic nature and low water solubility, PCBs are generally found at low concentrations in water
and at relatively high concentrations in sediment [15]. Individual PCB congeners have different physical
and chemical properties based on the degree of chlorination and position of chlorine substitution,
although differences with degree of chlorination are more significant [15]. Solubilities and octanol-water
partition coefficients for PCB congeners range over several orders of magnitude [16]. Octanol-water
partition coefficients, which are often used as estimators of the potential for bioconcentration, are highest
for the most chlorinated PCB congeners.
Dispersion of PCBs in the aquatic environment is a function of their solubility [15] while PCB mobility
within and sorption to sediment are a function of chlorine substitution pattern and degree of chlorination
[17]. The concentration of PCB s in sediments is a function of the physical characteristics of the sediment,
such as grain size [18,19] and total organic carbon content [18,19,20,21]. Fine sediments typically
contain higher concentrations of PCBs than coarser sediments because of more surface area [15].
Mobility of PCBs in sediment is generally quite low for the higher chlorinated biphenyls [17]. Therefore,
it is common for the lower chlorinated PCBs to have a greater dispersion from the original point source
[15]. Limited mobility and high rates of sedimentation could prevent some PCB congeners in the
sediment from reaching the overlying water via diffusion [17].
The persistence of PCBs in the environment is a result of their general resistance to degradation [16]. The
rate of degradation of PCB congeners by bacteria decreases with increasing degree of chlorination [22];
other structural characteristics of the individual PCBs can affect susceptibility to microbial degradation
to a lesser extent [16]. Photochemical degradation, via reductive dechlorination, is also known to occur
in aquatic environments; the higher chlorinated PCBs appear to be most susceptible to this process [21].
Toxicity of PCB congeners is dependent on the degree of chlorination as well as the position of chlorine
substitution. Lesser chlorinated congeners are more readily absorbed, but are metabolized more rapidly
62
-------
BIOACCUMULATION SUMMARY
AROCLOR 1260
than higher chlorinated congeners [23]. PCB congeners with no chlorine substituted in the ortho (2 and
2') positions but with four or more chlorine atoms at the meta (3 and 3') and para (4 and 4') positions can
assume a planar conformation that can interact with the same receptor as the highly toxic 2,3,7,8-
tetrachlorodibenzo-p-dioxin (TCDD) [24]. Examples of these more toxic, coplanar congeners are
3,3',4,4'-tetrachlorobiphenyl (PCB 77), 3,3',4,4',5-pentachlorobiphenyl (PCB 126), and 3,3',4,4',5,5'-
hexachlorobiphenyl (PCB 169). A method that has been proposed to estimate the relative toxicity of
mixtures is to use toxic equivalency factors (TEFs) [25]. With this method, relative potencies for
individual congeners are calculated by expressing their potency in relation to 2,3,7,8-TCDD. The
following TEFs have been recommended [25,26]:
Congener Class
3,3',4,4',5-PentaCB
3,3',4,4',5,5'-HexaCB
3,3',4,4'-TetraCB
Monoortho coplanar PCBs
Diortho coplanar PCBs
Recommended TEF
0.1
0.05
0.01
0.001
0.00002
Due to the toxicity, high Kow values, and highly persistent nature of many PCBs, they possess a high
potential to bioaccumulate and exert reproductive effects in higher-trophic-level organisms. Aquatic
organisms have a strong tendency to accumulate PCBs from water and food sources. The
bioconcentration factor for fish is approximately 50,000 [27]. This factor represents the ratio of
concentration in tissue to the ambient water concentration. Aquatic organisms living in association with
PCB-contaminated sediments generally have tissue concentrations equal to or greater than the
concentration of PCB in the sediment [27]. Once taken up by an organism, PCBs partition primarily into
lipid compartments [15]. Thus, differences in PCB concentration between species and between different
tissues within the same species may reflect differences in lipid content [15]. PCB concentrations in
polychaetes and fish have been strongly correlated to their lipid content [28]. Elimination of PCBs from
organisms is related to the characteristics of the specific PCB congeners present. It has been shown that
uptake and depuration rates in mussels are high for lower-chlorinated PCBs and much lower for higher-
chlorinated congeners [29, 30]. In some species, tissue concentrations of PCBs in females can be reduced
during gametogenesis because of PCB transfer to the more lipophilic eggs. Therefore, the transferred
PCBs are eliminated from the female during spawning [31,32]. Fish and other aquatic organisms
biotransform PCBs more slowly than other species, and they appear less able to metabolize, or excrete,
the higher chlorinated PCB congeners [31]. Consequently, fish and other aquatic organisms may
accumulate more of the higher chlorinated PCB congeners than is found in the environment [16].
The acute toxicity of PCBs appears to be relatively low, but results from chronic toxicity tests indicate
that PCB toxicity is directly related to the duration of exposure [1]. Toxic responses have been noted to
occur at concentrations of 0.03 and 0.014 ug/L in marine and freshwater environments, respectively [1].
The LC50 for grass shrimp exposed to PCBs in marine waters for 4 days was 6.1 to 7.8 |ig/L [1 ]. Chronic
toxicity of PCBs presents a serious environmental concern because of their resistance to degradation [33],
although the acute toxicity of PCBs is relatively low compared to that of other chlorinated hydrocarbons.
Sediment contaminated with PCBs has been shown to elicit toxic responses at relatively low
63
-------
BIOACCUMULATION SUMMARY AROCLOR 1260
concentrations. Sediment bioassays and benthic community studies suggest that chronic effects generally
occur in sediment at total PCB concentrations exceeding 370 |ig/kg [34].
A number of field and laboratory studies provide evidence of chronic sublethal effects on aquatic
organisms at low tissue concentrations [16]. Field and Dexter [16] suggest that a number of marine and
freshwater fish species have experienced chronic toxicity at PCB tissue concentrations of less than 1.0
mg/kg and as low as 0.1 mg/kg. Spies et al. [35] reported an inverse relationship between PCB
concentrations in starry flounder eggs in San Francisco Bay and reproductive success, with an effective
PCB concentration in the ovaries of less than 0.2 mg/kg. Monod [36] also reported a significant
correlation between PCB concentrations in eggs and total egg mortality in Lake Geneva char. PCBs have
also been shown to cause induction of the mixed function oxidase (MFO) system in aquatic animals, with
MFO induction by PCBs at tissue concentrations within the range of environmental exposures [16].
64
-------
Summary of Biological Effects Tissue Concentrations for Aroclor 1260
Species:
Taxa
Invertebrates
Clam, Macoma
nasuta
Concentration, Units in1:
Sediment Water
1 .2 mg/kg dw
(reference
station)
0.9 mg/kg dw
3.8 mg/kg dw
Tissue (Sample Type)
0.976 mg/kg
(variance = 4.6xl06,
n=5)
18.600 mg/kg
(variance = na; n=5)
9.170 mg/kg
(variance = 3.96xl08,
n=5)
Toxicity: Ability to Accumulate2:
Log Log
Effects BCF BAF BSAF
Survival
(out of 20):
19.8
(variance=0.2,
n=5)
5.2
(variance=6.2,
n=5)
19.8
(variance=0.2,
n=5)
Source:
Reference Comments3
[37] L; standard bioassay
with field collected
sediments with
multiple
contaminants.
Tissue burdens and
toxicity were
determined in
separate aquaria
after 20 and 10
days, respectively.
1 Concentration units based on wet weight unless otherwise noted.
2 BCF = bioconcentration factor, BAF = bioaccumulation factor, BSAF = biota-sediment accumulation factor.
3 L = laboratory study, spiked sediment, single chemical; F = field study, multiple chemical exposure; other unusual study conditions or observations noted.
-------
BIOACCUMULATION SUMMARY AROCLOR 1260
References
1. USEPA. 1980. Ambient water quality criteria document: Poly chlorinated biphenyls. EPA
440/5-80-068. (Cited in USEPA. 1996. Hazardous Substances Data Bank (HSDB). National
Library of Medicine online (TOXNET). U.S. Environmental Protection Agency, Office of Health
and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH.
February.)
2. Eisler, R. 1986. Poly chlorinated biphenyl hazards to fish, wildlife, and invertebrates: A synoptic
review. U.S. Fish Wildl. Serv. Biol. Rep. 85(1.7).
3. MacKay, D., W.Y. Shiu, and K.C. Ma. 1992. Illustrated handbook of physical-chemical
properties and environmental fate for organic chemicals. Vol. I, Monoaromatic hydrocarbons,
chlorobenzenes, and PCBs. Lewis Publishers, Boca Raton, FL.
4. Agency for Toxic Substances and Disease Registry. 1993. Toxicological profile for
poly chlorinated biphenyls. Prepared by Syracuse Research Corporation. Prepared for U.S.
Department of Health and Human Services, Public Health Service. April 1993.
5. USEPA. 1995. Integrated Risk Information System (IRIS). National Library of Medicine online
(TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental
Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. September.
6. Jones, P.O., J.P. Giesy, T.J. Kubiak, D.A. Verbrugge, J.C. Newstead, J.P. Ludwig, D.E. Tillit,
R. Crawford, N. De Galan, and G.T. Ankley. 1993. Biomagnification of bioassay-derived
2,3,7,8-tetrachlorodibenzo-j?-dioxin equivalents. Chemosphere 26:1203-1212.
7. Biddinger, G.R., and S.P. Gloss. 1984. The importance of trophic transfer in the
bioaccumulation of chemical contaminants in aquatic ecosystems. Residue Rev. 91:103-145.
8. Kay, S.H. 1984. Potential for biomagnification of contaminants within marine and freshwater
food webs. Technical Report D-84-7. U.S. Army Corps of Engineers, Waterways Experiment
Station, Vicksburg, MS.
9. USAGE. 1995. Trophic transfer and biomagnification potential of contaminants in aquatic
ecosystems. Environmental Effects of Dredging, Technical Notes EEDP-01-33. U.S. Army
Corps of Engineers, Waterways Experiment Station, Vicksburg, MS.
10. Thomann, R.V. 1989. Bioaccumulation model of organic chemical distribution in aquatic food
chains. Environ. Sci. Technol. 23:699.
11. Hoffman, D.J., C.P. Rice, and T.J. Kubiak. 1996. PCBs and dioxins in birds. In Environmental
contaminants in wildlife, ed. W.N. Beyer, G.H. Heinz, and A.W. Redmon-Horwood, pp. 165-207.
Lewis Publishers, Boca Raton, FL.
66
-------
BIOACCUMULATION SUMMARY AROCLOR 1260
12. Oliver, E.G., and AJ. Niimi. 1988. Trophodynamic analysis of polychlorinated biphenyl
congeners and other chlorinated hydrocarbons in the Lake Ontario ecosystem. Environ. Sci.
Technol. 22:388-397.
13. Rasmussen, J.B., DJ. Rowan, D.R.S. Lean, and J.H. Carey. 1990. Food chain structure in
Ontario lakes determines PCB levels in lake trout (Salvelinus namaycush) and other pelagic fish.
Can. J. Fish. Aquat. Sci. 47:2030-2038.
14. Rand, G.M., P.O. Wells, and L.S. McCarty. 1995. Chapter 1. Introduction to aquatic toxicology.
In Fundamentals of aquatic toxicology: Effects, environmental fate, and risk assessment, ed.
G.M. Rand, pp. 3-67. Taylor and Francis, Washington, DC.
15. Phillips, DJ.H. 1986. Use of organisms to quantify PCB s in marine and estuarine environments.
In PCBs and the environment, ed. J.S. Waid, pp.127-182. CRC Press, Inc., Boca Raton, FL.
16. Field, LJ. and R.N. Dexter. 1998. A discussion of PCB target levels in aquatic sediments.
Unpublished document. January 11, 1988.
17. Fisher, J.B., R.L. Petty, and W. Lick. 1983. Release of polychlorinated biphenyls from
contaminated lake sediments: Flux and apparent diffusivities of four individual PCBs. Environ.
Pollut. 5B: 121-132.
18. Pavlou, S.P., and R.N. Dexter. 1979. Distribution of polychlorinated biphenyls (PCB) in
estuarine ecosystems: Testing the concept of equilibrium partitioning in the marine environment.
Environ. Sci. Technol. 13:65-71.
19. Lynch, T.R., and H.E. Johnson. 1982. Availability of hexachlorobiphenyl isomer to benthic
amphipods from experimentally contaminated sediments. In Aquatic Toxicology and Hazard
Assessment: Fifth Conference, ASTM STP 766, ed. J.G. Pearson, R.B. Foster, and W.E. Bishop,
pp. 273-287. American Society of Testing and Materials, Philadelphia, PA.
20. Chou, S.F.J., and R.A. Griffin. 1986. Solubility and soil mobility of polychlorinated biphenyls.
In PCBs and the environment, ed. J. S. Waid, Vol. 1, pp. 101-120. CRC Press, Inc. Boca Raton,
Florida.
21. Sawhney, B.L. 1986. Chemistry and properties of PCBs in relation to environmental effects.
In PCBs and the environment, ed. J.S. Waid, pp. 47-65. CRC Press, Inc., Boca Raton, FL.
22. Furukawa, K. 1986. Modification of PCBs by bacteria and other microorganisms. In PCBs and
the environment, ed. J. S. Waid, Vol. 2, pp. 89-100. CRC Press, Inc. Boca Raton, Florida.
23. Bolger, M. 1993. Overview of PCB toxicology. Proceedings of the U.S. Environmental
Protection Agency's National Technical Workshop "PCBs in Fish Tissue," EPA/823-R-93-003.
U.S. Environmental Protection Agency, Office of Water, Washington, DC, May 10-11, 1993,
pp. 37-53.
67
-------
BIOACCUMULATION SUMMARY AROCLOR 1260
24. Erickson, M.D. 1993. Introduction to PCBs and analytical methods. Proceedings of the U.S.
Environmental Protection Agency's National Technical Workshop "PCBs in Fish Tissue,"
EPA/823-R-93-003. U.S. Environmental Protection Agency, Office of Water, Washington, DC,
May 10-11, 1993, pp. 3-9.
25. Safe, S. 1990. Polychlorinated biphenyls (PCBs), dibenzo-p-dioxins (PCDDs), dibenzofurans
(PCDFs), and related compounds: Environmental and mechanistic considerations which support
the development of toxic equivalency factors (TEFs). Critical Reviews in Toxicology 21(1):51-
26. USEPA. 1991. Workshop report on toxicity equivalency factors for polychlorinated biphenyl
congeners. EPA/625/3-91/020. U.S. Environmental Protection Agency. (Eastern Research
Group, Inc., Arlington, MA.)
27. Neff, J.M. 1984. Bioaccumulation of organic micropollutants from sediments and suspended
particulates by aquatic animals. Fres. Z. Anal. Chem. 319:132-136.
28. Shaw, G.R., and D. W. Connell. 1982. Factors influencing concentrations of polychlorinated
biphenyls in organisms from an estuarine ecosystem. Aust. J. Mar. Freshw. Res. 33:1057-1070.
29. Tanabe, S., R. Tatsukawa, and DJ.H. Phillips. 1987. Mussels as bioindicators of PCB pollution:
A case study on uptake and release of PCB isomers and congeners in green-lipped mussels
(Perna viridis) in Hong Kong waters. Environ. Pollut. 47:41-62.
30. Pruell, R. J., J. L. Lake, W. R. Davis, and J. G. Quinn.. 1986. Uptake and depuration of organic
contaminants by blue mussels (Mytilus edulis) exposed to environmentally contaminated
sediments. Mar. Biol. 91:497-508.
31. Lech, J.J., and R.E. Peterson. 1983. Biotransformation and persistence of polychlorinated
biphenyls (PCBs) in fish. In PCBs: Human and environmental hazards, ed. P.M. D'ltri and M.A.
Kamrin, pp. 187-201. Ann Arbor Science Publishers, Inc., Ann Arbor, MI.
32. Stout, V.F. 1986. What is happening to PCBs? Elements of effective environmental monitoring
as illustrated by an analysis of PCB trends in terrestrial and aquatic organisms. In PCBs and the
environment, ed. J.S. Waid. CRC Press, Inc., Boca Raton, FL.
33. Mearns, A.J., M. Malta, G. Shigenaka, D. MacDonald, M. Buchman, H. Harris, J. Golas, and G.
Lauenstein. 1991. Contaminant trends in the Southern California Bight: Inventory and
assessment. Technical Memorandum NOAA ORCA 62. National Oceanic and Atmospheric
Administration. Seattle, WA.
34. 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. NOAA Tech. Memo. NOS
OMA 52. National Oceanic and Atmospheric Administration, Seattle, WA.
68
-------
BIOACCUMULATION SUMMARY AROCLOR 1260
35. Spies, R. B., D. W. Rice, Jr., P. A. Montagna, and R. R. Ireland. 1985. Reproductive success,
xenobiotic contaminants and hepatic mixed-function oxidase (MFO) activity in Platichthys
stellatus populations from San Francisco Bay. Mar. Environ. Res. 17:117-121.
36. Monod, G. 1985. Egg mortality of Lake Geneva char (Salvelinus alpinus) contaminated by PCB
and DDT derivatives. Bull. Environ. Contam. Toxicol. 35:531-536.
37. Toxscan, Inc. 1990. Technical evaluation of environmental impact potential for propose d ocean
disposal of dredged material from Berth 256 Fire Station 111 in Los Angeles Harbor. Toxscan,
Inc., Marine Bioassay Laboratories Division, Watsonville, CA. Prepared for the Port of Los
Angeles, San Pedro, CA.
69
-------
70
-------
BIOACCUMULATION SUMMARY ARSENIC
Chemical Category: METAL
Chemical Name (Common Synonyms): ARSENIC CASRN: 7440-38-2
Chemical Characteristics
Solubility in Water: Insoluble [1] Half-Life: Not applicable, stable [1]
LogKow: - LogKoc: -
Human Health
Oral RfD: 3 x 10~4 mg/kg/day [2] Confidence: Medium, uncertainty factor = 3
Critical Effect: Hyperpigmentation, keratosis, and possible vascular complications
Oral Slope Factor: 1.5 x 10+0 per (mg/kg)/day [2] Carcinogenic Classification: A [2]
Wildlife
Partitioning Factors: Partitioning factors for arsenic in wildlife were not found in the literature.
Food Chain Multipliers: Food chain multipliers for arsenic in wildlife were not found in the literature.
Aquatic Organisms
Partitioning Factors: Arsenic is a metal that occurs in aquatic systems in a number of chemical forms.
The most prevalent form is arsenate, followed by arsenite, which usually is present at lower
concentrations. The arsenate ions can be methylated and form alkylated compounds (methylarsenic acid
and dimethylarsenic acid). In any aquatic environment only a small portion of the total arsenic
(approximately 0.1 percent) exists as methylated species. The arsenic methylation rate is strongly
correlated with sediment organic matter content in sediments and amount of sulfate-reducing bacteria.
Food Chain Multipliers: The simplified trophic transfer experiment conducted by Lindsay and Sanders
[11] effectively ended speculation of food chain transfer to the second trophic level. Arsenic is taken up
by aquatic organisms primarily through dietary exposure [3]
Toxicity/Bioaccumulation Assessment Profile
Arsenic (As) is accumulated by aquatic organisms primarily through dietary exposure [3]. The most toxic
form of arsenic in aquatic systems is As HI, follow by As V, and the least toxic forms are organic
complexes. The bioavailability of arsenic is not dependent on the concentration of acid-volatile sulfides
71
-------
BIOACCUMULATION SUMMARY ARSENIC
(AVS). Pore water concentrations of arsenic are two to three orders of magnitude higher than surface
water concentrations [4], a factor that can be of considerable lexicological importance to some benthic
organisms. It has been demonstrated that sediments are the major source of arsenic to the infaunal
organisms and the body burden is related to the concentration of extractable (IN HCL) arsenic normalized
for iron [5].
72
-------
Summary of Biological Effects Tissue Concentrations for Arsenic
Species:
Taxa
Invertebrates,
field-collected
Tubificidae
Helisoma
campanulata,
Snail
Concentration, Units in1:
Sediment Water
Total SEM Filt Nonfit
|ig/g n-g/g H-g/L ng/L
404 202 57 1740
102 24 54 158
68 25 72 138
46 11 29 72
11 3 23 31
4 <0.5 3 <22
9.78 |ig/g
1.15ng/g
26 |ig/g
18 |ig/g
17 M-g/g
Tissue (Sample Type)
M-g/g
34
15
13
27
3
3
6.96 mg/g
4.98 mg/g
7.38 mg/g
2.35 mg/g
5.95 mg/g
4.2 mg/kg
(whole body)4
16 mg/kg
(whole body)4
5.8 mg/kg
(whole body)4
4 mg/kg
(whole body)4
Toxicity:
Effects
Mortality,
ED16
Mortality,
NOED
Mortality,
NOED
Mortality,
NOED
Ability to Accumulate2: Source:
Log Log
BCF BAF BSAF Reference Comments3
[8] F
[7] L
[16] L; mixture of 4
arsenic compounds,
estimated body
burden from graph
[16] L; mixture of 4
arsenic compounds,
estimated body
burden from graph
[16] L; mixture of 4
arsenic compounds,
estimated body
burden from graph
[16] L; mixture of 4
arsenic compounds,
estimated body
burden from graph
-------
Summary of Biological Effects Tissue Concentrations for Arsenic
Species: Concentration, Units in1:
Taxa Sediment Water
Stagnicola
emarginata,
Snail
Mytilus
galloprovincialis,
Mussel
Ceriodaphnia dubia, l,120|ig/g 1295 |ig/L
Cladoceran , _„_ . 0_0_ „
2,720 |ig/g 3580 |ig/L
650 |ig/g 901 |jg/L
569 |ig/g 436 |jg/L
Tissue (Sample Type)
3.6 mg/kg
(whole body)4
3.6 mg/kg
(whole body)4
3.6 mg/kg
(whole body)4
3.6 mg/kg
(whole body)4
0.44-0.51 mg/kg
Toxicity: Ability to Accumulate2:
Log Log
Effects BCF BAF BSAF
Mortality,
NOED
Mortality,
NOED
Mortality,
NOED
Mortality,
NOED
0.047
70% mortality
70% mortality
20% mortality/
no reproduction
0% mortality/
no reproduction
Source:
Reference Comments3
[16] L; mixture of 4
arsenic compounds,
estimated body
burden from graph
[16] L; mixture of 4
arsenic compounds,
estimated body
burden from graph
[16] L; mixture of 4
arsenic compounds,
estimated body
burden from graph
[16] L; mixture of 4
arsenic compounds,
estimated body
burden from graph
[12] F
[4] L
-------
Summary of Biological Effects Tissue Concentrations for Arsenic
Species:
Taxa
Daphnia magna,
Cladoceran
Hyallela azteca,
Amphipod
Concentration, Units in1:
Sediment Water Tissue (Sample Type)
3.8 mg/kg
(whole body)4
9.8 mg/kg
(whole body)4
4.4 mg/kg
(whole body)4
4 mg/kg
(whole body)4
87 mg/kg
(whole body)4
33 mg/kg
(whole body)4
3580 |ig/g 1420 |ig/L
Toxicity: Ability to Accumulate2:
Log Log
Effects BCF BAF BSAF
Mortality,
NOED
Mortality,
NOED
Mortality,
NOED
Mortality,
NOED
Mortality,
ED50
Reproduction,
ED10
Growth
reduction
Source:
Reference
[16]
[16]
[16]
[16]
[6]
[6]
[4]
Comments3
L; mixture of 4
arsenic compounds,
estimated body
burden from graph,
tissues exposed 21 d
L; mixture of 4
arsenic compounds,
estimated body
burden from graph,
tissues exposed 21 d
L; mixture of 4
arsenic compounds,
estimated body
burden from graph,
tissues exposed 21 d
L; mixture of 4
arsenic compounds,
estimated body
burden from graph,
tissues exposed 21 d
L; lethal body
burden after 21 d
exposure
L; 10% reduction in
number of offspring
L
-------
Summary of Biological Effects Tissue Concentrations for Arsenic
Species: Concentration, Units in1:
Taxa Sediment Water
Hyallela azteca, Total SEM Filt Nonfilt
Amphipod |ig/g |ig/g |ig/L |ig/L
404 202 57 1740
102 24 54 158
68 25 72 138
46 11 29 72
11 3 23 31
4 <0.5 3 <22
Palaemonetes pugio,
Grass shrimp
Pteronarcys dorsata,
Giant black stonefly
Tissue (Sample Type)
M-g/g
7
12
4
2
1
0.4
1.15 mg/kg
(whole body)4
1.03 mg/kg
(whole body)4
1.28 mg/kg
(whole body)4
1.14 mg/kg
(whole body)4
8.4 mg/kg
(whole body)4
6 mg/kg
(whole body)4
7 mg/kg
(whole body)4
Toxicity:
Effects
Growth,
NOED
Growth,
NOED
Growth,
NOED
Growth,
NOED
Mortality,
NOED
Mortality,
NOED
Mortality,
NOED
Ability to Accumulate2: Source:
Log Log
BCF BAF BSAF Reference
[8]
[11]
[11]
[11]
[11]
[16]
[16]
[16]
Comments3
F
L; no effect on
growth
L; no effect on
growth
L; no effect on
growth
L; no effect on
growth
L; mixture of 4
arsenic compounds,
estimated body
burden from graph
L; mixture of 4
arsenic compounds,
estimated body
burden from graph
L; mixture of 4
arsenic compounds,
estimated body
burden from graph
-------
Summary of Biological Effects Tissue Concentrations for Arsenic
Species:
Taxa
Concentration, Units in1:
Sediment Water Tissue (Sample Type)
8.4 mg/kg
(whole body)4
Toxicity:
Effects
Mortality,
NOED
Ability
Log
BCF
to Accumulate2:
Log
BAF BSAF
Source:
Reference
[16]
Comments3
L; mixture of 4
arsenic compounds,
estimated body
burden from graph
Fishes
Oncorhynchus
mykiss,
Rainbow trout
8.4 mg/L
18.1 mg/L
240 mg/L
1.8 mg/kg
3.5 mg/kg
(0.18 mmol/kg)
[10]
Oncorhynchus
mykiss,
Rainbow trout
3 mg/kg
(whole body)4
4.7 mg/kg
(whole body)4
8.6 mg/kg
(whole body)4
13.5 mg/kg
(whole body)4
Growth,
NOED
Mortality,
LOED
Behavior,
ED50
Behavior,
ED50
[14] L; exposure to
arsenic for 21 d did
not affect growth at
the longest time
interval tested
[14] L; pre-exposure to
arsenic for 7 d
produced significant
increase in LC50
(reduced sensitivity
to exposure) at
shortest time
interval tested
[15] L; loss of
equilibrium,
mortality
[15] L; loss of
equilibrium,
mortality
-------
Summary of Biological Effects Tissue Concentrations for Arsenic
Species:
Taxa
Concentration, Units in1:
Toxicity: Ability to Accumulate2:
Log Log
Source:
Sediment Water Tissue (Sample Type) Effects BCF BAF BSAF Reference Comments3
8.1 mg/kg
(whole body)4
8.6 mg/kg
(whole body)4
Behavior,
ED50
Behavior,
ED50
[15]
[15]
L;loss of
equilibrium,
mortality
L;loss of
equilibrium,
mortality
Lepisosteus osseus, 673 |ig/g 186 [ig/L 0.051 mg/kg
Longnose gar
[9]
Esox lucius,
Northern pike
673 [ig/g 186 \iglL 0.025 mg/kg
[9]
Notemigonus 673 [ig/g 186 [ig/L 0.167 mg/kg
crysoleiicas, Golden
shiner
[9]
Notropis
atherinoides,
Emerald shiner
673 [ig/g 186 [ig/L 0.036 mg/kg
[9]
Notropis hudsonius, 673 [ig/g 186 [ig/L 0.03 mg/kg
Spottail shiner
[9]
Pimephales notatus, 673 [ig/g 186 [ig/L 0.0513 mg/kg
Bluntnose minnow
[9]
-------
Summary of Biological Effects Tissue Concentrations for Arsenic
Species:
Taxa
Pimephales
promelas,
Fathead minnow
Semotilus
atromaculatus,
Creek chub
Catostomus
commersoni,
White sucker
Concentration, Units in1:
Sediment Water
9. 10 Mg/g
9.78 Mg/g
1.25 Mg/g
26 Mg/g
15 Mg/g
18 Mg/g
17 Mg/g
17 M-g/g
11 M8/8
673 Mg/g 186 Mg/L
673 Mg/g 186 Mg/L
Toxicity:
Tissue (Sample Type) Effects
1.39mg/g
1.14mg/g
1.58mg/g
2.40 mg/g
1.76mg/g
0.66 mg/g
2.33 mg/g
2.22 mg/g
1.82 mg/g
2.36 mg/kg
0.132 mg/kg
Ability to Accumulate2: Source:
Log Log
BCF BAF BSAF Reference Comments3
[7] L
[9] F
[9] F
Fundulus diaphanus, 673 Mg/g
Banded killifish
186 Mg/L 0.101 mg/kg
[9]
Amblolites repestris, 673 Mg/g
Rock bass
186 Mg/L 0.128 mg/kg
[9]
Lepomis gibbosus,
Pumpkinseed
673 Mg/g 186 Mg/L 0.342 mg/kg
[9]
-------
oo
o
Summary of Biological Effects Tissue Concentrations for Arsenic
Species:
Concentration, Units in1:
Toxicity:
Ability to Accumulate2:
Source:
Taxa
Lepomis
macrochirus,
Bluegill
Sediment Water Tissue (Sample Type)
0.52 mg/kg
(whole body)4
Effects
Mortality,
NOED
Log
BCF
Log
BAF
BSAF Reference
[13]
Comments3
L; no effect on
mortality
Micropterus
salmoides
Largemouth bass
673 |ig/g 186 |ig/L
0.083 mg/kg
[9]
Percaflavescens
Yellow perch
673 |ig/g 186 |ig/L
0.077 mg/kg
[9]
Stizostedion vitreum 673 |ig/g
vitreum, Walleye
186 |ig/L
0.080 mg/kg
[9]
Concentration units based on wet weight unless otherwise noted.
2 BCF = bioconcentration factor, BAF = bioaccumulation factor, BSAF = biota-sediment accumulation factor.
3 L = laboratory study, spiked sediment, single chemical; F = field study, multiple chemical exposure; other unusual study conditions or observations noted.
4 This entry was excerpted directly from the Environmental Residue-Effects Database (ERED, www.wes.army.mil/el/ered, U.S. Army Corps of Engineers and U.S.
Environmental Protection Agency). The original publication was not reviewed, and the reader is strongly urged to consult the publication to confirm the information
presented here.
-------
BIOACCUMULATION SUMMARY ARSENIC
References
1. Weast handbook of chemistry and physics, 68th edition, 1987-1988,6-73. (Cited in: USEPA. 1995.
Hazardous Substances Data Bank (HSDB). National Library of Medicine online (TOXNET). U.S.
Environmental Protection Agency, Office of Health and Environmental Assessment, Environmental
Criteria and Assessment Office, Cincinnati, OH. September.)
2. USEPA. 1995. Integrated Risk Information System (IRIS). National Library of Medicine online
(TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental
Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. September.
3. Woodward, D.F., W.G. Brumbaugh, A.J. DeLonay, E.E. Little, and C.E. Smith. 1994. Effects on
rainbow trout fry of a metals-contaminated diet of benthic invertebrates from the Clark Fork River,
Montana. Tran. Amer. Fish. Society 123:51-62.
4. Top, K.M., J. Bleiler, S. Reed, C. George, and A. Putt. 1995. Bioavailability of metals and toxicity
identification evaluation of the sediment pore waters from Plow Shop Pond, Fort Devens,
Massachusetts. Abstract, 16th Annual Meeting, Society of Environmental Toxicology and
Chemistry, Vancouver, British Columbia, Canada, November 5-9, 1995.
5. Bryan, G.W., and WJ. Langston. 1992. Bioavailability, accumulation and effects of heavy metals
in sediments with special reference to United Kingdom estuaries: A review. Environ. Pollut.
76:89-131.
6. Enserink, E.L., J.L. Mass-Diepeveen, and CJ. Van Leeuwen. 1991. Combined effects of metals;
An ecotoxicological evaluation. Water Res. 25:679-687.
7. Krantzberg, G. 1994. Spatial and temporal variability in metal bioavailability and toxicity of
sediment from Hamilton Harbour, Lake Ontario. Environ. Toxicol. Chem. 13:1685-1698.
8. Ingersoll, C.G., W.G. Brumbaugh, FJ. Dwuer, and N.E. Kemble. 1994. Bioaccumulation of metals
by Hyalella azteca exposed to contaminated sediments from the Upper Clark Fork River, Montana.
Environ. Toxicol. Chem. 13:2013-2020.
9. Azcue, J.M., and D.G. Dixon. 1994. Effects of past mining activities on the arsenic concentration
in fish from Moira Lake, Ontario. Internal Assoc. Great Lakes Res. 20:717-724.
10. McGeachy, S.M., and D.G. Dixon. 1990. Effect of temperature on the chronic toxicity of arsenic
to rainbow trout (Oncorhynchus mykiss). Can. J. Fish. Aquat. Sci. 47:2228-2234.
11. Lindsay, D.M., and J.G. Sanders. 1990. Arsenic uptake and transfer in a simplified estuarine food
chain. Environ. Toxicol. Chem. 9:391-395.
12. Houkal, D., B. Rummel, and B. Shephard. 1996. Results of an in situ mussel bioassay in the Puget
Sound. Abstract, 17th Annual Meeting, Society of Environmental Toxicology and Chemistry,
Washington, DC, November 17-21, 1996.
81
-------
BIOACCUMULATION SUMMARY ARSENIC
13. Barrows, M.E., S.R. Petrocelli, K.J. Macek, and JJ. Carroll. 1980. Bioconcentration and elimination
of selected water pollutants by bluegill sunfish (Lepomis macrochirus). In Dynamics, exposure and
hazard assessment of toxic chemicals, ed. R. Haque, pp. 379-392.
14. Dixon, D.G., and J.B. Sprague. 1981. Acclimation-induced changes in toxicity of arsenic and
cyanide to rainbow trout, Salmo gairdneri Richardson. /. Fish Biol. 18: 579-589.
15. Mcgeachy, S.M., and D.G. Dixon. 1992. Whole-body arsenic concentrations in rainbow trout during
acute exposure to arsenate. Ecotoxicol Environ. Saf. 24:301-308.
16. 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. Arch. Environm. Contain. Toxicol. 9:
53-63.
82
-------
BIOACCUMULATION SUMMARY BENZO(A)ANTHRACENE
Chemical Category: POLYNUCLEAR AROMATIC HYDROCARBON (high molecular weight)
Chemical Name (Common Synonyms): BENZO(A)ANTHRACENE CASRN: 56-55-3
Chemical Characteristics
Solubility in Water: 0.014 mg/L at 25°C [1] Half-Life: No data [2]
Log Kow: 5.70 [3] Log Koc: 5.60 L/kg organic carbon
Human Health
Oral RfD: No data [4] Confidence: —
Critical Effect: —
Oral Slope Factor (Reference): No data [4] Carcinogenic Classification: No data [4]
Wildlife
Partitioning Factors: Partitioning factors for benzo(a)anthracene in wildlife were not found in the
literature.
Food Chain Multipliers: Food chain multipliers for benzo(a)anthracene in wildlife were not found in
the literature.
Aquatic Organisms
Partitioning Factors: Partitioning factors for benzo(a)anthracene in aquatic organisms were not found
in the literature.
Food Chain Multipliers: Food chain multipliers (FCMs) for trophic level 3 aquatic organisms were 12.8
(all benthic food web), 1.4 (all pelagic food web), and 8.0 (benthic and pelagic food web). FCMs for
trophic level 4 aquatic organisms were 20.2 (all benthic food web), 2.3 (all pelagic food web), and 10.2
(benthic and pelagic food web) [16].
Toxicity/Bioaccumulation Assessment Profile
The acute toxicity of hydrocarbons, including benzo(a)anthracene, to both fresh and salt water
crustaceans is largely nonselective, i.e., it is not primarily influenced by molecular structure, but is rather
controlled by organism-water partitioning which, for nonpolar organic chemicals, is in turn a reflection
83
-------
BIOACCUMULATION SUMMARY BENZO(A)ANTHRACENE
of aqueous solubility. The toxic effect is believed to occur at a relatively constant concentration within
the organism [5]. Toxicity of benzo(a)anthracene, as well as chrysene and pyrene, to striped bass
(Morone saxatilis) decreased as water salinity increased [6].
Bioavailability of sediment-associated polynuclear aromatic hydrocarbons (PAHs), e.g.,
benzo(a)anthracene, has been observed to decline with increased contact time [7]. The majority of
investigations have shown that aquatic organisms are able to release PAHs from their tissues rapidly when
they were returned to a clean environment. Mussels exposed to contaminated sediment rapidly
accumulated benzo(a)anthracene reaching maximum concentrations at day 20 [8]. The concentration
factors for mussels exposed to 675 ng/g of benzo(a)anthracene in sediment ranged from 2,470 to 35,700
[4]. Benzo(a)anthracene was rapidly taken up by the aquatic plant, Fontinalis antipyretica and the uptake
kinetics plateaued between 48 and 168 h of exposure [9]. Roy et al. [9] suggested that slow elimination
of benzo(a)anthracene from the plant tissue may be due to low aqueous solubility. Sediment-associated
benzo(a)anthracene can be accumulated from two sources: interstital water and ingested particles. The
accumulation kinetics of benzo(a)anthracene suggest that uptake occurs via the sediment interstitial water
and ingested material and is controlled by desorption from sediment particles and dissolved organic
matter [10]. Benzo(a)anthracene after 24 h exposure was accumulated by Daphnia pulex mostly from
the water, while lower-molecular-weight PAHs like napththalene and phenanthrene were accumulated
primarily through algal food [11].
Bioaccumulation of low-molecular-weight PAHs from sediments by Rhepoxynius abronius (amphipod)
and Armandia brevis (polychaete) was similar, however, a large difference in tissue concentration
between these two species was measured for high-molecular-weight PAHs including benzo(a)anthracene
[12]. Meador et al. [12] concluded that the low-molecular-weight PAHs were available to both species
from interstitial water, while sediment ingestion was a much more important uptake route for the high-
molecular-weight PAHs. The authors also indicated that bioavailability of the high-molecular-weight
PAHs to amphipods was significantly reduced due to their partitioning to dissolved organic carbon.
84
-------
Summary of Biological Effects Tissue Concentrations for Benzo(a)anthracene
Species:
Taxa
Invertebrates
Corbicula fluminea,
Asian clam
Macoma nasuta,
Clam
Daphnia pulex,
Cladoceran
Concentration, Units in1:
Sediment Water
59 |ig/kgOC
3,613 |ig/kg
OC
4.13ng/g
6.19ng/g
39.9 ng/g
39.5 ng/g
138 ng/g
146 ng/g
5.27 ng/L
Toxicity:
Tissue (Sample Type) Effects
508 |ig/kglipid
1,049 |ig/kglipid
16.5 ng/g
6.1 ng/g
14 ng/g
1 1 ng/g
66 ng/g
53 ng/g
1.6 ng/g
Ability to Accumulate2:
Log Log
BCF BAF BSAF
8.643
0.290
-0.21
-0.82
-0.62
-0.68
-0.36
-0.32
3.04
Source:
Reference
[15]
[15]
[13]
[13]
[13]
[13]
[13]
[13]
[11]
Comments3
F;%lipid = 0.61;
%sedOC= 1.19
F;%lipid = 0.61;
%sedOC= 1.19
F
F
F
F
F
F
L
Pontoporeia hoyi, 28 ng/g
Amphipod
72 ng/g
[10]
L
-------
oo
ON
Summary of Biological Effects Tissue Concentrations for Benzo(a)anthracene
Species:
Taxa
Fishes
Leuciscus idus,
Golden ide
Concentration, Units in1:
Sediment Water Tissue (Sample Type)
17.5 mg/kg (whole
body)
Toxicity:
Effects
Mortality,
NOED
Ability to Accumulate2:
Log Log
BCF BAF BSAF
Source:
Reference Comments3
[14] L; no effect on
survivorship in
days
3
Concentration units based on wet weight unless otherwise noted.
BCF = bioconcentration factor, BAF = bioaccumulation factor, BSAF = biota-sediment accumulation factor.
L = laboratory study, spiked sediment, single chemical; F = field study, multiple chemical exposure; other unusual study conditions or observations noted.
This entry was excerpted directly from the Environmental Residue-Effects Database (ERED, www.wes.army.mil/el/ered, U.S. Army Corps of Engineers and U.S.
Environmental Protection Agency). The original publication was not reviewed, and the reader is strongly urged to consult the publication to confirm the information
presented here.
-------
BIOACCUMULATION SUMMARY BENZO(A)ANTHRACENE
References
1. USEPA. 1980. Ambient water quality criteria document: Polynuclear aromatic hydrocarbons.
(Cited in: USEPA. 1995. Hazardous Substances Data Bank (HSDB). National Library of Medicine
online (TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental
Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. September
2. USEPA. 1989. Chemical fate rate constants for SARA section 313 chemicals and Superfund Health
Manual chemicals. Prepared by Chemical Hazard Assessment Division, Syracuse Research
Corporation, for U.S. Environmental Protection Agency, Office of Toxic Substances, Exposure
Evaluation Division, Washington, DC, and Environmental Criteria and Assessment Office,
Cincinnati, OH. August 11.
3. Karickhoff, S.W., and J.M. Long, 1995. Internal report on summary of measured, calculated, and
recommended log Kow values. Draft. Prepared by U.S. Environmental Protection Agency, Office of
Research and Development, Environmental Research Laboratory-Athens, for E. Southerland, Office
of Water, Office of Science and Technology, Standards and Applied Science Division, Washington,
DC. April 10.
4. USEPA. 1997. Integrated Risk Information System (IRIS). National Library of Medicine online
(TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental
Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. January.
5. Abernethy, S., A.M. Bobra, W.Y. Shiu, P.O. Wells and D. Mackay. 1986. Acute lethal toxicity of
hydrocarbons and chlorinated hydrocarbons to two planktonic crustaceans: The key role of
organism-water partitioning. Aquatic Tax. 8:163-174.
6. Palawski, D., J.B. Hunn, and F.J. Dwyer. 1985. Sensitivity of young striped bass to organic and
inorganic contaminants in fresh and saline waters. Trans. Am. Fish. Soc. 114:748-753.
7. Landrum, P.F., BJ. Eadie, and W.R. Faust. 1992. Variation in the bioavailability of polycyclic
aromatic hydrocarbons to the amphipod Diporeia (spp.) with sediment aging. Environ. Toxicol.
Chem. 11:1197-1208.
8. Pruell, R.J., and J.G. Quinn. 1987. Availability of PCBs and PAHs to Mytilus edulis from artificially
resuspended sediments. In Oceanic process in marine pollution, Vol. 1, ed. J.H. Capuzzo and D.R.
Kester. Robert E. Kriger Publishing Co., Malabor, FL.
9. Roy, S., J. Pellinen, C.K. Sen, and O. Hanninen. 1994. Benzo(a)anthracene and benzo(a)pyrene
exposure in the aquatic plant Fontinalis antipyretica: Uptake, elimination, and the responses of
biotransformation and antioxidant enzymes. Chemosphere 29:1301-1311.
10. Landrum, P.F. 1989. Bioavailability and toxicokinetics of polycyclic aromatic hydrocarbons sorbed
to sediments for the amphipod Pontoporeia hoyi. Environ. Sci. Technol. 23:588-595.
11. Trucco, R.G., N.R. Engelhardt, and B. Stacey. 1983. Toxicity, accumulation, and clearance of
aromatic hydrocarbons in Daphnia pulex. Environ. Pollut. 31:191-202.
87
-------
BIOACCUMULATION SUMMARY BENZO(A)ANTHRACENE
12. Meador, J.P., E. Casillas, C.A. Sloan, and U. Varanasi. 1995. Comparative bioaccumulation of
polycyclic aromatic hydrocarbons from sediments by two infaunal invertebrates. Mar. Ecol Prog.
Ser. 123:107-124.
13. Ferraro, S.P., H. Lee II, RJ. Ozretich, and D.T. Specht. 1990. Predicting bioaccumulation
potential: A test of a fugacity-based model. Arch. Environ. Contain. Toxicol 19:386-394.
14. Freitag, D., L. Ballhorn, H. Geyer and F. Korte. 1985. Environmental hazard profile of organic
chemicals: An experimental method for the assessment of the behaviour of organic chemicals in the
ecosphere by means of laboratory tests with 14C labelled chemicals. Chemosphere 14:1589-1616.
15. Pereira, W.E., J.L. Domagalski, F.D. Hostettler, L.R.Brown, and J.B. Rapp. 1996. Occurrence and
accumulation of pesticides and organic contaminants in river sediment, water, and clam tissues from
the San Joaquin River and Tributaries, California. Environ. Toxicol. Chem. 15: 172-180.
16. USEPA. 1998. Ambient water quality criteria derivation methodology: Human health. Technical
support document. EPA-822-B-98-005. U.S. Environmental Protection Agency. Office of Water,
Washington, DC. Final Draft.
-------
BIOACCUMULATION SUMMARY BENZO(A)PYRENE
Chemical Category: POLYNUCLEAR AROMATIC HYDROCARBON (high molecular weight)
Chemical Name (Common Synonyms): BENZO(A)PYRENE CASRN: 50-32-8
Chemical Characteristics
Solubility in Water: 0.0038 mg/L at 25°C [1] Half-Life: 5.7 d - 1.45 yrs based on aerobic soil
die-away test data at 10-30°C [2]
Log Kow: 6.11 [3] Log Koc: 6.01 L/kg organic carbon
Human Health
Oral RfD: No Data [4] Confidence: —
Critical Effect: Forestomach cancer in mice
Oral Slope Factor: 7.3 x 10+0 per (mg/kg)/day [4] Carcinogenic Classification: B2 [4]
Wildlife
Partitioning Factors: Partitioning factors for benzo(a)pyrene in wildlife were not found in the literature.
Food Chain Multipliers: Food chain multipliers for benzo(a)pyrene in wildlife were not found in the
literature.
Aquatic Organisms
Partitioning Factors: Partitioning factors for benzo(a)pyrene in aquatic organisms were not found in
the literature.
Food Chain Multipliers: Trophic tranfer of benzo(a)pyrene metabolites has been demonstrated between
polychaetes and bottom-feeding fish [5]. The diatom Thalassiosira pseudonana cultured in 10 |ig/L of
benzo(a)pyrene and subsequently fed to larvae of the hard clam Mercenaria mercenaria accumulated
42.2 jig/g while clams accumulated only 18.6 |ig/g [6]. The rate of direct uptake by the algae was thus
approximately 20 times faster than the rate of trophic transfer. Dobroski and Epifanio [6] concluded that
direct uptake and trophic transfer (2 |ig/g/day) are equally important in accumulation of benzo(a)pyrene.
Food chain multipliers (FCMs) for trophic level 3 aquatic organisms were 18.5 (all benthic food web),
1.6 (all pelagic food web), and 11.3 (benthic and pelagic food web). FCMs for trophic level 4 aquatic
organisms were 37.4 (all benthic food web), 3.1 (all pelagic food web), and 17.8 (benthic and pelagic
food web) [42].
89
-------
BIOACCUMULATION SUMMARY BENZO(A)PYRENE
Toxicity/Bioaccumulation Assessment Profile
Bioavailability of sediment-associated polynuclear aromatic hydrocarbon (PAHs), including
benzo(a)pyrene has been observed to decline with increased contact time [7]. Oikari and Kukkonene [8]
established a relationship between dissolved organic matter including the percentage of hydrophobic acids
and accumulation of benz(a)pyrene. They observed that the bioavailability of benzo(a)pyrene decreases
in waters with dissolved organic carbon having more high-molecular-weight hydrophobic acids. The
reduced bioavailability has been observed for benzo(a)pyrene accumulation from field-collected
sediments compared with laboratory spiked sediments [9]. Mean accumulation of benzo(a)pyrene
declined by a factor of three in Chironomus riparius exposed to sediment stored one week versus the
sediment stored for eight weeks [10]. The concentrations of benzo(a)pyrene in whole sediment and pore
water were 0.27-80.9 ng/g and 0.004-0.913 mg/mL, respectively [10].
Short-term exposures (24-h) to 1 mg/L benzo(a)pyrene averaged 8.27 nmol in fish tissue. Of this total,
67 percent was accumulated in the gallbladder or gut, indicating rapid metabolism and excretion [11].
The bioaccumulation of benzo(a)pyrene can be influenced by the lipid reserves [12]. In an experiment
conducted by Clements et al. [13], chironomidae larvae rapidly accumulated benzo(a)pyrene from spiked
sediment and tissue concentrations were directly proportional to sediment concentrations. However, the
level of benzo(a)pyrene in bluegill that were fed contaminated chironomids was generally low, indicating
either low uptake or rapid metabolism. According to McCarthy [14], accumulation of hydrophobic
chemicals like benzo(a)pyrene in aqueous systems appears to depend on the amount of chemical in
solution and on the amount sorbed to particles entering the food chain. Uptake and accumulation of
benzo(a)pyrene was reduced by 97 percent due to sorption to organic matter [14].
Studies that report body burdens of the parent compound may, depending on the species, grossly
underestimate total bioaccumulation of benzo(a)pyrene and their metabolites [15]. Kane-Driscoll and
McElroy [15] concluded that the body burden of the parent compound may represent less than 10 percent
of the actual total body burden of parent plus metabolites. The accumulation kinetics of benzo(a)pyrene
suggest that uptake occurs largely via the sediment interstitial water and is controlled by desorption from
sediment particles and dissolved organic matter [16]. Accumulation of benzo(a)pyrene from water was
not affected by the simultaneous presence of naphthalene or PCB [17].
Kolok et al. [18] showed that the concentration of benzo(a)pyrene equivalents in shad (Dorosoma
cepedianum) increases when the fish ventilate water turbid with benzo(a)pyrene spiked sediments. Also
the turbid water, not sediment ingestion, appears to be a significant source of benzo(a)pyrene for gizzard
shad.
Bioaccumulation of low-molecular-weight PAHs from sediments by Rhepoxynius abronius (amphipod)
and Armandia brevis (polychaete) was similar, however, a large difference in tissue concentration
between these two species was measured for high-molecular-weight PAHs including benzo(a)pyrene [19].
Meador et al. [19] concluded that the low-molecular-weight PAHs were available to both species from
interstitial water, while sediment ingestion was a much more important uptake route for the high-
molecular-weight PAHs. The authors also indicated that bioavailability of the high-molecular-weight
PAHs to amphipods was significantly reduced due to their partitioning to dissolved organic carbon.
90
-------
Summary of Biological Effects Tissue Concentrations for Benzo(a)pyrene
Species:
Concentration, Units in1:
Toxicity:
Ability to Accumulate2:
Source:
Log Log
Taxa Sediment Water Tissue (Sample Type) Effects BCF BAF BSAF Reference Comments3
Invertebrates
Nereis diversicolor, 236.6 pmol/g
Polychaeta worm
95.2 pmol/g
[15]
Scolecolepides 184.2 pmol/g
viridis,
Polychaeta worm
119 pmol/g
[15] F
Leitoscoloplos 475.8 pmol/g
fragilis,
Polychaeta worm
3540 pmol/g
[15] F
Thais haemostoma,
Snail
DDL
1.45-3.89 ng/kg
[23] F
Physa sp., Snail
3.39 |ig/L 259.6 |ig/kg
[20]
Dreissena
polymorpha,
Zebra mussel
3.1 -4.7xl06mg/g
[12] L; depending on the
lipid content
Mytilus edulis,
Mussel
3.2 mg/kg
(whole body)4
Physiological,
ED50
[30] L; 50% reduction in
feeding, clearance
rate, and tolerance
to aerial exposure
-------
Summary of Biological Effects Tissue Concentrations for Benzo(a)pyrene
Species:
Taxa
Macotna nasuta,
Clam
Macoma nasuta,
Clam
Macomona liliana,
Mollusc
Concentration, Units in1: Toxicity: Ability to Accumulate2:
Log Log
Sediment Water Tissue (Sample Type) Effects BCF BAF BSAF
0.161 mg/kg Physiological,
(whole body)4 LOED
3.2 mg/kg Physiological,
(whole body)4 LOED
3.2 mg/kg Reproduction,
(whole body)4 LOED
9.2 ng/g 50 ng/g -0.07
4.7ng/g 1.4 ng/g -1.30
70 ng/g 22 ng/g -0.68
99 ng/g 45 ng/g -0.48
228 ng/g 62 ng/g -0.70
440 ng/g 66 ng/g -0.70
3,533 |ig/kg 189.2 |ig/kg lipid 0.0536
OC
Source:
Reference
[30]
[30]
[30]
[12]
[21]
[21]
[21]
[21]
[21]
[40]
Comments3
L; elevated activity
of superoxide
dismutase (SOD)
L; inhibition of
superoxide
dismutase (SOD)
and catalase activity
L, reduced
gametogenesis,
reproductive
success rate
F
F
F
F
F
F
F, %lipid = 2.95;
%sed OC = 0.30
-------
Summary of Biological Effects Tissue Concentrations for Benzo(a)pyrene
Species:
Taxa
Austrovenus
stutchburyi, Mollusc
Sphaeriiim corneum,
Fingernail Clam
Concentration, Units in1:
Sediment Water
68,767 ng/kg
OC
2,864 ng/kg
OC
2,440 ng/kg
OC
1,021 ng/kg
OC
3,533 ng/kg
OC
68,767 |ig/kg
OC
2,864 |ig/kg
OC
2,440 |ig/kg
OC
1,021 |ig/kg
OC
Toxicity:
Tissue (Sample Type) Effects
845.5 |ig/kg lipid
1 66.9 |ig/kg lipid
261.8|ig/kglipid
48.6|ig/kg lipid
19.2|ig/kglipid
24.6 |ig/kg lipid
18.8|ig/kglipid
14.5 |ig/kg lipid
1 1 .0 |ig/kg lipid
1 .25 mg/kg Mortality,
(whole body)4 NOED
Ability to Accumulate2:
Log Log
BCF BAF BSAF
0.0123
0.0583
0.1073
0.0476
0.0054
0.0004
0.0066
0.0059
0.0108
Source:
Reference
[40]
[40]
[40]
[40]
[40]
[40]
[40]
[40]
[40]
[28]
Comments3
F, %lipid = 2.33;
%sed OC = 0.73
F, %lipid = 2.57;
%sed OC = 0.22
F, %lipid = 2.04;
%sed OC = 0.25
F, %lipid=3.13;
%sed OC = 0.48
F, %lipid = 5.62;
%sed OC = 0.30
F, %lipid=5.21;
%sed OC = 0.73
F, %lipid = 4.85;
%sed OC = 0.22
F, %lipid = 3.87;
%sed OC = 0.25
F, %lipid = 4.27;
%sed OC = 0.48
L; no effect on
survivorship in 120
hours
-------
Summary of Biological Effects Tissue Concentrations for Benzo(a)pyrene
Species: Concentration, Units in1: Toxicity:
Taxa Sediment Water Tissue (Sample Type) Effects
Corbicula fluminea, 84 |ig/kg 180.3 |ig/kg lipid
Asian Clam OC
6,387 ng/kg 245.9 |ig/kg lipid
OC
Mercenaria 0.00221 mg/kg Physiological,
mercenaria, (whole body)4 LOED
Quahog Clam,
0.00221 mg/kg Mortality,
(whole body)4 NOED
Daphnia magna,
Cladoceran
Daphnia magna,
Cladoceran
Ability to Accumulate2:
Log Log
BCF BAF BSAF
2.146
0.039
3.90
(without
organic
matter)
3.00
(with
organic
matter)
Source:
Reference Comments3
[41] F, %lipid=0.61;
%sedOC=1.19
[41] F, %lipid=0.61;
%sedOC= 1.19
[27] L;impaired ability
to clear
flavobacterium,
exp_conc = < 0.001
[27] L; no effect on
mortality, exp_conc
= <0.001
[14] L
[14] L
-------
Summary of Biological Effects Tissue Concentrations for Benzo(a)pyrene
Species:
Taxa
Pontoporeia hoyi,
Amphipod
Chironomus
riparius, Midge
Chironomus
riparius, Midge
Chironomus
riparius, Midge
Culexpipiens
quinquefasciatus,
Mosquito larva
Concentration, Units in1:
Sediment Water Tissue (Sample Type)
15.5 ng/g 32 ng/g
4 10 ng/g 3 ng/mL 600 ng/g
40 ng/g 3.5 ng/mL 400 ng/g
30 ng/g 2.2 ng/mL 270 ng/g
3,920 ng/kg 2,160 ng/L 720 |ig/kg
4,290 ng/kg 1,680 ng/L 252 |ig/kg
4,035 |ig/kg 2,640 ng/L 720 |ig/kg
0.23 mg/kg
(whole body)4
0.09 mg/kg
(whole body)4
0.04 mg/kg
(whole body)4
1 .9 mg/kg
(whole body)4
3.39 |ig/L 73.1 |ig/kg
Toxicity:
Effects
Behavior,
NOED
Behavior,
NOED
Behavior,
NOED
Mortality,
NOED
Ability to Accumulate2: Source:
Log Log
BCF BAF BSAF Reference
[16]
4.74 [22]
[13]
[13]
[13]
[38]
[38]
[38]
[28]
[21]
Comments3
L
L
L
L
L
L; no effect on
swimming behavior
L; no effect on
swimming behavior
L; no effect on
swimming behavior
L; no effect on
survivorship in 120
hours
L
-------
Summary of Biological Effects Tissue Concentrations for Benzo(a)pyrene
Species:
Taxa
Asterias rubens,
Starfish
Concentration, Units in1:
Sediment Water Tissue (Sample Type)
37.8 mg/kg
(pyloric caeca)4
40 mg/kg
(whole body)4
2.15 mg/kg
(pyloric caeca)4
13.2 mg/kg
(pyloric caeca)4
2.5 mg/kg
(whole body)4
10 mg/kg
(whole body)4
0.5 mg/kg
(whole body)4
10 mg/kg
(whole body)4
2.5 mg/kg
(whole body)4
Toxicity: Ability to Accumulate2:
Log Log
Effects BCF BAF BSAF
Physiological,
ED 100
Physiological,
ED100
Physiological,
LOED
Physiological,
LOED
Physiological,
LOED
Physiological,
LOED
Mortality,
NOED
Mortality,
NOED
Mortality,
NOED
Source:
Reference
[29]
[29]
[29]
[29]
[29]
[29]
[29]
[29]
[29]
Comments3
L; 346% induction
of benzo(a)pyrene
hydroxylase activity
L; 346% induction
of benzo(a)pyrene
hydroxylase activity
L; 200% induction
of benzo(a)pyrene
hydroxylase activity
L; 200% induction
of benzo(a)pyrene
hydroxylase activity
L; 200% induction
of benzo(a)pyrene
hydroxylase activity
L; 200% induction
of benzo(a)pyrene
hydroxylase activity
L; no effect on
mortality
L; no effect on
mortality
L; no effect on
mortality
-------
Summary of Biological Effects Tissue Concentrations for Benzo(a)pyrene
Species:
Taxa
Fishes
Poeciliopsis
monoacha,
Concentration, Units in1:
Sediment Water Tissue (Sample Type)
10 mg/kg
(whole body)4
40 mg/kg
(whole body)4
0.053 mg/kg
(pyloric caeca)4
0.5 mg/kg
(whole body)4
3.96 nmol/L 8.27 nmol
Toxicity: Ability to Accumulate2:
Log Log
Effects BCF BAF BSAF
Mortality,
NOED
Mortality,
NOED
Physiological,
NOED
Physiological,
NOED
48-h LC50 3.75
mg/L
Source:
Reference
[29]
[29]
[29]
[29]
[11]
Comments3
L; no effect on
mortality
L; no effect on
mortality
L; no effect on
benzo(a)pyrene
hydroxylase activity
L; no effect on
benzo(a)pyrene
hydroxylase activity
L
Viviparius
Oncorhynchus
mykiss
(Salmo gairdneri),
Rainbow trout
5 |ig/egg 32,090 cpm (egg)
injection 25,448 cpm (fry)
[24]
14-day 21,839 cpm fry)
35-day 8,922 cpm (fry)
-------
Summary of Biological Effects Tissue Concentrations for Benzo(a)pyrene
Species:
Taxa
Oncorhynchus
mykiss,
Rainbow trout
Concentration, Units in1:
Sediment Water Tissue (Sample Type)
0.35 mg/kg
(whole body)4
30 mg/kg
(whole body)4
12.3 mg/kg
(whole body)4
1.93 mg/kg
(whole body)4
7.18 mg/kg
(whole body)4
10.2 mg/kg
(whole body)4
12.3 mg/kg
(whole body)4
Toxicity: Ability to Accumulate2:
Log Log
Effects BCF BAF BSAF
Physiological,
LOED
Physiological,
LOED
Development,
NA
Reproduction,
NA
Reproduction,
NA
Reproduction,
NA
Reproduction,
NA
Source:
Reference
[34]
[34]
[35]
[35]
[35]
[35]
[35]
Comments3
L; hepatic enzyme
induction
L; induction of
hepatic mixed
function oxidases
L; gross
abnormalities in
alevins noted at all
test concentrations
0.08 mg/L and
above, significant
increase relative to
the control
L; hatchability not
significantly
reduced
L; hatchability not
significantly
reduced
L; hatchability not
significantly
reduced
L; hatchability not
significantly
reduced
-------
Summary of Biological Effects Tissue Concentrations for Benzo(a)pyrene
Species:
Taxa
Cyprinus carpio,
Common carp
Gambusia affinis,
Mosquito fish
Lepomis
macrochirus,
Bluegill sunfish
Dorosoma
cepedianum,
Gizzard shad
Concentration, Units in1: Toxicity:
Sediment Water Tissue (Sample Type) Effects
155 mg/kg (liver)4 Physiological,
NA
3.39 |ig/L 14.1 |ig/kg
1 |ig/L 39,000 ng/g
(gall bladder)
1 |ig/L 4,600 ng/g (liver)
1 |ig/L 2,200 ng/g (viscera)
1 |ig/L 250 ng/g (brain)
1 |ig/L 370 ng/g (carcass)
Ability to Accumulate2:
Log Log
BCF BAF BSAF
4.15
3.20
2.89
1.95
2.11
3.62
Source:
Reference
[39]
[20]
[25]
[25]
[25]
[25]
[25]
[18]
Comments3
L; significant
increase in EROD
enzyme and P450
1A protein content
L
L
L
L
L
L
L
-------
o
o
Summary of Biological Effects Tissue Concentrations for Benzo(a)pyrene
Species:
Taxa
Dorosoma
cepedianum,
Gizzard shad
Concentration, Units in1:
Sediment Water Tissue (Sample Type)
10 mg/kg
(whole body)4
0.0289 mg/kg
(whole body)4
0.0283 mg/kg
(whole body)4
50 mg/kg
(whole body)4
0.0257 mg/kg
(whole body)4
Toxicity: Ability to Accumulate2:
Log Log
Effects BCF BAF BSAF
Physiological,
LOED
Physiological,
LOED
Physiological,
LOED
Physiological,
NA
Physiological,
NA
Source:
Reference Comments3
[37] L; statistically
significant,
maximum (llx)
induction of
ethoxyresorufin-o-
deethylase (EROD)
[37] L; statistically
significant induction
of ethoxyresorufin-
o-deethylase
(EROD)
[37] L; statistically
significant induction
of ethoxyresorufin-
o-deethylase
(EROD)
[37] L; lOx induction of
ethoxyresorufin-o-
deethylase (EROD)
[37] L; statistically
significant induction
of ethoxyresorufin-
o-deethylase
(EROD)
-------
Summary of Biological Effects Tissue Concentrations for Benzo(a)pyrene
Species:
Taxa
Concentration, Units in1:
Toxicity:
Ability to Accumulate2:
Log Log
Sediment Water Tissue (Sample Type) Effects BCF BAF BSAF
Source:
Reference Comments3
0.0265 mg/kg
(whole body)4
0.1 mg/kg
(whole body)4
0.0337 mg/kg
(whole body)4
0.0201 mg/kg
(whole body)4
1 mg/kg
(whole body)4
0.0239 mg/kg
(whole body)4
0.0196 mg/kg
(whole body)4
Physiological,
NA
Physiological,
NOED
Physiological,
NOED
Physiological,
NOED
Physiological,
NOED
Physiological,
NOED
Physiological,
NOED
[37] L; statistically
significant induction
of ethoxyresorufin-
o-deethylaste
(EROD)
[37] L; no induction of
ethoxyresorufin-o-
deethylase (EROD)
[37] L; no induction of
ethoxyresorufin-o-
deethylase (EROD)
[37] L; no induction of
ethoxyresorufin-o-
deethylase (EROD)
[37] L; no induction of
ethoxyresorufin-o-
deethylase (EROD)
[37] L; no induction of
ethoxyresorufin-o-
deethylase (EROD)
[37] L; no induction of
ethoxyresorufin-o-
deethylase (EROD)
-------
Summary of Biological Effects Tissue Concentrations for Benzo(a)pyrene
Species: Concentration, Units in1:
Taxa Sediment Water
Ictalurus punctatus,
Channel catfish
Leiicisciis idus,
Golden ide
Citharichthys 3 |ig/L
stigmaeus,
Sand dab
Psettichthys
melanostictus,
Sand sole
Tissue (Sample Type)
100 mg/kg
(whole body)4
0.1 mg/kg
(whole body)4
24 mg/kg
(whole body)4
130 ng/g (liver),
10 ng/g (gut),
400 ng/g (gill),
30 ng/g (flesh),
150 ng/g (heart)
2.1 mg/kg
(whole body)4
2.1 mg/kg
(whole body)4
Toxicity: Ability to Accumulate2:
Log Log
Effects BCF BAF BSAF
Physiological,
LOED
Physiological,
LOED
Mortality,
NOED
Reproduction,
ED50
Development,
LOED
Source:
Reference Comments3
[31] L; significant
decrease in
neurotransmitter
levels
[32] L; five to six-fold
induction of
cytochrome P450
[33] L; no effect on
survivorship in 3
days
[25] L; accumulation
within 1 h
[36] L; reduced hatching
success
[36] L; larval
abnormalities
-------
Summary of Biological Effects Tissue Concentrations for Benzo(a)pyrene
Species:
Taxa
Concentration, Units in1:
Toxicity:
Ability to Accumulate2:
Source:
Log Log
Sediment Water Tissue (Sample Type) Effects BCF BAF BSAF Reference Comments3
Oligocottiis
maculosus,
Tidepool sculpins
0.5 ng/L 120 ng/g (liver),
160ng/g(gut),
200 ng/g (gill),
130 ng/g (flesh),
70 ng/g (heart)
[25] L; accumulation
within 1 h
Concentration units based on wet weight unless otherwise noted.
BCF = bioconcentration factor, BAF = bioaccumulation factor, BSAF = biota-sediment accumulation factor.
L = laboratory study, spiked sediment, single chemical; F = field study, multiple chemical exposure; other unusual study conditions or observations noted.
This entry was excerpted directly from the Environmental Residue-Effects Database (ERED, www.wes.army.mil/el/ered, U.S. Army Corps of Engineers and U.S.
Environmental Protection Agency). The original publication was not reviewed, and the reader is strongly urged to consult the publication to confirm the information presented
here.
-------
BIOACCUMULATION SUMMARY BENZO(A)PYRENE
References
1. MacKay, D., and Shin Wy; /. Chem. Eng. Data 22:399 (1977). Weast handbook of chemistry and
physics, 68th edition, 1987-1988, B-73. (Cited in: USEPA. 1995. Hazardous Substances Data
Bank(HSDB). National Library of Medicine online (TOXNET). U.S. Environmental Protection
Agency, Office of Health and Environmental Assessment, Environmental Criteria and Assessment
Office, Cincinnati, OH. September.)
2. USEPA. 1989. Chemical fate rate constants for SARA section 313 chemicals and Superfund
Health Evaluation Manual Chemicals. Prepared by Chemical Hazard Assessment Division,
Syracuse Research Corporation, for U.S. Environmental Protection Agency, Office of Toxic
Substances, Exposure Evaluation Division, Washington, DC, and Environmental Criteria and
Assessment Office, Cincinnati, OH. August 11.
3. Karickhoff, S.W., and J.M. Long, 1995. Internal report on summary of measured, calculated, and
recommended log Kow values. Draft. Prepared by U.S. Environmental Protection Agency, Office
of Research and Development, Environmental Research Laboratory-Athens, for E. Southerland,
Office of Water, Office of Science and Technology, Standards and Applied Science Division,
Washington, DC. April 10.
4. USEPA. 1997. Integrated Risk Information System (IRIS). National Library of Medicine online
(TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental
Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. January.
5. McElroy, A.E., and J.D. Sisson. 1989. Trophic transfer of benzo[a]pyrene metabolites between
benthic marine organisms. Mar. Environ. Res. 28:265-269.
6. Dobroski, C.J., Jr., and Epifanio. 1980. Accumulation of benzo[a]pyrene in a larval bivalve via
trophic transfer. Can. J. Fish. Aquat. Sci. 37:2318-2322.
7. Landrum, P.F., B.J. Eadie, and W.R. Faust. 1992. Variation in the bioavailability of polycyclic
aromatic hydrocarbons to the amphipod Diporeia (spp.) with sediment aging. Environ. Toxicol.
Chem. 11:1197-1208.
8. Kukkonen, J.V.K., and P.F. Landrum. 1998. Effect of particle-xenobiotic contact time on
bioavailablility of sediment-associated benzo(a)pyrene by benthic amphipod, Diporeia spp. Aquat.
Toxicol. 42:229-242.
9. Varanasi, U., W.L. Reichert, J.E. Stein, D.W. Brown, and H.R. Sanborn. 1985. Bioavailability and
biotransformation of aromatic hydrocarbons in benthic organisms exposed to sediment from an
urban estuary. Environ. Sci. Technol. 19:836-841.
10. Harkey, G.A., P.F. Landrum, and S.J. Klaine. 1994. Comparison of whole-sediment, elutriate and
pore-water exposures for use in assessing sediment-associated organic contaminants in bioassays.
Environ. Toxicol. Chem. 13:1315-1329.
104
-------
BIOACCUMULATION SUMMARY BENZO(A)PYRENE
11. Goddard, K.A., RJ. Schultz, and JJ. Stegeman. 1987. Uptake, toxicity, and distribution of
benzo[a]pyrene and monooxygenase induction in the topminnows Poeciliopsis monacha and
Poeciliopsis lucida. Drug Metab. Disposition 15:449-455.
12. Bruner, K.A., S.W. Fisher, and P.P. Landrum. 1994. The role of the zebra mussel, Dreissena
polymorpha, in contaminant cycling: 1. The effect of body size and lipid content on the
bioconcentration of PCBs and PAHs. Great Lakes Res. 20:725-734.
13. Clements, W.H., J.T. Oris, and T.E. Wissing. 1993. Accumulation and food chain transfer of
fluoranthene and benzo[a]pyrene in Chironomus riparius and Lepomis macrochirus. Arch.
Environ. Contam. Toxicol. 26:261-266.
14. McCarthy, J.F. 1983. Role of particulate organic matter in decreasing accumulation of polynuclear
aromatic hydrocarbons by Daphnia magna. Arch. Environ. Contam. Toxicol. 12:559-568.
15. Kane-Driscoll, S., and A.E. McElroy. 1996. Bioaccumulation and metabolism of benzo[a]pyrene
in three species of polychaete worms. Environ. Toxicol. Chem. 15:1401-1410.
16. Landrum, P.P. 1989. Bioavailability and toxicokinetics of polycyclic aromatic hydrocarbons sorbed
to sediments for the amphipod Pontoporeia hoyi. Environ. Sci. Technol. 23:588-595.
17. Former, A.R., and L.V. Sick. 1985. Simultaneous accumulations of naphthalene, aPCB mixture
and benzo(a)pyrene by the oyster, Crassostrea virginica. Bull. Environ. Contam. Toxicol. 34:256-
264.
18. Kolok A.S., J.N. Huckins, J.D. Petty, and J.T. Oris. 1996. The role of water ventilation and
sediment ingestion in the uptake of benzo(a)pyrene in gizzard shad (Dorsoma cepedianuni).
Environ. Toxicol. Chem. 15:1752-1759.
19. Meador, J.P., E. Casillas, C.A. Sloan, and U. Varanasi. 1995. Comparative bioaccumulation of
polycyclic aromatic hydrocarbons from sediments by two infaunal invertebrates. Mar. Ecol. Prog.
Ser. 123: 107-124.
20. Po-Yung, L, R.L. Metcalf, N. Plummer, and D. Mandel. 1977. The environmental fate of three
carcinogens: Benzo-(a)-pyrene, benzidine, and vinyl chloride evaluated in laboratory model
ecosystems. Arch. Environm. Contam. Toxicol. 6:129-142.
21. Ferraro, S.P., H.Lee U, RJ. Ozretich, and D.T.Specht. 1990. Predicting bioaccumulation potential:
A test of a fugacity-based model. Arch. Environ. Contam. Toxicol. 19:386-394.
22. Eadie, B.J., P.P. Landrum, and W.Faust. 1982. Polycyclic aromatic hydrocarbons in sediments,
pore water and the amphipod Pontoporeia hoyi from Lake Michigan. Chemosphere 11:847-858.
23. Rostad, C.E., and W.E. Pereira. 1987. Creosote compounds in snails obtained from Pensacola Bay,
Florida, near an onshore hazardous-waste site. Chemosphere 16:2397-2404.
105
-------
BIOACCUMULATION SUMMARY BENZO(A)PYRENE
24. Black, J.J., E. Maccubbin, and CJ. Johnston. 1988. Carcinogenicity of benzo[a]pyrene in rainbow
trout resulting from embryo microinjection. Aquatic Tox. 13:297-308.
25. Lee, R.F., and G.H. Dobbs. 1972. Uptake, metabolism and discharge of polycyclic aromatic
hydrocarbons by marine fish. Mar. Biol. 17:201-208.
26. Spacie, A., P.P. Landrum, and GJ. Leversee. 1983. Uptake, depuration, and biotransformation
of anthracene and benzo[a]pyrene in blugill sunfish. Ecotox. Environ. Saf. 7:330-341.
27. Anderson, R.S., C.S. Giam, P.P. Ray, and M.R. Tripp. 1981. Pffects of environmental pollutants
on immunological competency of the clam Mercenaria mercenaria: Impaired bacterial clearance.
Aquat. Toxicol. 1:187-195.
28. Borchert, J., P. Karbe, and J. Westendorf. 1997. Uptake and metabolism of benzo(a)pyrene
absorbed to sediment by the freshwater invertebrate species Chironomus riparius and Sphaerium
corneum. Bull. Environ. Contain. Toxicol. 58:158-165.
29. Den Besten, P.J., P. Pemaire, D.R. Pivingstone, B. Woodin, JJ. Stegeman, HJ. Herwin, and W.
Seinen. 1993. Time-course and dose-response of the apparent induction of the cytochrome P450
monooxygenase system of pyloric caeca microsomes of the female sea star Asterias rubens P. by
benzo[a]pyrene and polychlorinated biphenyls. Aquat. Toxicol. 26:23-40.
30. Permian, R.H.M., C.P. Groenink, B. Sandee, and H. Hummel. 1995. Response of the blue mussel
Mytilus edulis P. following exposure to PAHs or contaminated sediment.. Mar. Environ. Res.
39:169-173.
31. Fingerman, S., and P.C. Short, Jr. 1983. Changes in neurotransmitter levels in channel catfish after
exposure to benzo(a)pyrene, naphthalene, and Aroclor 1254. Bull. Environ. Contam. Toxicol.
30:147-151.
32. Fingerman, S.W., P.A. Brown, M. Pynn, and P.C. Short, Jr. 1983. Responses of channel catfish
to xenobiotics: Induction and partial characterization of a mixed function oxygenase. Arch.
Environ. Contam. Toxicol. 12:195-201.
33. Freitag, D., P. Ballhorn, H. Geyer and F. Korte. 1985. Environmental hazard profile of organic
chemicals: An experimental method for the assessment of the behaviour of organic chemicals in
the ecosphere by means of laboratory tests with 14C labelled chemicals. Chemosphere 14:1589-
1616.
34. Gerhart, P.M., and R.H. Carlson. 1978. Hepatic mixed-function oxidase activity in rainbow trout
exposed to several polycyclic aromatic hydrocarbons. Environ. Res. 17:284-295.
35. Hannah, J.B., J.P. Hose, M.P. Pandolt, B.S. Miller, S.P. Felton, and W.T. Iwaoka. 1982.
Benzo(a)pyrene-induced morphologic and developmental abnormalities in rainbow trout. Arch.
Environm. Contam. Toxicol. 11:727-734.
106
-------
BIOACCUMULATION SUMMARY BENZO(A)PYRENE
36. Hose, J.E., J.B. Hannah, D. Dijulio, M.L. Landolt, B.S. Miller, W.T. Iwaoka, and S.P. Felton. 1982.
Effects of benzo(a)pyrene on early development in flatfish. Arch. Environ. Contain. Toxicol.
11:167-171.
37. Levine, S.L., J.T. Oris, and T.E. Wissing. 1994. Comparison of P-450al monooxygenase induction
in gizzard shad (Dorosoma cepedianum) following intraperitoneal injection or continuous
waterborne-exposure with benzo[a]pyrene: Temporal and dose-dependent studies. Aquat. Toxicol
30:61-75.
38. Lydy, M.J., K.A. Bruner, D.M. Fry, and S.W. Fisher. 1990. Effects of sediment and the route of
exposure on the toxicity and accumulation of neutral lipophilic and moderately water soluble
metabolizable compounds in the midge, Chironomus riparius. In Aquatic toxicology and risk
assessment, Vol. 13, ed. W.G. Landis, et.al., pp. 140-164. American Society for Testing and
Materials, Philadelphia, PA.
39. Van Der Weidern, M.E.J., F.H.M. Hanegraaf, M.L. Eggens, M. Celander, W. Seinen, and M. Ven
Den Berg. 1994. Temporal induction of cytochrome P450 la in the mirror carp (Cyprinus carpio)
after administration of several polycyclic aromatic hydrocarbons. Environ. Toxicol. Chem. 13: 797-
802.
40. Hickey, C.W., D.S. Roper, P.T. Holland, and T.M. Trower. 1995. Accumulation of organic
contaminants in two sediment-dwelling shellfish with contrasting feeding modes: Deposit
(Macomona liliana) and filter-feeding (Austovenus stutchburi). Arch. Environ. Contain. Toxicol.
11:221-231.
41. Pereira, W.E., J.L. Domagalski, F.D. Hostettler, L.R. Brown, and J.B. Rapp. 1996. Occurrence
and accumulation of pesticides and organic contaminants in river sediment, water, and clam tissues
from the San Joaquin River and tributaries, California. Environ. Toxicol. Chem. 15:172-180.
42. USEPA. 1998. Ambient water quality criteria derivation methodology: Human health. Technical
support document. EPA-822-B-98-005. U.S. Environmental Protection Agency, Office of Water,
Washington, DC. Final Draft.
107
-------
108
-------
BIOACCUMULATION SUMMARY
BENZO(B)FLUORANTHENE
Chemical Category: POLYNUCLEAR AROMATIC HYDROCARBON (high molecular weight)
Chemical Name (Common Synonyms): BENZO(B)FLUORANTHENE CASRN: 205-99-2
Chemical Characteristics
Solubility in Water: 0.0012 mg/L [1]
Log Kow: 6.20 [3]
Half-Life: 360 days - 1.67 yrs based on aerobic soil
die-away test data [2]
Log Koc: 6.09 L/kg organic carbon
Oral RfD: No data [4]
Critical Effect: —
Human Health
Confidence:
Oral Slope Factor (Reference): No data [4] Carcinogenic Classification: No data [4]
Wildlife
Partitioning Factors: Partitioning factors for benzo(b)fluoranthene in wildlife were not found in the
literature.
Food Chain Multipliers: Food chain multipliers for benzo(b)fluoranthene in wildlife were not found
in the literature.
Aquatic Organisms
Partitioning Factors: Partitioning factors for benzo(b)fluoranthene in aquatic organisms were not
found in the literature.
Food Chain Multipliers: Food chain multipliers for benzo(b)fluoranthene in aquatic organisms were
not found in the literature.
Toxicity/Bioaccumulation Assessment Profile
The acute toxicity of hydrocarbons, including benzo(b)fluoranthene, to both fresh and salt water
crustaceans is largely nonselective, i.e., it is not primarily influenced by molecular structure, but is rather
controlled by organism-water partitioning which, for nonpolar organic chemicals, is in turn a reflection
of aqueous solubility. The toxic effect is believed to occur at a relatively constant concentration within
the organism [5].
109
-------
BIOACCUMULATION SUMMARY BENZO(B)FLUORANTHENE
Bioavailability of sediment-associated polynuclear aromatic hydrocarbons (PAHs), e.g.,
benzo(b)fluoranthene, has been observed to decline with increased contact time [6]. The majority of
investigations have shown that aquatic organisms are able to release PAHs from their tissues rapidly when
they were returned to a clean environment. The apparent effects threshold concentration of 4,500 ng/g
was established for benzo(b)fluoranthene based on effects observed in the marine amphipod Rhepoxynius
abronius [7].
Bioaccumulation of low- molecular-weight PAHs from sediments by Rhepoxynius abronius (amphipod)
and Armandia brevis (polychaete) was similar, however, a large difference in tissue concentration
between these two species was measured for high-molecular-weight PAHs including
benzo(b)fluoranthene [8]. Meador et al. [8] concluded that the low-molecular-weight PAHs were
available to both species from interstitial water, while sediment ingestion was a much more important
uptake route for the high-molecular-weight PAHs. The authors also indicated that bioavailability of the
high-molecular-weight PAHs to amphipods was significantly reduced due to their partitioning to
dissolved organic carbon.
110
-------
Summary of Biological Effects Tissue Concentrations for Benzo(b)fluoranthene
Species:
Taxa
Invertebrates
Crassostrea
virginica, Oyster
Diporeia spp,
Amphipod
Concentration, Units in1:
Sediment Water
18 ng/g
2.9 ng/g
9.9 ng/g
27 nmol/g
Toxicity:
Tissue (Sample Type) Effects
18 ng/g
27 ng/g
40 ng/g
321 nmol/g
Ability to Accumulate2: Source:
Log Log
BCF BAF BSAF Reference
[9]
[9]
[9]
[6]
Comments3
F
F
F
L
1 Concentration units based on wet weight unless otherwise noted.
2 BCF = bioconcentration factor, BAF = bioaccumulation factor, BSAF = biota-sediment accumulation factor.
3 L = laboratory study, spiked sediment, single chemical; F = field study, multiple chemical exposure; other unusual study conditions or observations noted.
-------
BIOACCUMULATION SUMMARY BENZO(B)FLUORANTHENE
References
1. Sims, R.C., and M.R. Overcash. Res. Rev. 88:1-68 (1983). (Cited in: USEPA. 1995. Hazardous
Substances Data Bank (HSDB). National Library of Medicine online (TOXNET). U.S.
Environmental Protection Agency, Office of Health and Environmental Assessment,
Environmental Criteria and Assessment Office, Cincinnati, OH. September.)
2. USEPA. 1989. Chemical fate rate constants for SARA section 313 chemicals and Superfund
Health Manual chemicals. Prepared by Chemical Hazard Assessment Division, Syracuse
Research Corporation, for U.S. Environmental Protection Agency, Office of Toxic Substances,
Exposure Evaluation Division, Washington, DC, and Environmental Criteria and Assessment
Office, Cincinnati, OH. August 11.
3. Karickhoff, S.W., and J.M. Long. 1995. Internal report on summary of measured, calculated, and
recommended log Kow values. Draft. Prepared by U.S. Environmental Protection Agency, Office
of Research and Development, Environmental Research Laboratory-Athens, for E. Southerland,
Office of Water, Office of Science and Technology, Standards and Applied Science Division,
Washington, DC. April 10.
4. USEPA. 1997. Integrated Risk Information System (IRIS). National Library of Medicine online
(TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental
Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. January.
5. Abernethy, S., A.M. Bobra, W.Y. Shiu, P.O. Wells, and D. MacKay. 1986. Acute lethal toxicity
of hydrocarbons and chlorinated hydrocarbons to two planktonic crustaceans: The key role of
organism-water partitioning. Aquat. Tax. 8:163-174.
6. Landrum, P.F., BJ. Eadie, and W.R. Faust. 1992. Variation in the bioavailability of polycyclic
aromatic hydrocarbons to the amphipod Diporeia (spp.) with sediment aging. Environ. Tax. Chem.
11:1197-1208.
7. Ingersoll, C.G., and M.K. Nelson. 1990. Testing sediment toxicity with Hyalella azteca
(Amphipoda) and Chironomus riparius (Diptera). In Aquatic toxicology and risk assessment:
ASTM STP 1096, ed. W.G. Landis and W.H. van der Schalie, pp. 93-109. American Society for
Testing and Materials, Philadelphia, PA.
8. Meador, J.P., E. Casillas, C.A. Sloan, and U. Varanasi. 1995. Comparative bioaccumulation of
polycyclic aromatic hydrocarbons from sediments by two infaunal invertebrates. Mar. Ecol. Prog.
Ser. 123:107-124.
9. Sanders, M. 1995. Distribution of polycyclic aromatic hydrocarbons in oyster (Crassostrea
virginica) and surface sediment from two estuaries in South Carolina. Arch. Environ. Contam.
Toxicol. 28:397-405.
112
-------
BIOACCUMULATION SUMMARY
BENZO(G,H,I)PERYLENE
Chemical Category: POLYNUCLEAR AROMATIC HYDROCARBON (high molecular weight)
Chemical Name (Common Synonyms): BENZO(G,H,I)PERYLENE CASRN: 191-24-2
Chemical Characteristics
Solubility in Water: Insoluble in water [1]
Log Kow: 6.70 [3]
Half-Life: 590 d - 650 days based on aerobic
soil die-away test data at 30°. [2]
Log Koc: 6.59 L/kg organic carbon
Human Health
Oral RfD: No data [4]
Critical Effect: —
Oral Slope Factor (Reference): No data [4]
Confidence:
Carcinogenic Classification: No data [4]
Wildlife
Partitioning Factors: Partitioning factors for benzo(g,h,i)perylene in wildlife were not found in the
literature.
Food Chain Multipliers: Food chain multipliers for benzo(g,h,i)perylene in wildlife were not found in
the literature.
Aquatic Organisms
Partitioning Factors: Partitioning factors for benzo(g,h,i)perylene in aquatic organisms were not found
in the literature.
Food Chain Multipliers: An ecotoxicological in situ study conducted at the Baltic Sea, showed that the
tissue residue concentration of benzo(g,h,i)perylene decreased with increasing trophic level [5]. The
relatively high theoretical flux through the food chain was not possible to detect.
113
-------
BIOACCUMULATION SUMMARY BENZO(G,H,I)PERYLENE
Toxicity/Bioaccumulation Assessment Profile
The acute toxicity of hydrocarbons, including benzo(g,h,i)perylene, to both fresh and salt water
crustaceans is largely nonselective, i.e., it is not primarily influenced by molecular structure, but is rather
controlled by organism-water partitioning which, for nonpolar organic chemicals, is in turn a reflection
of aqueous solubility. The toxic effect is believed to occur at a relatively constant concentration within
the organism [5].
The majority of investigations have shown that aquatic organisms are able to release polynuclear aromatic
hydrocarbons (PAHs), e.g., benzo(g,h,i)perylene, from their tissues rapidly when they were returned to
clean environment. Tanacredl and Cardenas [6] reported that Mercenaria mercenaria exposed to PAHs
accumulated them to high levels in their tissues and failed to release them when returned to clean seawater
over the 45-day depuration period. Unlike other marine organisms, this "sequestering" in molluscs may
support the apparent inability to metaboilize PAHs to more water soluble and thus easily secreted polar
metabolites.
Bioaccumulation of low-molecular-weight PAHs from sediments by Rhepoxynius abronius (amphipod)
and Armandia brevis (polychaete) was similar; however, a large difference in tissue concentration
between these two species was measured for high-molecular-weight PAHs including benzo(g,h,i)perylene
[7]. Meador et al. [7] concluded that the low-molecular-weight PAHs were available to both species from
interstitial water, while sediment ingestion was a much more important uptake route for the high-
molecular-weight PAHs. The authors also indicated that bioavailability of the high-molecular-weight
PAHs to amphipods was significantly reduced due to their partitioning to dissolved organic carbon.
114
-------
Summary of Biological Effects
Species:
Taxa
Invertebrates
Mytilus edulis,
Mussels
Crassostrea
virginica, Oyster
Pontoporeia hoyi,
Amphipod
Fishes
Cypriniis carpio,
Common carp
Concentration, Units
Sediment Water
0.4 ng/g
122.1 ng/g
31.1 ng/g
75.1 ng/g
5.4 ng/g
5.7 ng/g
6.2 ng/g
6.7 ng/g
0.4 ng/g
16.1 ng/g
400 ng/g 5 ng/mL
in1:
Tissue (Sample Type)
13 ng/g
10 ng/g
16 ng/g
27 ng/g
12 ng/g
14 ng/g
18 ng/g
10 ng/g
10 ng/g
10 ng/g
16 ng/g
DDL
29.6 mg/kg (liver)4
Tissue Concentrations for Benzo(g,h,i)perylene
Toxicity: Ability to Accumulate2: Source:
Log Log
Effects BCF BAF BSAF Reference
[8]
[10]
[10]
[10]
[10]
[10]
[10]
[10]
[10]
[10]
[10]
[9]
Physiological, [11]
NOED
Comments3
F
F
F
F
F
F
F
F
F
F
L
L; no significant increase in
EROD enzyme and P450 la
protein content
-------
Summary of Biological Effects Tissue Concentrations for Benzo(g,h,i)perylene
Species:
Taxa
Concentration, Units in1: Toxicity: Ability to Accumulate2: Source:
Log Log
Sediment Water Tissue (Sample Type) Effects BCF BAF BSAF Reference Comments3
Wildlife
Somateria
mollissima, Eider
duck
2 ng/g
[8]
Concentration units based on wet weight unless otherwise noted.
2 BCF = bioconcentration factor, BAF = bioaccumulation factor, BSAF = biota-sediment accumulation factor.
3 L = laboratory study, spiked sediment, single chemical; F = field study, multiple chemical exposure; other unusual study conditions or observations noted.
4 This entry was excerpted directly from the Environmental Residue-Effects Database (ERED, www.wes.army.mil/el/ered, U.S. Army Corps of Engineers and U.S.
Environmental Protection Agency). The original publication was not reviewed, and the reader is strongly urged to consult the publication to confirm the information
presented here.
-------
BIOACCUMULATION SUMMARY BENZO(G,H,I)PERYLENE
References
1. Pearlman, R.S. et al. /. Phys. Chem. Ref. Data 13: 555-562 (1984) as cited in USEPA, Health and
Environmental Effects Profile for Benzo(ghi)perylene, p.l (1987) EPA/600/X-87/395. (Cited in:
USEPA. 1995. Hazardous Substances Data Bank (HSDB). National Library of Medicine online
(TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental
Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. September.)
2. USEPA. 1989. Chemical fate rate constants for SARA section 313 chemicals and Superfund
Health Manual chemicals. Draft. Prepared by Chemical Hazard Assessment Division, Syracuse
Research Corporation, for U.S. Environmental Protection Agency, Office of Toxic Substances,
Exposure Evaluation Division, Washington, DC, and Environmental Criteria and Assessment
Office, Cincinnati, OH. August 10.
3. Karickhoff, S.W., and J.M. Long. 1995. Internal report on summary of measured, calculated, and
recommended log Kow values. Prepared by U.S. Environmental Protection Agency, Office of
Research and Development, Environmental Research Laboratory-Athens, for E. Southerland,
Office of Water, Office of Science and Technology, Standards and Applied Science Division,
Washington, DC. April 10, draft.
4. USEPA. 1997. Integrated Risk Information System (IRIS). National Library of Medicine online
(TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental
Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. January.
5. Abernethy, S., A.M. Bobra, W.Y. Shiu, P.G.Weils, and D. MacKay. 1986. Acute lethal toxicity
of hydrocarbons and chlorinated hydrocarbons to two planktonic crustaceans: The key role of
organism-water partitioning. Aquatic Tox. 8:163-174.
6. Tanacredl, J.T., and R.R. Cardenas. 1991. Biodepuration of polynuclear aromatic hydrocarbons
from a bivalve mollusc Mercenaria mercenaria L. Environ. Sci. Technol. 25:1453-1461.
7. Meador, J.P., E.Casillas, C.A. Sloan, and U. Varanasi. 1995. Comparative bioaccumulation of
polycyclic aromatic hydrocarbons from sediments by two infaunal invertebrates. Mar. Ecol. Prog.
Ser. 123:107-124.
8. Broman, D., C. Naf, I. Lundbergh, and Y. Zebuhr. 1990. An in situ study on the distribution,
biotransformation and flux of polycyclic aromatic hydrocarbons (PAHs) in an aquatic food chain
(sQSton-Mytilus edulis L - Somateria mollissima L.) from the Baltic: An ecotoxicological
perspective. Environ. Tox. Chem. 9:429-442.
9. Eadie, B.J., P.F. Landrum, and W. Faust. 1982. Polycyclic aromatic hydrocarbons in sediments,
pore water and the amphipod Pontoporeia hoyi from Lake Michigan. Chemosphere 11:847-858.
10. Sanders, M. 1995. Distribution of polycyclic aromatic hydrocarbons in oyster (Crassostrea
virginica) and surface sediment from two estuaries in South Carolina. Arch. Environ. Contain.
Toxicol. 28:397-405.
117
-------
BIOACCUMULATION SUMMARY BENZO(G,H,I)PERYLENE
11. Van Der Weidern, M.E.J., F.H.M. Hanegraaf, M.L. Eggens, M. Celander, W. Seinen, and M. Ven
Den Berg. 1994. Temporal induction of cytochrome P450 la in the mirror carp (Cyprinus carpio)
after administration of several polycyclic aromatic hydrocarbons. Environ. Toxicol Chem. 13:
797-802.
118
-------
BIOACCUMULATION SUMMARY BENZO(K)FLUORANTHENE
Chemical Category: POLYNUCLEAR AROMATIC HYDROCARBON (high molecular weight)
Chemical Name (Common Synonyms): BENZO(K)FLUORANTHENE CASRN: 207-08-9
Chemical Characteristics
Solubility in Water: Insoluble in water [1] Half-Life: 2.49 yrs - 5.86 yrs based on aerobic
soil die-away test data [2]
Log Kow: 6.20 [3] Log Koc: 6.09 L/kg organic carbon
Human Health
Oral RfD: No data [4] Confidence: —
Critical Effect: —
Oral Slope Factor (Reference): Not available [4] Carcinogenic Classification: B2 [4]
Wildlife
Partitioning Factors: Partitioning factors for benzo(k)fluoranthene in wildlife were not found in the
literature.
Food Chain Multipliers: Food chain multipliers for benzo(k)fluoranthene in wildlife were not found in
the literature.
Aquatic Organisms
Partitioning Factors: The only partitioning factors for benzo(k)fluoranthene in aquatic organisms found
in the literature were log BAFs of -0.68 to 0.01 for the clam Macoma nasuta [9].
Food Chain Multipliers: An ecotoxicological in situ study conducted at the Baltic Sea [5] showed that
the tissue residue concentration of benzo(k)fluoranthene decreased with increasing trophic level. The
relatively high theoretical flux through the food chain was not possible to detect.
Toxicity/Bioaccumulation Assessment Profile
The acute toxicity of hydrocarbons, including benzo(k)fluoranthene, to both fresh and salt water
crustaceans is largely nonselective, i.e., it is not primarily influenced by molecular structure, but is rather
controlled by organism-water partitioning which, for nonpolar organic chemicals, is in turn a reflection
119
-------
BIOACCUMULATION SUMMARY BENZO(K)FLUORANTHENE
of aqueous solubility. The toxic effect is believed to occur at a relatively constant concentration within
the organism [6].
The majority of investigations have shown that aquatic organisms are able to release polynuclear aromatic
hydrocarbons (PAHs), e.g., benzo(k)fluoranthene, from their tissues rapidly when they were returned to
clean environment. The apparent effects threshold concentration of 4500 ng/g for benzo(k)fluoranthene
was established based on effects observed in the marine amphipod Rhepoxynius abronius [7].
Bioaccumulation of low-molecular-weight PAHs from sediments by Rhepoxynius abronius (amphipod)
and Armandia brevis (polychaete) was similar, however, a large difference in tissue concentration
between these two species was measured for high-molecular-weight PAHs including
benzo(k)fluoranthene [8]. Meador et al. [8] concluded that the low-molecular-weight PAHs were
available to both species from interstitial water, while sediment ingestion was a much more important
uptake route for the high-molecular-weight PAHs. The authors also indicated that bioavailability of the
high-molecular-weight PAHs to amphipods was significantly reduced due to their partitioning to
dissolved organic carbon.
120
-------
Summary of Biological Effects Tissue Concentrations for Benzo(k)fluoranthene
Species:
Taxa
Invertebrates
Mytilus edulis,
Blue mussel
Crassostrea
virginica,
Eastern oyster
Macoma nasuta,
Clam
Wildlife
Somateria
mollissima,
Eider duck
1 Concentration
Concentration,
Sediment
1.5 ng/g
36 ng/g
59.6 ng/g
127.5 ng/g
, 14.1 ng/g
17 ng/g
121 ng/g
156 ng/g
390 ng/g
610 ng/g
units based on wet
Units in1: Toxicity:
Water Tissue (Sample Type) Effects
44 ng/g
14 ng/g
85 ng/g
65 ng/g
61 ng/g
92 ng/g
24 ng/g
59 ng/g
87 ng/g
128 ng/g
96 ng/g
4.3 ng/g
weight unless otherwise noted.
Ability to Accumulate2:
Log Log
BCF BAF BSAF
0.009 or
0.01
-0.66
-0.48
-0.39
-0.51
-0.68
Source:
Reference
[5]
[10]
[10]
[10]
[9]
[9]
[9]
[9]
[9]
[9]
[5]
Comments3
F
F
F
F
F
F
F
F
F
F
F
2 BCF = bioconcentration factor, BAF = bioaccumulation factor, BSAF = biota-sediment accumulation factor.
3 L = laboratory
T^Viic Antr\r ™?Q<
study, spiked sediment, single chemical; F = field study, multiple chemical
? Av^ArntArl HirA^tl\r frnm thf» THtTuirnrimfntQl Rfcirhif-lH fff»rtc Pi^tshQCf1 fTnli
exposure; other unusual study conditions or observations noted.
JTnT^ \X7\X7\X7 \x7f»c Qrrm7 mi 1 /V»l /Wf»rl TT*\ Arrm7 f^nrnc nf Tnnainf^rc 9n
and U.S.
Environmental Protection Agency). The original publication was not reviewed, and the reader is strongly urged to consult the publication to confirm the information
presented here.
-------
BIOACCUMULATION SUMMARY BENZO(K)FLUORANTHENE
References
1. Weast handbook of chemistry and physics, 60th edition, 1979, C-180. (Cited in: USEPA. 1995.
Hazardous Substances Data Bank (HSDB). National Library of Medicine online (TOXNET). U.S.
Environmental Protection Agency, Office of Health and Environmental Assessment, Environmental
Criteria and Assessment Office, Cincinnati, OH. September.)
2. USEPA. 1989. Chemical fate rate constants for SARA section 313 chemicals and Superfund Health
Manual chemicals. Prepared by Chemical Hazard Assessment Division, Syracuse Research
Corporation, for U.S. Environmental Protection Agency, Office of Toxic Substances, Exposure
Evaluation Division, Washington, DC, and Environmental Criteria and Assessment Office,
Cincinnati, OH. August 11.
3. Karickhoff, S.W., and J.M. Long. 1995. Internal report on summary of measured, calculated, and
recommended log Kow values. Draft. Prepared by U.S. Environmental Protection Agency, Office
of Research and Development, Environmental Research Laboratory-Athens, for E. Southerland,
Office of Water, Office of Science and Technology, Standards and Applied Science Division,
Washington, DC. April 10.
4. USEPA. 1997. Integrated Risk Information System (IRIS). National Library of Medicine online
(TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental
Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. January.
5. Broman, D., C. Naf, I. Lundbergh, and Y. Zebuhr. 1990. An in situ study on the distribution,
biotransformation and flux of polycyclic aromatic hydrocarbons (PAHs) in an aquatic food chain
(sQSton-Mytilus edulis L - Somateria mollissima L.) from the Baltic: An ecotoxicological
perspective. Environ. Toxicol. Chem. 9:429-442.
6. Abernethy, S., A.M. Bobra, W.Y. Shiu, P.G.WeUs, and D. MacKay. 1986. Acute lethal toxicity of
hydrocarbons and chlorinated hydrocarbons to two planktonic crustaceans: The key role of
organism-water partitioning. Aquat. Tox. 8:163-174.
7. Ingersoll, C.G., and M.K. Nelson. 1990. Testing sediment toxicity with Hyalella azteca
(Amphipoda) and Chironomus riparius (Diptera). In Aquatic Toxicology and Risk Assessment:
ASTM STP 1096, ed. W.G. Landis and W.H. van der Schalie, pp. 93-109. American Society for
Testing and Materials, Philadelphia, PA.
8. Meador, J.P., E. Casillas, C.A. Sloan, and U. Varanasi. 1995. Comparative bioaccumulation of
polycyclic aromatic hydrocarbons from sediments by two infaunal invertebrates. Mar. Ecol. Prog.
Ser. 123:107-124.
9. Ferraro, S.P., H. Lee U, RJ. Ozretich, and D.T. Specht. 1990. Predicting bioaccumulation potential:
A test of a fugacity-based model. Arch. Environ. Contain. Toxicol. 19:386-394.
10. Sanders, M. 1995. Distribution of polycyclic aromatic hydrocarbons in oyster (Crassostrea
virginica) and surface sediment from two estuaries in South Carolina. Arch. Environ. Contain.
Toxicol. 28:397-405.
122
-------
BIOACCUMULATION SUMMARY CADMIUM
Chemical Category: METAL (Divalent)
Chemical Name (Common Synonyms): CADMIUM CASRN: 7440-43-9
Chemical Characteristics
Solubility in Water: Insoluble [1] Half-Life: Not applicable, stable [1]
LogKow: - LogKoc: -
Human Health
Oral RfD: 5 x 10~4 mg/kg-day [2] Confidence: High, uncertainty factor =10
Critical Effect: Significant proteinuria, presence of protein in urine
Oral Slope Factor: Not available [2] Carcinogenic Classification: Bl [2]
Wildlife
Partitioning Factors: Partitioning factors for cadmium in wildlife were not found in the
literature.
Food Chain Multipliers: Food chain multipliers for cadmium in wildlife were not found in the
literature.
Aquatic Organisms
Partitioning Factors: Cadmium in the water column can partition to dissolved and particulate organic
carbon. The more important issues related to water column concentrations of cadmium are water
hardness (i.e., calcium concentration), pH, and metal speciation since the divalent cadmium ion is
believed to be responsible for observed biological effects. Cadmium speciation yields primarily the
divalent form of the metal, Cd+2, between pH values of 4.0 and 7.0 [3]. In addition, the concentration of
acid-volatile sulfides is known to be an important factor controlling the toxicity and bioaccumulation of
cadmium in sediments.
Food Chain Multipliers: Most studies reviewed contained data which suggest that cadmium is not a
highly mobile element in aquatic food webs, and there appears to be little evidence to support the general
occurrence of biomagnification of cadmium within marine or freshwater food webs [4,5,6,7].
123
-------
BIOACCUMULATION SUMMARY CADMIUM
Toxicity/Bioaccumulation Assessment Profile
Cadmium does not appear to be a highly mobile element under typical conditions in most aquatic habitats
[4]. Additional studies reviewed by Kay [4] indicated that no maternal transfer of cadmium was observed
in zebrafish and that the cadmium content of bird eggs did not appear to be a good indicator of
environmental exposure to cadmium. Tissue residue-toxicity relationships can also be variable because
organisms might sequester metal in various forms that can be analytically measurable as tissue residue
but might actually be stored in unavailable forms within the organism as a form of detoxification [8].
Whole body residues might also not be indicative of effects concentrations at the organ level because
concentrations in target organs, such as the kidneys and liver, may be 20 times higher than whole body
residues [9]. The application of "clean" chemical analytical and sample preparation techniques is also
critical in the measurement of metal tissue residues. After evaluating the effects of sample preparation
techniques on measured concentrations of metals in the edible tissue of fish, Schmitt and Finger [10]
concluded that there was little direct value in measuring copper, zinc, iron, or manganese tissue residues
in fish because they do not bioaccumulate to any appreciable extent. Cadmium and lead were the only
ones found to be of potential concern in edible fish tissue based on the results from Schmitt and Finger's
study of "clean" chemical techniques, although Wiener and Stokes [11] suggested that cadmium did not
generally accumulate to any appreciable extent in the edible muscle tissue of fish.
Rule and Alden [26] studied the relationship between uptake of cadmium and copper from the sediment
by the blue mussel (Mytilus edulis), grass shrimp (Palaemonetes pugio), and hard clam (Mercenaria
mercenarid). The uptake of cadmium by the blue mussel significantly increased as a function of
increasing cadmium concentration in sediment. However, the uptake of cadmium increased when copper
was added to the sediments. The uptake of cadmium by the grass shrimp exhibited a pattern similar to that
of the mussel, while the uptake of cadmium by the hard clam was low compared to the other two species
and related only to the cadmium concentration in sediment.
The experiments performed by Meador [28] revealed that the response of the amphipods Rhepoxynius
abronius and Eohaustorius estuarius to cadium decreased two- to threefold for animals held in the
laboratory for several weeks compared to organisms recently collected from the field.
124
-------
Summary of Biological Effects Tissue Concentrations for Cadmium
Species:
Taxa
Plants
Scenedesmiis obliquus,
Freshwater colonial
green algae
Concentration, Units in1:
Sediment Water Tissue (Sample Type)
2,340 mg/kg
(whole body)5
658 mg/kg
(whole body)5
3,030 mg/kg
(whole body)5
Toxicity:
Effects
Growth,
LOED
Growth,
LOED
Growth,
NOED
Ability to Accumulate2 Source:
Log Log
BCF BAF BSAF Reference Comments3
[31] L; significant
inhibition of
growth (27%
reduction from
control)
[31] L;39%
reduction in
population
growth from
controls
[31] L;no
significant
inhibition of
growth
Eichhornia crassipes,
Water hyacinth
11.4 mg/kg (leaf)5 Growth,
LOED
262 mg/kg (root)5
49.6 mg/kg (stem)5
Growth,
LOED
Growth,
LOED
[47]
[47]
[47]
F; reduced
growth rate,
chlorosis
F; reduced
growth rate,
chlorosis
F; reduced
growth rate,
chlorosis
-------
Summary of Biological Effects Tissue Concentrations for Cadmium
Species: Concentration, Units in1: Toxicity:
Taxa Sediment Water Tissue (Sample Type) Effects
1 1 .4 mg/kg (leaf)5 Morphology,
LOED
262 mg/kg (root)5 Morphology,
LOED
49.6 mg/kg (stem)5 Morphology,
LOED
20.8 mg/kg (leaf)5 Growth, NA
45.8 mg/kg (leaf)5 Growth, NA
578 mg/kg (root)5 Growth, NA
1,300 mg/kg (root)5 Growth, NA
Ability to Accumulate2 Source:
Log Log
BCF BAF BSAF Reference
[47]
[47]
[47]
[47]
[47]
[47]
[47]
Comments3
F; chlorosis,
browning,
necrosis,
waterlogging of
tissues
F; chlorosis,
browning,
necrosis,
waterlogging of
tissues
F; chlorosis,
browning,
necrosis,
waterlogging of
tissues
F; reduced
growth rate,
chlorosis
F; reduced
growth rate,
chlorosis
F; reduced
growth rate,
chlorosis
F; reduced
growth rate,
chlorosis
-------
Summary of Biological Effects Tissue Concentrations for Cadmium
Species: Concentration, Units in1: Toxicity: Ability to Accumulate2
Log Log
Taxa Sediment Water Tissue (Sample Type) Effects BCF BAF BSAF
84.8 mg/kg (stem)5 Growth, NA
159 mg/kg (stem)5 Growth, NA
20.8 mg/kg (leaf)5 Morphology,
NA
45.8 mg/kg (leaf)5 Morphology,
NA
578 mg/kg (root)5 Morphology,
NA
1,300 mg/kg (root)5 Morphology,
NA
Source:
Reference Comments3
[47] F; reduced
growth rate,
chlorosis
[47] F; reduced
growth rate,
chlorosis
[47] F; chlorosis,
browning,
necrosis,
waterlogging of
tissues
[47] F; chlorosis,
browning,
necrosis,
waterlogging of
tissues
[47] F; chlorosis,
browning,
necrosis,
waterlogging of
tissues
[47] F; chlorosis,
browning,
necrosis,
waterlogging of
tissues
-------
to summary 01 Biological mtects i issue concentrations tor cadmium
Species: Concentration, Units in1:
Taxa Sediment Water Tissue (Sample Type)
84.8 mg/kg (stem)5
159 mg/kg (stem)5
8 mg/kg (leaf)5
142 mg/kg (root)5
27.8 mg/kg (stem)5
8 mg/kg (leaf)5
142 mg/kg (root)5
27.8 mg/kg (stem)5
Toxicity:
Effects
Morphology,
NA
Morphology,
NA
Growth,
NOED
Growth,
NOED
Growth,
NOED
Morphology,
NOED
Morphology,
NOED
Morphology,
NOED
Ability to Accumulate2 Source:
Log Log
BCF BAF BSAF Reference
[47]
[47]
[47]
[47]
[47]
[47]
[47]
[47]
Comments3
F; chlorosis,
browning,
necrosis,
waterlogging of
tissues
F; chlorosis,
browning,
necrosis,
waterlogging of
tissues
F; no effect on
growth
F; no effect on
growth
F; no effect on
growth
F; no effect on
plant
appearance
F; no effect on
plant
appearance
F; no effect on
plant
appearance
-------
Summary of Biological Effects Tissue Concentrations for Cadmium
Species:
Taxa
Invertebrates
Lumbriculus
variegatus,
Oligochaete
Najas qiiadulepensis,
Southern naiad
Neanthes
arenaceodentata,
Polychaete
Concentration, Units in1:
Sediment Water Tissue (Sample Type)
670 mg/kg
(whole body)5
3 10 mg/kg
(whole body)5
10.3 mg/kg
(whole body)5
67 mg/kg
(whole body)5
67 mg/kg
(whole body)5
4.5 mg/kg
(whole body)5
0.22 mg/kg
(whole body)5
0.028 mg/kg
(whole body)5
Toxicity: Ability to Accumulate2
Log Log
Effects BCF BAF BSAF
Mortality,
LOED
Mortality,
NOED
Development,
LOED
Reproduction,
ED 100
Behavior,
LOED
Behavior,
NOED
Behavior,
NOED
Behavior,
NOED
Source:
Reference
[32]
[32]
[35]
[46]
[46]
[46]
[46]
[46]
Comments3
L; 40%
mortality
L; no effect on
mortality
L; reductions in
chlorophyll and
stolon
development
L; reproductive
failure
L; reduced tube
building,
sluggish
behavior
L; no effect on
behavior
L; no effect on
behavior
L; no effect on
behavior
-------
Summary of Biological Effects Tissue Concentrations for Cadmium
Species: Concentration, Units in1:
Taxa Sediment Water Tissue (Sample Type)
0.0028 mg/kg
(whole body)5
67 mg/kg
(whole body5
4.5 mg/kg
(whole body)5
0.22 mg/kg
(whole body)5
0.028 mg/kg
(whole body )5
0.0028 mg/kg
(whole body)5
4.5 mg/kg
(whole body)5
0.22 mg/kg
(whole body)5
0.028 mg/kg
(whole body)5
0.0028 mg/kg
(whole body)5
Toxicity: Ability to Accumulate2
Log Log
Effects BCF BAF BSAF
Behavior,
NOED
Mortality,
NOED
Mortality,
NOED
Mortality,
NOED
Mortality,
NOED
Mortality,
NOED
Reproduction,
NOED
Reproduction,
NOED
Reproduction,
NOED
Reproduction,
NOED
Source:
Reference
[46]
[46]
[46]
[46]
[46]
[46]
[46]
[46]
[46]
[46]
Comments3
L; no effect on
behavior
L; no effect on
survival
L; no effect on
survival
L; no effect on
survival
L; no effect on
survival
L; no effect on
survival
L; no effect on
reproduction
L; no effect on
reproduction
L; no effect on
reproduction
L; no effect on
reproduction
-------
Summary of Biological Effects Tissue Concentrations for Cadmium
Species:
Taxa
Neanthes virens,
Polychaete - Sandworm
Helisoma sp.,
Snail
Dreissena polymorpha,
Zebra mussel
Mytilus edulis,
Blue mussel
Concentration, Units in1:
Sediment Water Tissue (Sample Type)
106 mg/kg
(whole body)5
78 mg/kg
(whole body)5
290 mg/kg
(whole body)5
625 mg/kg
(whole body)5
300 mg/kg
(whole body)5
460 mg/kg
(whole body)5
Day 27:
539-598 |ig/g
0.96-1. 06 mmol/kg
30 mg/kg
(whole body)5
Toxicity: Ability to Accumulate2
Log Log
Effects BCF BAF BSAF
Behavior,
LOED
Physiological,
LOED
Physiological,
LOED
Mortality,
ED50
Mortality,
NOED
Mortality,
NOED
50% mortality
Growth,
NOED
Source:
Reference
[33]
[33]
[33]
[32]
[32]
[32]
[19]
[53]
Comments3
L; lethargy
L; total
glycogen
reduced,
increase in
ascorbic acid
L; increase in
ascorbic acid
content
L; 50%
mortality
L; no effect on
mortality
L; no effect on
mortality
L
L
-------
Summary of Biological Effects Tissue Concentrations for Cadmium
Species: Concentration, Units in1:
Taxa Sediment Water Tissue (Sample Type)
30 mg/kg
(whole body)5
6.45 mg/kg
(whole body)5
4.22 mg/kg
(whole body)5
8.06 mg/kg
(whole body)5
3.74 mg/kg
(whole body)5
8.06 mg/kg
(whole body)5
8.06 mg/kg
(whole body)5
Toxicity: Ability to Accumulate2
Log Log
Effects BCF BAF BSAF
Mortality,
NOED
Mortality,
NOED
Mortality, NA
Mortality, NA
Mortality, NA
Mortality, NA
Physiological,
NOED
Source:
Reference
[53]
[26]
[60]
[60]
[60]
[60]
[60]
Comments3
L; highest body
burden reported
L; estimated
wet weight
L; decreased
anoxic survival
time (Control
10.7 days)
L; decreased
anoxic survival
time (Control
10.7 days)
L; decreased
anoxic survival
time (Control
13 days)
L; decreased
anoxic survival
time (Control
10.7 days)
L; no
significant
changes in
adenylate
energy charge
or glycogen
content
-------
Summary of Biological Effects Tissue Concentrations for Cadmium
Species:
Taxa
Mytilus
galloprovincialis,
Mussel
Crassostrea virginica,
Oyster
Daphnia magna,
Cladoceran
Concentration, Units in1: Toxicity: Ability to Accumulate2
Log Log
Sediment Water Tissue (Sample Type) Effects BCF BAF BSAF
0.57-0.92 mg/kg 0.416
18.2mg/kg Reproduction,
(whole body)5 NOED
54 mg/kg Reproduction,
(whole body)5 NOED
Day 21: LOEC
2.36 |ig/g
Week 20: LOEC
17.4 |ig/g
Day 21: 10% mortality
2.0 mmol/kg
Source:
Reference Comments3
[27] F
[62] L; no reduced
viability of
gametes after
exposure of
adults in 21 ppt
seawater
[62] L; 24%
reduction in
viability of
gametes after
exposure of
adults in 21 ppt
seawater
[20] F
[17] L
[21] L
-------
Summary of Biological Effects Tissue Concentrations for Cadmium
Species:
Taxa
Daphnia magna,
Cladoceran
Daphnia galeata
mendotae, Cladoceran
Concentration, Units in1:
Sediment Water Tissue (Sample Type)
1.7 mg/kg
(whole body)5
221 mg/kg
(whole body)5
10.3 mg/kg
(whole body) 5
3.5 mg/kg
(whole body)
5.7 mg/kg
(whole body) 5
8.6 mg/kg
(whole body)5
Toxicity: Ability to Accumulate2
Log Log
Effects BCF BAF BSAF
Reproduction,
ED10
Mortality,
ED50
Growth,
LOED
Mortality,
LOED
Mortality, NA
Mortality, NA
Source:
Reference Comments3
[21] L; 10%
reduction in
number of
offspring
[21] L; lethal body
burden after
21 -day
exposure
[48] L; increased
weight of
individual
animals
[48] L; reduced
longevity,
increased
prenatal
mortality
[48] L; reduced
longevity,
increased
prenatal
mortality
[48] L; reduced
longevity,
increased
prenatal
mortality
-------
Summary of Biological Effects Tissue Concentrations for Cadmium
Species:
Taxa
Folsomia Candida,
Cladoceran
Gammarusfossarum,
Amphipod
Moina macrocopa,
Cladoceran
Concentration, Units in1:
Sediment Water Tissue (Sample Type)
10.3 mg/kg
(whole body)5
3.5 mg/kg
(whole body)5
5.7 mg/kg
(whole body)5
8.6 mg/kg
(whole body)5
60 |ig/g
Day 14:
60-70 |ig/g
16.4 mg/kg
(whole body)5
16.4 mg/kg
(whole body)5
Toxicity: Ability to Accumulate2
Log Log
Effects BCF BAF BSAF
Mortality, NA
Growth,
NOED
Growth,
NOED
Growth,
NOED
LOEC
50% mortality
Reproduction,
ED 100
Growth,
LOED
Source:
Reference
[48]
[48]
[48]
[48]
[22]
[18]
[42]
[42]
Comments3
L; reduced
longevity,
increased
prenatal
mortality
L; no effect on
individual
weight
L; no effect on
individual
weight
L; no effect on
individual
weight
F
L
L; no
reproduction
after 12 days
L; reduced
growth
-------
Summary of Biological Effects Tissue Concentrations for Cadmium
Species:
Taxa
Hyallela azteca,
Amphipod
Pontoporeia affinis,
Amphipod
(juveniles, 105-460 d)
Pontoporeia affinis,
Amphipod
Concentration, Units in1:
Sediment Water Tissue (Sample Type)
16.4 mg/kg
(whole body)5
10.6 mg/kg
(whole body)5
10.6 mg/kg
(whole body)5
8 mg/kg
(whole body)5
Week 6:
15.2 ng/g
Day 460:
80-90 |ig/g
(0.14 mmol/kg)
1 1 mg/kg
(whole body)5
6 mg/kg
(whole body)5
6 mg/kg
(whole body)5
Toxicity: Ability to Accumulate2
Log Log
Effects BCF BAF BSAF
Mortality,
LOED
Reproduction,
LOED
Mortality,
NOED
Reproduction,
NOED
LOAEC
LOEC
Mortality,
LOED
Reproduction,
LOED
Mortality,
NOED
Source:
Reference
[42]
[42]
[42]
[42]
[17]
[16]
[58]
[58]
[58]
Comments3
L; reduced
survival
L; reduced
brood size
L; no effect on
survival
L; no effect on
brood size
L
L
L
L; percent
malformed
eggs
L
-------
Summary of Biological Effects Tissue Concentrations for Cadmium
Species:
Taxa
Balaniis crenatus,
Barnacle
Mysidopsis bahia,
Mysid
Concentration, Units in1:
Sediment Water Tissue (Sample Type)
3 mg/kg
(whole body)5
2 mg/kg
(whole body)5
10 mg/kg
(whole body)5
52 mg/kg
(whole body)5
1.29 mg/kg
(whole body)5
1.29 mg/kg
(whole body)5
Toxicity: Ability to Accumulate2
Log Log
Effects BCF BAF BSAF
Reproduction,
NOED
Mortality,
NOED
Mortality,
NOED
Behavior,
NOED
Growth,
LOED
Physiological,
LOED
Source:
Reference Comments3
[58] L; Percent
malformed
eggs
[59] L; body burden
estimated from
graph
[59] L; body burden
estimated from
graph
[55] L; regulation of
metals endpoint
- summer
experiment
[34] L; reduction in
growth, mean
dry weight of
animals
[34] L; altered O:N
ratio, shift
towards lipid
utilization with
increasing
cadmium
concentration
-------
Summary of Biological Effects Tissue Concentrations for Cadmium
Species:
Taxa
Concentration, Units in1:
Toxicity:
Ability to Accumulate2
Log Log
Sediment Water Tissue (Sample Type) Effects BCF BAF BSAF
Source:
Reference Comments3
2.38 mg/kg
(whole body)5
4.36 mg/kg
(whole body)5
2.38 mg/kg
(whole body)5
4.36 mg/kg
(whole body)5
Growth, NA
Growth, NA
Physiological,
NA
[34]
[34]
[34]
Physiological,
NA
[34]
L; reduction in
growth, mean
dry weight of
animals
L; reduction in
growth, mean
dry weight of
animals
L; altered O:N
ratio, shift
towards lipid
utilization with
increasing
cadmium
concentration
L; altered O:N
ratio, shift
towards lipid
utilization with
increasing
cadmium
concentration
Oniscus asellus,
Isopod
Day 91:
8.15mmol/kg
[23]
50% mortality
Porcellio scaber,
Isopod
Day 63:
5.40 mmol/kg
3.77 mmol/kg
[23]
50% mortality
50% mortality
-------
Summary of Biological Effects Tissue Concentrations for Cadmium
Species:
Taxa
Concentration, Units in1:
Toxicity:
Ability to Accumulate2
Log Log
Sediment Water Tissue (Sample Type) Effects BCF BAF BSAF
Source:
Reference Comments3
Palaemonetes pugio,
Grass shrimp
0.9 mg/kg
(whole body)5
2.6 mg/kg
(whole body)5
Mortality,
NOED
Mortality, NA
[26]
[61]
5.8 mg/kg
(whole body)5
Mortality, NA
[61]
7 mg/kg
(whole body)5
Mortality, NA
[61]
L; estimated
wet weight
L; 20%
increased
mortality over
control in 5 ppt
water; no
statistical
analysis
L; 22%
increased
mortality over
control in 5 ppt
water; no
statistical
analysis
L; 25%
increased
mortality over
control in 5 ppt
water; no
statistical
analysis
Palaemonetes pugio,
Grass shrimp
Day 21:
4.0 |ig/g
25% mortality
[14]
L
-------
Summary of Biological Effects Tissue Concentrations for Cadmium
Species: Concentration, Units in1: Toxicity: Ability to Accumulate2 Source:
Log Log
Taxa Sediment Water Tissue (Sample Type) Effects BCF BAF BSAF Reference Comments3
Callianassa
aiistraliensis,
Mole shrimp
Day 14: 50% mortality [15] L
4.8 |ig/g
Cambams latimanus,
Crayfish
14.9 mg/kg
(whole body)5
14.9 mg/kg
(whole body)5
14.9 mg/kg
(whole body)5
Growth,
NOED
[13]
Mortality,
NOED
Physiological,
NOED
[13]
[13]
L; no
significant
difference from
control growth
at lowest test
concentration
L; no
significant
difference from
control
mortality
L; no
significant
difference from
control
temperature
sensitivity at
lowest test
concentration
Cambams latimanus,
Crayfish
Month 5:
4.4 |ig/g
LOEC
[13]
-------
Summary of Biological Effects Tissue Concentrations for Cadmium
Species:
Taxa
Orconectes virilis,
Crayfish
Orconectes
propinquus,
Crayfish
Chironomiis gr.
thummi, Midge
Glyptotendipes pattens,
Midge
Concentration, Units in1:
Sediment Water Tissue (Sample Type)
Day 14:
5.6 |ig/g
534 mg/kg
(whole body)5
0.1 56 mg/kg
(whole body)5
20 mg/kg
(whole body)5
20 mg/kg
(whole body)5
30 mg/kg
(whole body)5
50 mg/kg
(whole body)5
Toxicity: Ability to Accumulate2
Log Log
Effects BCF BAF BSAF
25% mortality
Mortality,
NOED
Morphology,
NOED
Behavior,
LOED
Growth,
LOED
Behavior, NA
Behavior, NA
Source:
Reference
[12]
[39]
[45]
[44]
[44]
[44]
[44]
Comments3
L
L; 7% mortality
after 190.5
hours, probably
not significant
F; 4th instar
larvae
L; modified
feeding
behavior,
reduced net
spinning
activity
L; reduced
biomass
L; modified
feeding
behavior,
reduced net
spinning
activity
L; lethargy
-------
Summary of Biological Effects Tissue Concentrations for Cadmium
Species: Concentration, Units in1:
Taxa Sediment Water Tissue (Sample Type)
72 mg/kg
(whole body)5
138 mg/kg
(whole body)5
30 mg/kg
(whole body)5
50 mg/kg
(whole body)5
72 mg/kg
(whole body)5
138 mg/kg
(whole body)5
10 mg/kg
(whole body)5
18 mg/kg
(whole body)5
10 mg/kg
(whole body)5
18 mg/kg
(whole body)5
Toxicity: Ability to Accumulate2
Log Log
Effects BCF BAF BSAF
Behavior, NA
Behavior, NA
Growth, NA
Growth, NA
Growth, NA
Growth, NA
Behavior,
NOED
Behavior,
NOED
Growth,
NOED
Growth,
NOED
Source:
Reference
[44]
[44]
[44]
[44]
[44]
[44]
[44]
[44]
[44]
[44]
Comments3
L; lethargy
L; lethargy
L; reduced
biomass
L; reduced
biomass
L; reduced
biomass
L; reduced
biomass
L; no effect on
feeding
behavior or
activity level
L; no effect on
feeding
behavior or
activity level
L; no effect on
biomass
L; no effect on
biomass
-------
Summary of Biological Effects Tissue Concentrations for Cadmium
Species:
Taxa
Orchesella cincta,
Springtail
Tomocerus minor,
Springtail
Concentration, Units in1:
Sediment Water Tissue (Sample Type)
10 mg/kg
(whole body)5
18 mg/kg
(whole body)5
20 mg/kg
(whole body)5
30 mg/kg
(whole body)5
50 mg/kg
(whole body)5
72 mg/kg
(whole body)5
138 mg/kg
(whole body)5
Day 49:
0.07 mmol/kg
Day 63:
0.13 mmol/kg
Toxicity: Ability to Accumulate2
Log Log
Effects BCF BAF BSAF
Mortality,
NOED
Mortality,
NOED
Mortality,
NOED
Mortality,
NOED
Mortality,
NOED
Mortality,
NOED
Mortality,
NOED
50% mortality
50% mortality
Source:
Reference
[44]
[44]
[44]
[44]
[44]
[44]
[44]
[23]
[23]
Comments3
L; no effect on
mortality in 96
hours
L; no effect on
mortality in 96
hours
L; no effect on
mortality in 96
hours
L; no effect on
mortality in 96
hours
L; no effect on
mortality in 96
hours
L; no effect on
mortality in 96
hours
L; no effect on
mortality in 96
hours
F
F
-------
Summary of Biological Effects Tissue Concentrations for Cadmium
Species:
Taxa
Platynothrus peltifer,
Oribatid mite
Classenia sabulosa,
Stonefly
Hesperoperla paciflca,
Stonefly
Isogenoides sp.,
Stonefly
Pteronarcys
californica, Stonefly
Hydropsyche sp.,
Caddisfly
Concentration, Units
Sediment Water
<0.3 |ig/g
3.5 ng/g
6.6 |ig/g
<0.3 |ig/g
3.5 ng/g
6.6 |ig/g
<0.3 |ig/g
3.5 ng/g
6.6 |ig/g
<0.3 |ig/g
3.5 ng/g
6.6 |ig/g
in1: Toxicity: Ability to Accumulate2 Source:
Log Log
Tissue (Sample Type) Effects BCF BAF BSAF Reference Comments3
Day 63: 50% mortality [23] F
0.42 mmol/kg
0.1 ng/g [24] F
ND
1.4|ig/g
0.2 ng/g [24] F
ND
1.0|ig/g
<0.4 |ig/g [24] F
1.4|ig/g
1.8 |ig/g
0.1 |ig/g [24] F
ND
1.0|ig/g
9.8 mg/kg Mortality, [38] L; mortality in
(whole body)5 LOED one day
17.4 mg/kg Mortality, [38] L; mortality in
(whole body)5 LOED two days
29.8 mg/kg Mortality, [38] L; mortality in
(whole body)5 LOED four days
-------
Summary of Biological Effects Tissue Concentrations for Cadmium
Species:
Taxa
Hydropsyche spp.,
Caddisfly
Arctopsyche grandis,
Caddisfly
Concentration, Units in1:
Sediment Water Tissue (Sample Type)
0.118mg/kg
(whole body)5
0.0934 mg/kg
(whole body)5
16 mg/kg
(whole body)5
24.8 mg/kg
(whole body)5
4 1.8 mg/kg
(whole body)5
0.202 mg/kg
(whole body)5
0.284 mg/kg
(whole body)5
<0.3 |ig/g 0.2 |ig/g
3.5 |ig/g 2.2 |ig/g
6.6 |ig/g 2.8 |ig/g
<0.3 |ig/g 0.2 |ig/g
3.5 |ig/g ND4
6.6|ig/g 1.4|ig/g
Toxicity:
Effects
Mortality,
LOED
Mortality,
LOED
Mortality,
NOED
Mortality,
NOED
Mortality,
NOED
Mortality,
NOED
Mortality,
NOED
Ability to Accumulate2 Source:
Log Log
BCF BAF BSAF Reference
[38]
[38]
[38]
[38]
[38]
[38]
[38]
[24]
[24]
Comments3
L; mortality in
one day
L; mortality in
two days
L; no effect on
mortality in one
day
L; no effect on
mortality in one
day
L; no effect on
mortality in one
day
L; no effect on
mortality in one
day
L; no effect on
mortality in one
day
F
F
-------
Summary of Biological Effects Tissue Concentrations for Cadmium
Species:
Taxa
Asterias rubens,
Starfish
Fishes
Oncorhynchiis mykiss,
Rainbow trout
Concentration, Units in1:
Sediment Water Tissue (Sample Type)
0.03 mg/kg (gonad)5
0.14 mg/kg (gonad)5
16.4 mg/kg
(whole body)5
101 mg/kg
(whole body)5
0.84 mg/kg
(whole body)5
0.71 mg/kg
(whole body)5
0.21 mg/kg
(whole body)5
Toxicity: Ability to Accumulate2
Log Log
Effects BCF BAF BSAF
Development,
LOED
Development,
LOED
Mortality,
ED100
Mortality,
ED 100
Mortality,
ED 100
Behavior,
LOED
Morphology,
LOED
Source:
Reference
[37]
[37]
[29]
[29]
[29]
[29]
[29]
Comments3
combined,
estimated wet
weight adult
males
combined,
estimated wet
weight adult
females
L; complete
mortality of
alevins within
10 hours
L; complete
mortality of
eggs within 32
hours
L; complete
mortality of
alevins within
320 hours
L; erratic
swimming
L; deformed
vertebrae,
blood clots in
fins
-------
Summary of Biological Effects Tissue Concentrations for Cadmium
Species: Concentration, Units in1:
Taxa Sediment Water Tissue (Sample Type)
0.21 mg/kg
(whole body)5
10 mg/kg
(whole body)5
0.0599 mg/kg
(whole body)5
6.4 mg/kg
(whole body)5
3.74 mg/kg
(whole body)5
4 mg/kg
(whole body)5
2.2 mg/kg
(whole body)5
Toxicity: Ability to Accumulate2
Log Log
Effects BCF BAF BSAF
Mortality,
LOED
Physiological,
LOED
Mortality,
NOED
Mortality,
ED50
Mortality,
ED50
Mortality,
ED50
Mortality,
ED50
Source:
Reference
[29]
[30]
[41]
[51]
[51]
[51]
[51]
Comments3
L; hatching
alevins unable
to break free
from egg
membrane,
died
L; induction of
metallothionein
L; no effect on
mortality
L; hardness:
279 mg/L
CaCO3
L; Hardness:
279 Mg/L
CaCO3
L; hardness:
70 mg/L
CaCO3
L; hardness:
70 mg/L
CaCO3
-------
Summary of Biological Effects Tissue Concentrations for Cadmium
Species:
Taxa
Salmo salar, Atlantic
Salmon
Concentration, Units in1:
Sediment Water Tissue (Sample Type)
0.26 mg/kg
(yolk sac/stomach)5
0.26 mg/kg
(yolk sac/stomach)5
0.05 mg/kg
(yolk sac/stomach)5
0.05 mg/kg
(yolk sac/stomach)5
Toxicity:
Effects
Growth,
LOED
Mortality,
LOED
Growth,
NOED
Mortality,
NOED
Ability to Accumulate2 Source:
Log Log
BCF BAF BSAF Reference Comments3
[52] L; yolk
sac/stomach
weight - graph
and table
interpretation
[52] L; yolk
sac/stomach
weight - graph
and table
interpretation
[52] L; yolk
sac/stomach
weight - graph
and table
interpretation
[52] L; yolk
sac/stomach
weight - graph
and table
interpretation
Salvelinusfontinalis,
Brook trout
3.4 |ig/g
Week 38:
10 |ig/g, kidney
2 |ig/g, liver
[25]
L
-------
Summary of Biological Effects Tissue Concentrations for Cadmium
Species:
Taxa
Concentration, Units in1:
Toxicity:
Ability to Accumulate2
Log Log
Sediment Water Tissue (Sample Type) Effects BCF BAF BSAF
Source:
Reference Comments3
Salvelinusfontinalis,
Brook Trout
0.175 mg/kg (liver)5 Mortality,
LOED
0.232 mg/kg (liver)5 Growth, NA
0.203 mg/kg (liver)5
144 mg/kg
(whole body)5
Mortality,
NOED
Mortality,
LOED
[40]
[40]
[40]
[40]
L; significant
mortality in
10.5|ig/Lat 15
days and 1.91
|ig/L at 7 days,
but no body
burdens
measured
L; no
significant
effect on
growth
L
L; significantly
reduced
survival at
lowest test
concentration,
exp_conc =
<3.6
-------
Summary of Biological Effects Tissue Concentrations for Cadmium
Species:
Taxa
Concentration, Units in1:
Toxicity:
Ability to Accumulate2
Log Log
Sediment Water Tissue (Sample Type) Effects BCF BAF BSAF
Source:
Reference Comments3
0.742 mg/kg (liver)5
Physiological,
LOED
[40]
144 mg/kg
(whole body)5
Physiological,
LOED
[40]
L; significantly
increased
metallothionein
in whole body
tissues at
lowest test
concentration;
no correlation
between
metallothionein
concentration
and mortality
or whole body
tissue residues,
exp_conc =
<3.6
L; significantly
increased
metallothionein
in whole body
tissues at
lowest test
concentration;
no correlation
between
metallothionein
and mortality
or whole body
tissue residues,
exp_conc =
<3.6
-------
Summary of Biological Effects Tissue Concentrations for Cadmium
Species:
Taxa
Jordanella floridae,
American flagfish
Concentration, Units in1:
Sediment Water Tissue (Sample Type)
0.4 mg/kg
(whole body)5
0.4 mg/kg
(whole body)5
6 mg/kg
(whole body)5
0.4 mg/kg
(whole body)5
0.09 mg/kg
(whole body)5
6 mg/kg
(whole body)5
Toxicity: Ability to Accumulate2
Log Log
Effects BCF BAF BSAF
Mortality,
LOED
Mortality,
LOED
Growth,
NOED
Mortality,
NOED
Mortality,
NOED
Reproduction,
NOED
Source:
Reference Comments3
[56] L; body burden
estimated from
graph, fish
initially
exposed as
embryos
[56] L; body burden
estimated from
graph, fish not
exposed as
embryos
[56] L; body burden
estimated from
graph
[56] L; body burden
estimated from
graph, fish not
exposed as
embryos
[56] L; body burden
estimated from
graph, fish
initially
exposed as
embryos
[56] L; body burden
estimated from
graph
-------
Summary of Biological Effects Tissue Concentrations for Cadmium
Species:
Taxa
Poecilia reticulata,
Guppy
Cyprinodon variegatus,
Sheepshead minnow
Concentration, Units in1:
Sediment Water Tissue (Sample Type)
20 mg/kg
(whole body)5
10 mg/kg
(whole body)5
35 mg/kg
(whole body)5
8 mg/kg
(whole body)5
0.5 mg/kg
(whole body)5
1.2 mg/kg
(whole body)5
0.8 mg/kg
(whole body)5
0.9 mg/kg
(whole body)5
Toxicity: Ability to Accumulate2
Log Log
Effects BCF BAF BSAF
Growth,
LOED
Growth,
NOED
Mortality,
NOED
Mortality,
ED50
Growth,
LOED
Mortality,
LOED
Growth, NA
Development,
LOED
Source:
Reference
[57]
[57]
[57]
[43]
[43]
[43]
[43]
[49]
Comments3
L; total length
of females
L; total length
of females
L
L; 50%
reduction in
survival
L; reduction in
body length
within 10 days
L; 14%
reduction in
survival
L; reduction in
body length
within 10 days
L; decreased
time to hatch
-------
Summary of Biological Effects Tissue Concentrations for Cadmium
Species:
Taxa
Platichthysflesus,
European flounder
Concentration, Units in1: Toxicity: Ability to Accumulate2
Log Log
Sediment Water Tissue (Sample Type) Effects BCF BAF BSAF
17.2 mg/kg (kidney)5 Biochemical,
LOED
21.6 mg/kg (liver)5 Biochemical,
LOED
1 .82 mg/kg (ovary)5 Biochemical,
LOED
33.2 mg/kg (kidney)5 Biochemical,
NOED
43.8 mg/kg (liver)5 Biochemical,
NOED
Source:
Reference Comments3
[54] L; females -
Cd + estradiol
injection:
RNA:DNA
ratio
[54] L; females -
Cd + estradiol
injection:
RNA:DNA
ratio
[54] L; females -
Cd + estradiol
injection:
RNA:DNA
ratio
[54] L; males -
Cd + estradiol
injection:
RNA:DNA
ratio
[54] L; males -
Cd + estradiol
injection:
RNA:DNA
ratio
-------
Summary of Biological Effects Tissue Concentrations for Cadmium
Species: Concentration, Units in1: Toxicity: Ability to Accumulate2
Log Log
Taxa Sediment Water Tissue (Sample Type) Effects BCF BAF BSAF
4.66 mg/kg (ovary)5 Biochemical,
NOED
17.2 mg/kg (kidney)5 Mortality,
NOED
33.2 mg/kg (kidney)5 Mortality,
NOED
43.8 mg/kg (liver)5 Mortality,
NOED
21.6 mg/kg (liver)5 Mortality,
NOED
4.66 mg/kg (ovary)5 Mortality,
NOED
1 .82 mg/kg (ovary)5 Mortality,
NOED
Source:
Reference
[54]
[54]
[54]
[54]
[54]
[54]
[54]
Comments3
L; males -
Cd + estradiol
injection:
RNA:DNA
ratio
L; females -
Cd + estradiol
injection:
survival
L; males -
Cd + estradiol
injection:
survival
L; males -
Cd + estradiol
injection:
survival
L; females -
Cd + estradiol
injection:
survival
L; males -
Cd + estradiol
injection:
survival
L; females -
Cd + estradiol
injection:
survival
-------
Summary of Biological Effects Tissue Concentrations for Cadmium
Species:
Taxa
Pleiironectes
americanus,
Winter flounder
Concentration, Units in1:
Sediment Water Tissue (Sample Type)
1 mg/kg
(whole body)5
Toxicity:
Effects
Physiological,
LOED
Ability to Accumulate2
Log Log
BCF BAF BSAF
Source:
Reference
[36]
Comments3
L; induction of
metallothionein
Wildlife
Ambystoma gracile,
Salamander
140 mg/kg
(whole body)5
6.28 mg/kg
(whole body)5
4.7 mg/kg
(whole body)5
71.7 mg/kg
(whole body)5
Behavior,
LOED
Growth,
LOED
Growth,
LOED
Behavior,
NOED
[50]
[50]
[50]
[50]
L; significant
reduction in
regurgitation/
food retention
L; significant
reduction in
both length and
weight
L; significant
reduction in
both length and
weight
L; no
significant
increase in
regurgitation/
food retention
-------
Summary of Biological Effects Tissue Concentrations for Cadmium
Species: Concentration, Units in1:
Taxa Sediment Water Tissue (Sample Type)
43.5 mg/kg
(whole body)5
3.75 mg/kg
(whole body)5
145 mg/kg
(whole body)5
1.62 mg/kg
(whole body)5
43.5 mg/kg
(whole body)5
Toxicity:
Effects
Growth,
NOED
Growth,
NOED
Growth,
NOED
Growth,
NOED
Mortality,
NOED
Ability to Accumulate2 Source:
Log Log
BCF BAF BSAF Reference Comments3
[50] L; no
significant
reduction in
length or
weight at
highest test
concentration
[50] L; no
significant
reduction in
length or
weight
[50] L; no
significant
reduction in
length or
weight at
highest test
concentration
[50] L; no
significant
reduction in
length or
weight
[50] L; no
significant
increase in
mortality at
highest test
concentration
-------
Summary of Biological Effects Tissue Concentrations for Cadmium
Species:
Taxa
Concentration, Units in1:
Sediment Water Tissue (Sample Type)
145 mg/kg
(whole body)5
Toxicity:
Effects
Mortality,
NOED
Ability to Accumulate2
Log Log
BCF BAF BSAF
Source:
Reference Comments3
[50] L; no
significant
increase in
mortality at
highest test
concentration
4.13 mg/kg
(whole body)5
Mortality,
NOED
[50]
L; no
significant
increase in
mortality at
highest test
concentration
Concentration units based on wet weight unless otherwise noted.
BCF = bioconcentration factor, BAF = bioaccumulation factor, BSAF = biota-sediment accumulation factor.
L = laboratory study, spiked sediment, single chemical; F = field study, multiple chemical exposure; other unusual study conditions or observations noted.
ND = not detected.
This entry was excerpted directly from the Environmental Residue-Effects Database (ERED, www.wes.army.mil/el/ered, U.S. Army Corps of Engineers and U.S.
Environmental Protection Agency). The original publication was not reviewed, and the reader is strongly urged to consult the publication to confirm the information
presented here.
-------
BIOACCUMULATION SUMMARY CADMIUM
References
I. Merck index, 10th ed., 1983, p. 223. (Cited in: USEPA. 1995. Hazardous Substances Data Bank
(HSDB). National Library of Medicine online (TOXNET). U.S. Environmental Protection Agency,
Office of Health and Environmental Assessment, Environmental Criteria and Assessment Office,
Cincinnati, OH. September.)
2. USEPA. 1995. Integrated Risk Information System (IRIS). National Library of Medicine online
(TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental
Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. September.
3. Stephenson, M., and G.L. Mackie. 1989. A laboratory study of the effects of waterborne cadmium,
calcium, and carbonate concentrations on cadmium concentrations in Hyalella azteca (Crustacea:
Amphipoda). Aquat. Toxicol 15:53-62.
4. Kay, S.H. 1985. Cadmium in aquatic food webs. Residue Rev. 96:13-43.
5. Timmermans, K.R., B.VanHattum, M.H.S. Kraak, and C. Davids. 1989. Trace metals in a littoral
foodweb: Concentrations in organisms, sediment and water. Set Total Environ. 87/88:477-494.
6. Wren, C.D., and G.L. Stephenson. 1991. The effect of acidification on the accumulation and
toxicity of metals to freshwater invertebrates. Environ. Pollut. 71:205-241.
7. Timmermans, K.R., E. Spijkerman, and M. Tonkes. 1992. Cadmium and zinc uptake by two
species of aquatic invertebrate predators from dietary and aqueous sources. Can. J. Fish. Aquat. Sci.
49:655-662.
8. Klerks, P.L., and P.R. Bartholomew. 1991. Cadmium accumulation and detoxification in a Cd-
resistant population of the oligochaete Limnodrilus hoffmeisteri. Aquat. Toxicol. 19:97-112.
9. McKinney, J. 1993. Metals bioavailability and disposition kinetics research needs workshop. July
18-19, 1990. Toxicol. Environ. Chem. 38:1-71.
10. Schmitt, C.J., and S.E. Finger. 1987. The effects of sample preparation on measured concentrations
of eight elements in edible tissues of fish from streams contaminated by lead mining. Arch. Environ.
Contain. Toxicol. 16:185-207.
11. Wiener, J.G., and P.M. Stokes. 1990. Enhanced bioaccumulation of mercury, cadmium and lead
in low-alkalinity waters: An emerging regional environmental problem. Environ. Toxicol. Chem.
9(7):821-823.
12. Mirenda, RJ. 1986. Toxicity and accumulation of cadmium in the crayfish, Orconectes virilis
(Hagen). Arch. Environ. Contain. Toxicol. 15:401-407.
13. Thorp, J.H., J.P. Giesy, and S.A. Wineriter. 1979. Effects of chronic cadmium exposure on crayfish
survival, growth, and tolerance to elevated temperatures. Arch. Environ. Contain. Toxicol. 8:449-
456.
158
-------
BIOACCUMULATION SUMMARY CADMIUM
14. Vernberg, W.B., PJ. DeCoursey, M. Kelly, and D.M. Johns. 1977. Effects of sublethal
concentrations of cadmium on adult Palaemonetes pugio under static and flow-through conditions.
Bull. Environ. Contain. Toxicol. 17:16-23.
15. Ahsanullah, M., D.S. Negilski, and M.C. Mobley. 1981. Toxicity of zinc, cadmium and copper
to the shrimp Callianassa australiensis. HI. Accumulation of metals. Mar. Biol. 64:311-316.
16. Sundelin, B. 1983. Effect of cadmium on Pontoporeia affinis (Crustacea:Amphipoda) in the
laboratory soft-bottom microcosms. Mar. Biol. 74:203-212.
17. Borgmann, U., W.P. Norwood, and I.M. Babirad. 1991. Relationship between chronic toxicity and
bioaccumulation of cadmium in Hyalella azteca. Can. J. Fish. Aquat. Sci. 48:1055-1060.
18. Abel, T., and F. Barlocher. 1988. Uptake of cadmium by Gammarus fossarum (Amphipoda) from
food and water. /. Appl. Ecol 25:223-231.
19. Kraak, M.H.S., D. Lavy, W.H.M. Peelers, and C. Davids. 1992. Chronic ecotoxicity of copper and
cadmium to the zebra mussel Dreissenapolymorpha. Arch. Environ. Contam. Toxicol. 23:363-369.
20. USAGE. 1987. Use of Daphnia magna to predict consequences of bioaccumulation.
Environmental Effects of Dredging-Technical Notes, EEDP-01-7. U.S. Army Corps of Engineers,
Waterways Experiment Station, Vicksburg, MS.
21. Enserink, E.L., J.L. Maas-Diepeveen, and CJ. Van Leeuwen. 1991. Combined effects of metals:
An ecotoxicological evaluation. Water Res. 25(6):679-687.
22. Hopkin, S.P. 1990. Species-specific differences in the net assimilation of zinc, cadmium, lead,
copper and iron by the terrestrial isopods Oniscus asellus and Porcellio scaber. J. Appl. Ecol.
27:460-474.
23. Crommentuijn, T., C.J.A.M. Doodeman, A. Doornekamp, J.J.C. van der Pol, J.J.M. Bedaux, and
C.A.M. van Gestel. 1994. Lethal body concentrations and accumulation patterns determine time-
dependent toxicity of cadmium in soil arthropods. Environ. Toxicol. Chem. 13:1781-1789.
24. Cain, D.J., S.N. Luoma, J.L. Carter, and S.V. Fend. 1992. Aquatic insects as bioindicators of trace
element contamination in cobble-bottom rivers and streams. Can. J. Fish. Aquat. Sci. 49:2141-2154.
25. Benoit, D.A., E.N. Leonard, G.M. Christensen, and J.T. Fiandt. 1976. Toxic effects of cadmium
on three generations of brook trout (Salvelinusfontinalis). Trans. Amer. Fish. Soc. 105:550-560.
26. Rule J.H., and R.W. Alden III. 1996. Interactions of Cd and Cu in anaerobic estuarine sediments.
II. Bioavailability, body burdens and respiration effects as related to geochemical partitioning.
Environ. Toxicol. Chem. 15:466-471.
27. Houkal, D., B. Rummel, and B. Shephard. 1996. Results of an in situ mussel bioassay in the Puget
Sound. Abstract, 17th Annual Meeting, Society of Environmental Toxicology and Chemistry,
Washington, DC, November 17-21, 1996.
159
-------
o BIOACCUMULATION SUMMARY CADMIUM
28. Meador, J.P. 1993. The effect of laboratory holding on the toxicity response of marine infaunal
amphipods to cadium and tributyltin. /. Exp. Mar. Biol. Ecol. 174:227-242.
29. Beattie, J.H., and D. Pascoe. 1978. Cadmium uptake by rainbow trout, Salmo gairdneri eggs and
alevins. /. Fish. Biol. 13:631-637.
30. Bonham, K., M. Zararullah, and L. Gedamu. 1987. The rainbow trout metailothioneins: Molecular
cloning and characterization of two distinct cDNA sequences. DNA 6:519-528.
31. Cain, J.R., D.C. Paschal, and C.M. Hayden. 1980. Toxicity and bioaccumulation of cadmium in the
colonial green alga Scenedesmus obliquus. Arch. Environ. Contam. Toxicol. 9:9-16.
32. Carlson, A.R., G.L. Phipps, V.R. Mattson, P.A. Kosian, and A.M. Cotter. 1991. The role of acid-
volatile sulfide in determining cadmium bioavailability and toxicity in freshwater sediments.
Environ. Toxicol. Chem. 10:1309-1319.
33. Carr, R.S., and J.M. Neff. 1982. Biochemical indices of stress in the sandworm Neanthes virens
(Sars). II. Sublethal responses to cadmium. Aquat. Toxicol. 2:319-333.
34. Carr, R.S., J.W. Williams, F.I. Saksa, R.L. Buhl, and J.M. Neff. 1985. Bioenergetic alterations
correlated with growth, fecundity and body burden of cadmium for mysids (Mysidopsis bahia).
Environ. Toxicol. Chem. 4:181-188.
35. Cearley, J.E., and R.L. Coleman. 1973. Cadmium toxicity and accumulation in southern naiad. Bull.
Environ. Contam. Toxicol. 9:100-101.
36. Chan, K.M., W.S. Davidson, C.L. Hew, and G.L. Fletcher. 1989. Molecular cloning of
metallothionein cDNA and analysis of metailothionein gene expression in winter flounder tissues.
Can. J. Zool. 67:2520-2527.
37. Den Besten, P.J., HJ. Herwig, D.I. Zandee, and P.A. Voogt. 1989. Effects of cadmium and PCBs
on reproduction of the sea star Asterias rubens: Aberrations in the early development. Exotox.
Environ. Saf. 18:173-180.
38. Dressing, S.A., R.P. Maas, and C.M. Weiss. 1982. Effects of chemical speciation on the
accumulation of cadmium by the caddisfly, Hydropsyche sp. Bull. Environ. Contam. Toxicol.
28:172-180.
39. Gillespie, R., T. Reisine, and E.J. Massaro. 1977. Cadmium uptake by the crayfish, Orconectes
propinquus propinquus (Girard). Environ. Res. 13:364-368.
40. Hamilton, S.J., Mehrle, P.M., and J.R. Jones. 1987. Cadmium-saturation technique for measuring
metallothionein in brook trout. Trans. Am. Fish. Soc. 116(4):541-550.
41. Handy, R.D. 1992. The assessment of episodic metal pollution. I. Uses and limitations of tissue
contaminant analysis in rainbow trout (Oncorhynchus mykiss) after short waterborne exposure to
cadmium or copper. Arch. Environ. Contam. Toxicol. 22:74-81.
160
-------
BIOACCUMULATION SUMMARY CADMIUM
42. Hatakeyama, S., and M. Yasuno. 1981. The effects of cadmium-accumulated Chlorella on the
reproduction of Moina macrocopa (Cladocera). Ecotoxicol Environ. Saf. 5:341-350.
43. Hatakeyama, S., and M. Yasuno. 1982. Accumulation and effects of cadmium on guppy (Poecilia
reticulatd) fed cadmium-dosed cladocera (Moina macrocopa). Bull. Environ. Contain. Toxicol.
29:159-166.
44. Heinis, F., Timmermans, K.R., and W.R. Swain. 1990. Short-term sublethal effects of cadmium on
the filter feeding chironomid larvae Glyptotendipes pattens (Meigen) (Diptera). Aquat. Toxicol.
16:73-86.
45. Janssens De Bisthoven, L.G., K.R. Timmermans, and F. Ollevier. 1992. The concentration of
cadmium, lead, copper, and zinc in Chironomus gr. thummi larvae (Diptera, Chironomidae) with
deformed versus normal antennae. Hydrobiologia 239:141-149
46. Jenkins, K.D., and A.Z. Mason. 1988. Relationships between subcellular distributions of cadmium
and perturbations in reproduction in the polychaete Neanthes arenaceodentata. Aquat. Toxicol.
12:229-244.
47. Kay, S.H., W.T. Haller, and L.A. Garrard. 1984. Effects of heavy metals on water hyacinths
(Eichhornia crassipes (mart.) Solms). Aquat. Toxicol. 5:117-128.
48. Marshall, J.S. 1978. Population dynamics of daphnia Galeata mendotae as modified by chronic
cadmium stress. /. Fish. Res. Bd. Can. 35:461-469.
49. Meteyer, M.J., D.A. Wright, and F.D. Martin. 1988. Effect of cadmium on early developmental
stages of the sheepshead minnow (Cyprinodon variegatus). Environ. Toxicol. Chem. 7:321-328.
50. Nebeker, A.V., et al. 1995. Effects of cadmium on growth and bioaccumulation in the northwestern
salamander, Ambystoma gracile. Arch. Environ. Contam. Toxicol. 29:492-503.
51. Pascoe, D., S.A. Evans, and J. Woodworth. 1986. Heavy metal toxicity to fish and the influence of
water hardness. Arch. Environ. Contam. Toxicol. 15:481-487.
52. Peterson, R.H., J.L. Metcalfe, and S. Ray. 1983. Effects of cadmium on yolk utilization, growth, and
survival of Atlantic salmon alevins and newly feeding fry. Arch. Environ. Contam. Toxicol. 12:37-
44.
53. Poulsen, E., H.U. Riisgard, and F. Mohlenberg. 1982. Accumulation of cadmium and bioenergetics
in the mussel Mytilus edulis. Mar. Biol. 68:25-29.
54. Povlsen, A.F., B. Korsgaard, and P. Bjerregaard. 1990. The effect of cadmium on vitellogenin
metabolism in estradiol-induced flounder (Platichyhys flesus (L.)) males and females. Aquat.
Toxicol. 17:253-262.
55. Powell, M.I., and K.N. White. 1990. Heavy metal accumulation by barnacles and its implications
for their use as biological monitors. Mar. Environ. Res. 30:91-118.
161
-------
BIOACCUMULATION SUMMARY CADMIUM
56. Spehar, R.L., E.N. Leonard, and D.L. Defoe. 1978. Chronic effects of cadmium and zinc mixtures
on flagfish (Jordanellafloridae). Trans. Am. Fish. Soc. 107(2):354-360.
57. Spehar, R.L. 1976. Cadmium and zinc toxicity to flagfish, Jordanellafloridae. J. Fish. Res. Board
Can., Vol. 33.
58. Sundelin, B. 1983. Effects of cadmium on Pontoporeia affinis (Crustacea: amphipods) in laboratory
soft-bottom microcosms. Mar. Biol 74:203-212.
59. Sundelin, B. 1984. Single and combined effects of lead and cadmium on Pontoporeia affinis
(Crustacea, Amphipoda) in laboratory soft-bottom microcosms. In Ecotoxicological testing for the
marine environment, Vol. 2, ed. G. Persoone, E. Jaspers, and C. Claus. State University of Ghent
and Institute of Marine Scientific Research, Bredene, Belgium.
60. Velduizen-Tsoerkan, M.B., D.A. Holwerda, and D.I. Zandee. 1991. Anoxic survival time and
metabolic parameters as stress indices in sea mussels exposed to cadmium or polychlorinated
biphenyls. Arch. Environ. Contain. Toxicol. 20:259-265.
61. Vernberg, W.B., P.J. Decoursey, M. Kelly, and D.M. Johns. 1977. Effects of sublethal
concentrations of cadmium on adult Palaemonetes pugio under static and flow-through conditions.
Bull. Environ. Contamin. Toxicol. 17:16-24.
62. Zaroogian, G.E., and G. Morrison. 1981. Effect of cadmium body burdens in adult Crassostrea
virginica on fecundity and viability of larvae. Bull. Environ. Contain. Toxicol. 27:344-348.
162
-------
BIOACCUMULATION SUMMARY CHLORDANE
Chemical Category: PESTICIDE (ORGANOCHLORINE)
Chemical Name (Common Synonyms): CHLORDANE CASRN: 57-74-9
Chemical Characteristics
Solubility in Water: 0.1 mg/Lat 20 - 30°C [1] Half-Life: 283 days - 3.8 yrs based on
unacclimated aerobic river
die-away test and reported soil
grab sample data [2]
Log Kow: 6.32 [3] Log Koc: 6.21 L/kg organic carbon
Human Health
Oral RfD: 6 x 10~5 mg/kg/day [4] Confidence: Low, uncertainty factor = 1000
Critical Effect: Regional liver hypertrophy in female rats; hepatocellular carcinomas in mice
Oral Slope Factor: 1.3 x 10+0 per (mg/kg)/day [4] Carcinogenic Classification: B2 [4]
Wildlife
Partitioning Factors: Partitioning factors for chlordane in wildlife were not found in the literature.
Food Chain Multipliers: Food chain multipliers for chlordane in wildlife were not found in the
literature.
Aquatic Organisms
Partitioning Factors: The major components of technical chlordane include gamma chlordane (24
percent), alpha chlordane (19 percent), and /raws-nonachlor (7 percent). Alpha chlordane is
environmentally more stable and therefore more persistent than gamma chlordane. Oxychlordane is an
epoxide metabolite formed in mammalian liver. It is persistent and much more toxic than its parent
chemicals [5].
Food Chain Multipliers: In a marine ecosystem the chlordane compounds (nonachlor and
oxychlordane) increased significantly with trophic levels from zooplankton to marine mammals [6].
Although the results of the study reported by Kawano et al. [6] indicated a small difference in the
chlordane composition in zooplankton from the North Pacific, Bering Sea, and Antarctic, they also
revealed a significant difference in chlordane composition between Dall's porpoise and the Weddell seal.
TVans'-chlordane was present in the seal but not in the porpoise, and the percentage composition of
oxychlordane in the seal was larger than that in the porpoise. Furthermore, the compositional percentage
163
-------
BIOACCUMULATION SUMMARY CHLORDANE
of oxychlordane in the Adelie penguin and thick-billed murre was much higher than that in the other
organisms. Marine mammals and seabirds accumulated chlordane via food. Biomagnification of total
chlordanes through the food chain is strongly evident in marine mammals. Chlordanes are concentrated
gradually from zooplankton, through squid and fish, to porpoises and dolphins [7,8]. Chlordane residues
in marine mammals are positively correlated with lipid content and not with the age of the animal [9].
Food chain multipliers (FCMs) for cis- or /raws-chlordane for trophic level 3 aquatic organisms were 21.7
(all benthic food web), 1.6 (all pelagic food web), and 13.2 (benthic and pelagic food web). FCMs for
trophic level 4 aquatic organisms were 49.5 (all benthic food web), 3.5 (all pelagic food web), and 23.3
(benthic and pelagic food web) [26].
Toxicity/Bioaccumulation Assessment Profile
Chlordane adversely affected sensitive species of fish and aquatic invertebrates at concentrations of 0.2
to 2.0 ug/L. Specifically, survival of shrimp and crabs was reduced at water concentrations of 0.2 to 2.0
|ig/L, while survival of freshwater and marine fishes was reduced between 1.7 and 3.0 |ig/L. Generally,
the uptake of chlordane by aquatic organisms is high, ranging from 216.8 |ig organic carbon cleared per
gram organism per hour for Diporeia spp. to 358 ug organic carbon cleared per gram organism per hour
for Chironomus riparius [10]. Accumulation of chlordane by Diporeia spp., C. riparius, or Lumbriculus
variegatus from whole sediment exposures was greater than that from the elutriate or pore water. Neither
species was able to metabolize chlordane. A study by Wilcock et al. [11] has shown that the bivalve
Macomona liliana can accumulate chlordane bound to sediment at depths below 2 cm. Animals
constantly exposed to contaminated sediment accumulated more (5,728 ppb lipid) than those able to feed
alternatively on contaminated and uncontaminated sediments (3,617 and 2,756 ppb). An in situ study of
the uptake and elimination by adult intertidal benthic infauna of chlordane from contaminated sediment
has shown large differences in accumulation between deposit- and suspension-feeding species [12]. In
the case of surface feeders, these differences can be attributed to direct exposure to high initial
concentration of chlordane in surficial sediments. The extract from the chlordane residues obtained from
Lake Michigan lake trout was significantly more toxic (3 to 5 times) than the chlordane used in
agricultural applications. Gooch et al. [13] suggested that the increased toxicity of these extracts was due
to the presence of the stable metabolite heptachlor epoxide and oxychlordane. Chlordane is persistent
in the environment; measurable residues in sediment were found 2.8 years after application to the
overlying water column [5]. More than 80 percent of the fish sampled from the Kansas River had
detectable chlordanes in their tissue [14]. Residues of c^-chlordane and /raws-chlordane were the most
abundant and persistent of the chlordane components measured in fish tissues in a U.S. study conducted
aproximately 10 years after the termination of the agricultural use of chlordanes [15]. In birds, technical
chlordane and its metabolite oxychlordane are frequently elevated in tissues with high lipid content. In
northern gannets, the half-time persistence of a's-chlordane, c^-nonachlor, and oxychlordane was
estimated at 11, 199, and 35 years [16].
164
-------
Summary of Biological Effects Tissue Concentrations for Chlordane
Species: Concentration, Units in1:
Taxa Sediment Water
Invertebrates
Liimbriculiis 125 ng/g
variegatus,
Oligochaete worm
1,406 ng/g
DDL4
Crassostrea virginica,
Eastern oyster
Tissue (Sample Type)
28, 197 ng/g
23,031 ng/g3
0.03 n/kg
0.02 mg/kg
(whole body)5
2.2 mg/kg
(whole body)
0.3 mg/kg
(whole body)5
0.075 mg/kg
(whole body)
0.6 mg/kg
(whole body)5
0.78 mg/kg
(whole body)
6.5 mg/kg
(whole body)5
Toxicity:
Effects
Growth,
ED18
Growth,
ED28
Growth,
ED28
Growth,
ED30
Growth,
ED30
Growth,
ED33
Growth,
ED33
Ability to Accumulate2: Source:
Log Log
BCF BAF BSAF Reference
[10]
[17]
[22]
[22]
[22]
[22]
[22]
[22]
Comments3
F
F
L; exposure media
65% heptachlor
(technical grade)
L; exposure media
65% heptachlor
(technical grade)
L; exposure media
65% heptachlor
(technical grade)
L; exposure media
65% heptachlor
(technical grade)
L; exposure media
65% heptachlor
(technical grade)
L; exposure media
65% heptachlor
(technical grade)
L; exposure media
65% heptachlor
(technical grade)
-------
ON
ON
Summary of Biological Effects Tissue Concentrations for Chlordane
Species: Concentration, Units in1:
Taxa Sediment Water
Crassostrea virginica,
Eastern oyster
Tissue (Sample Type)
1.9 mg/kg
(whole body)5
14 mg/kg
(whole body)
5.6 mg/kg
(whole body)5
47 mg/kg
(whole body)
0.022 mg/kg
(whole body)5
27 mg/kg
(whole body)5
1 1 mg/kg
(whole body)
Toxicity:
Effects
Growth,
ED78
Growth,
ED78
Growth,
ED95
Growth,
ED95
Growth,
NOED
Growth,
LOED
Growth,
NOED
Ability to Accumulate2: Source:
Log Log
BCF BAF BSAF Reference
[22]
[22]
[22]
[22]
[22]
[23]
[23]
Comments3
L; exposure media
65% heptachlor
(technical grade)
L; exposure media
65% heptachlor
(technical grade)
L; exposure media
65% heptachlor
(technical grade)
L; exposure media
65% heptachlor
(technical grade)
L; exposure media
65% heptachlor
(technical grade)
L; estimated LOED -
no statistical
summary in text
L; estimated NOED -
no statistical
summary in text
Corbicula fluminea,
Asian clam
21.7|ig/kg
OC
2,400 |ig/kg lipid
L04 [21] F; frans-chlordane;
%lipid not reported;
%sed OC = 2.30
-------
Summary of Biological Effects Tissue Concentrations for Chlordane
Species:
Taxa
Concentration, Units in1:
Sediment Water
Toxicity:
Tissue (Sample Type) Effects
Ability to Accumulate2:
Source:
Log
BCF
Log
BAF
BSAF Reference Comments3
Gonatopsis borealis,
Eight-armed squid
czs-chlordane:
15(11-18)
fraws-chlordane:
8.1 (6.3-9.9)
czs-nonachlor:
2.4 (2.2-2.8) |ig/kg
fraws-nonachlor:
18 (14-20) |ig/kg
oxychlordane:
1.2 (0.8-1.60) n-g/kg
total chlordanes:
44 (35-52) |ig/kg
[5]
F; lipid samples
Diporeia sp.,
Amphipod
493 ng/g
430 ng/g
23,729 ng/g
40,086 ng/g
[10]
Euphasia siiperba,
Krill
czs-chlordane:
0.58 ng/kg
fraws-chlordane:
0.51 ng/kg
cw-nonachlor:
0.22 ng/kg
fran^-nonachlor:
0.8 ng/kg
oxychlordane:
0.1 |ig/kg
[6]
Palaemonetes pugio,
Grass shrimp
4.5 mg/kg
(whole body)
Mortality,
LOED
[23] L; estimated LOED •
no statistical
summary in text
ON
-J
-------
ON
oo
Summary of Biological Effects Tissue Concentrations for Chlordane
Species:
Taxa
Penaeiis diioramm,
Pink shrimp
Concentration, Units in1:
Sediment Water Tissue (Sample Type)
4.8 mg/kg
(whole body)
1.7 mg/kg
(whole body)
0.71 mg/kg
(whole body)5
Toxicity:
Effects
Mortality,
NOED
Mortality,
LOED
Mortality,
NOED
Ability to Accumulate2: Source:
Log Log
BCF BAF BSAF Reference
[23]
[23]
[23]
Comments3
L; estimated NOED -
no statistical
summary in text
L; estimated LOED -
no statistical
summary in text
L; estimated NOED -
no statistical
summary in text
Homarus americanus,
American lobster
cw-chlordane:
80-100 |ig/kg,
hepatopancreas
frans-chlordane:
80-100 |ig/kg,
hepatopancreas
cw-nonachlor:
30 ng/kg,
hepatopancreas
frans-nonachlor:
(380-440) |ig/kg,
hepatopancreas
[5]
Chironomus ripariiis,
Midge
1,663 ng/g
1,741 ng/g
16,224 ng/g
8,417 ng/g
[10]
-------
Summary of Biological Effects Tissue Concentrations for Chlordane
Species:
Taxa
Fishes
Oncorhynchus, Salmo,
Salvelinus sp.,
Salmonids
Salmonids
Osmerus mordax,
Smelt; Oncorhynchus
velinus, Coho salmon
Cypriniis carpio, Carp
Cypriniis carpio, Carp
Concentration, Units in1: Toxicity:
Sediment Water Tissue (Sample Type) Effects
0.000034 19 ng/kg
Hg/L
77.8 ng/kg 172.7 |ig/kg lipid
OC
2.1ng/g 34pg/L 3.6ng/g
19 ng/g
2.5 ng/g 18 ng/g
437.5 ng/kg 217.9 |ig/kg lipid
OC
145.3 |ig/kg 1 10.7 |ig/kg lipid
OC
112.1 |ig/kg 161.3 |ig/kg lipid
OC
Ability to Accumulate2: Source:
Log Log
BCF BAF BSAF Reference
5.75 [20]
2.22 [20]
2.00 [25]
4.77 [25]
[18,20]
46.3 [18,19]
33.4
0.498 [24]
0.762 [24]
1.439 [24]
Comments3
F; frans-chlordane,
% lipid = 1 1
F; frans-chlordane;
%lipid= ll;%sed
OC = 2.70
F; frans-chlordane
F; cw-chlordane
F; median BSAFs
calculated in [18]
from field data in
[20]
F; median BSAFs
calculated in [18]
from field data in
[19]
F; frans-chlordane;
%lipid = 7.8; %sed
OC = 0.80
F; frans-chlordane;
%lipid = 8.4; %sed
OC= 1.79
F; frans-chlordane;
%lipid = 9.3; %sed
OC=1.16
-------
-J
o
Summary of Biological Effects Tissue Concentrations for Chlordane
Species:
Taxa
Cyprinus carpio, Carp
Catastomus
commersoni,
White sucker
Catastomus
commersoni,
White sucker
Concentration, Units in1:
Sediment Water
212.5 ng/kg
OC
128.5 |ig/kg
OC
86.21 ng/kg
OC
437.5 ng/kg
OC
145.3 |ig/kg
OC
112.1 jig/kg
OC
212.5 ng/kg
OC
128.5 |ig/kg
OC
86.21 ng/kg
OC
Toxicity:
Tissue (Sample Type) Effects
294.9 |ig/kg lipid
1 90.5 |ig/kg lipid
258.1 |ig/kg lipid
132.5|ig/kglipid
1 89.9 |ig/kg lipid
266.7 |ig/kg lipid
1 92.8 |ig/kg lipid
519 |ig/kg lipid
533.3 |ig/kg lipid
Ability to Accumulate2: Source:
Log Log
BCF BAF BSAF Reference
1.3878 [24]
1.4825 [24]
2.9939 [24]
0.301 [24]
1.307 [24]
2.379 [24]
0.9073 [24]
4.0389 [24]
6.1861 [24]
Comments3
F; cw-chlordane;
%lipid = 7.8; %sed
OC = 0.80
F; cw-chlordane;
%lipid = 8.4; %sed
OC=1.79
F; cw-chlordane;
%lipid = 9.3; %sed
OC= 1.16
F; frans-chlordane;
%lipid = 8.3; %sed
OC = 0.8
F; frans-chlordane;
%lipid = 7.9; %sed
OC=1.79
F; fran^-chlordane;
%lipid = 4.5; %sed
OC= 1.16
F; cw-chlordane;
%lipid = 8.3; %sed
OC = 0.8
F; cw-chlordane;
%lipid = 7.9; %sed
OC=1.79
F; cw-chlordane;
%lipid = 4.5; %sed
OC= 1.16
-------
Summary of Biological Effects Tissue Concentrations for Chlordane
Species: Concentration, Units in1:
Taxa Sediment Water
Cyprinodon variegatus,
Sheepshead minnow
Tissue (Sample Type)
909 mg/kg
(whole body)
1.2 mg/kg
(whole body)5
0.019 mg/kg
(whole body)
0.01 mg/kg
(whole body)5
17.5 mg/kg
(whole body)
2 mg/kg
(whole body)5
3.9 mg/kg
(whole body •*
32 mg/kg
(whole body)5
47 mg/kg
(whole body)
6.1 mg/kg
(whole body)5
Toxicity:
Effects
Mortality,
ED35
Mortality,
ED35
Mortality,
EDS
Mortality,
ED5
Mortality,
ED50
Mortality,
ED50
Mortality,
ED60
Mortality,
ED60
Mortality,
ED85
Mortality,
ED85
Ability to Accumulate2: Source:
Log Log
BCF BAF BSAF Reference
[22]
[22]
[22]
[22]
[22]
[22]
[22]
[22]
[22]
[22]
Comments3
L; exposure media
65% heptachlor
(technical grade)
L; exposure media
65% heptachlor
(technical grade)
L; exposure media
65% heptachlor
(technical grade)
L; exposure media
65% heptachlor
(technical grade)
L; exposure media
65% heptachlor
(technical grade)
L; exposure media
65% heptachlor
(technical grade)
L; exposure media
65% heptachlor
(technical grade)
L; exposure media
65% heptachlor
(technical grade)
L; exposure media
65% heptachlor
(technical grade)
L; exposure media
65% heptachlor
(technical grade)
-------
Summary of Biological Effects Tissue Concentrations for Chlordane
Species: Concentration, Units in1:
Taxa Sediment Water Tissue (Sample Type)
Cyprinodon variegatus, 28 1 mg/kg
Sheepshead minnow (whole body)
3. 18 mg/kg
(whole body)5
3. 18 mg/kg
(whole body)5
0.6 mg/kg
(whole body)
87 mg/kg
(whole body)5
1.38 mg/kg
(whole body)
1.38 mg/kg
(whole body)
Lagodon rhomboides, 16. 6 mg/kg
Pinfish (whole body)
Leiostomus mnthurus, 0.16 mg/kg
Spot (whole body)
Toxicity: Ability to Accumulate2:
Log Log
Effects BCF BAF BSAF
Mortality,
LOED
Mortality,
LOED
Reproduction,
LOED
Mortality,
NOED
Mortality,
NOED
Mortality,
NOED
Reproduction,
NOED
Mortality,
LOED
Mortality,
ED25
Source:
Reference
[23]
[23]
[23]
[23]
[23]
[23]
[23]
[23]
[22]
Comments3
L; estimated LOED -
no statistical
summary in text
L
L; hatching success
of fry from exposed
parents
L; estimated NOED -
no statistical
summary in text
L; estimated NOED -
no statistical
summary in text
L
L; hatching success
of fry from exposed
parents
L; estimated LOED -
no statistical
summary in text
L; exposure media
65% heptachlor
(technical grade)
-------
Summary of Biological Effects Tissue Concentrations for Chlordane
Species: Concentration, Units in1:
Taxa Sediment Water Tissue (Sample Type)
0.55 mg/kg
(whole body)5
0.89 mg/kg
(whole body)
0.22 mg/kg
(whole body)5
3.3 mg/kg
(whole body)
0.94 mg/kg
(whole body)5
1.6 mg/kg
(whole body)
7.1 mg/kg
(whole body)5
0.7 mg/kg
(whole body)
3.5 mg/kg
(whole body)5
0.01 mg/kg
(whole body)
Toxicity:
Effects
Mortality,
ED25
Mortality,
ED35
Mortality,
ED35
Mortality,
ED40
Mortality,
ED40
Mortality,
ED70
Mortality,
ED70
Mortality,
ED85
Mortality,
ED85
Mortality,
NOED
Ability to Accumulate2: Source:
Log Log
BCF BAF BSAF Reference
[22]
[22]
[22]
[22]
[22]
[22]
[22]
[22]
[22]
[22]
Comments3
L; exposure media
65% heptachlor
(technical grade)
L; exposure media
65% heptachlor
(technical grade)
L; exposure media
65% heptachlor
(technical grade)
L; exposure media
65% heptachlor
(technical grade)
L; exposure media
65% heptachlor
(technical grade)
L; exposure media
65% heptachlor
(technical grade)
L; exposure media
65% heptachlor
(technical grade)
L; exposure media
65% heptachlor
(technical grade)
L; exposure media
65% heptachlor
(technical grade)
L; exposure media
65% heptachlor
(technical grade)
-------
Summary of Biological Effects Tissue Concentrations for Chlordane
Species:
Taxa
Cottiis cognatus,
Slimy sculpin
Concentration, Units in1:
Sediment Water Tissue (Sample Type)
0.01 mg/kg
(whole body)
0.01 mg/kg
(whole body)5
0.01 mg/kg
(whole body)
2.1 ng/g 34 g/L 30 ng/kg
77.8 |ig/kg 375 |ig/kg lipid
OC
Toxicity:
Effects
Mortality,
NOED
Mortality,
NOED
Mortality,
NOED
Ability to Accumulate2: Source:
Log Log
BCF BAF BSAF Reference
[22]
[22]
[22]
5.95 2.47 [18,20]
4.821 [20]
Comments3
L; exposure media
65% heptachlor
(technical grade)
L; exposure media
65% heptachlor
(technical grade)
L; exposure media
65% heptachlor
(technical grade)
F; frans-chlordane,
% lipid = 8
F; frans-chlordane;
%lipid = 8; %sed OC
= 2.70
Pimelodus albicans, 3.4 ng/g 0.8 ng/L 2.9 |ig/g
Oligosarcusjenynsi,
Prochilodus platensis
20 [18,21] F; median BSAFs
calculated in [18]
from field data in
[21]
Prochilodus platensis, 20 |ig/kg
Curimata OC
Pimelodus albicans, 20 |ig/kg
Mandi OC
4,600 |ig/kg lipid
1,000 |ig/kg lipid
230 [21] F; frans-chlordane;
%lipid not reported;
%sed OC = 1
50 [21] F; frans-chlordane;
%lipid not reported;
%sed OC = 1
-------
Summary of Biological Effects Tissue Concentrations for Chlordane
Species:
Taxa
Concentration, Units in1:
Toxicity:
Ability to Accumulate2:
Log Log
Sediment Water Tissue (Sample Type) Effects BCF BAF BSAF
Source:
Reference Comments
Wildlife
Ducks
0.83 [18,19] F; median BSAFs
19.5 calculated in [18]
from field data in
[19]
Concentration units based on wet weight unless otherwise noted.
BCF = bioconcentration factor, BAF = bioaccumulation factor, BSAF = biota-sediment accumulation factor.
L = laboratory study, spiked sediment, single chemical; F = field study, multiple chemical exposure; other unusual study conditions or observations noted.
BDL = Below detection limit.
This entry was excerpted directly from the Environmental Residue-Effects Database (ERED, www.wes.army.mil/el/ered, U.S. Army Corps of Engineers and U.S.
Environmental Protection Agency). The original publication was not reviewed, and the reader is strongly urged to consult the publication to confirm the information
presented here.
-------
BIOACCUMULATION SUMMARY CHLORDANE
References
1. Merck index, 11th ed., 1989, p. 321. (Cited in: USEPA. 1995. Hazardous Substances Data Bank
(HSDB). National Library of Medicine online (TOXNET). U.S. Environmental Protection Agency,
Office of Health and Environmental Assessment, Environmental Criteria and Assessment Office,
Cincinnati, OH. September.)
2. USEPA. 1989. Chemical fate rate constants for SARA section 313 chemicals and Superfund Health
Manual chemicals. Prepared by Chemical Hazard Assessment Division, Syracuse Research
Corporation, for U.S. Environmental Protection Agency, Office of Toxic Substances, Exposure
Evaluation Division, Washington, DC, and Environmental Criteria and Assessment Office,
Cincinnati, OH. August 11.
3. Karickhoff, S.W., and J.M. Long. 1995. Internal report on summary of measured, calculated, and
recommended log Kow values. Draft. Prepared by U.S. Environmental Protection Agency, Office
of Research and Development, Environmental Research Laboratory-Athens, for E. Southerland,
Office of Water, Office of Science and Technology, Standards and Applied Science Division,
Washington, DC. April 10.
4. USEPA. 1997. Integrated Risk Information System (IRIS). National Library of Medicine online
(TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental
Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. January.
5. Fish and Wildlife Service. 1990. Chlordane hazards to fish, wildlife, and invertebrates: A synoptic
review. Biological Report 85(1.21).
6. Kawano, M., T. Inoue, T. Wada, H. Hidaka, and R. Tatsukawa. 1988. Bioconcentration and
residue patterns of chlordane compounds in marine animals: Invertebrates, fish, mammals and
seabirds. Environ. Sci. Technol. 22:792-797.
7. Kawano, M., S. Matsushita, T. Inoue, H. Tanaka, and R. Tatsukawa. 1986. Biological
accumulation of chlordane compounds in marine organisms from the northern North Pacific and
Bering Sea. Mar. Pollut. Bull. 17:512-516.
8. Muir, D.C.G., C.A. Ford, R.E.A. Stewart, T.G. Smith, R.F. Addison, M.E. Zinck, and P. Beland.
1990. Organochlorine contaminants in belugas, Delphinapterus leucas from Canadian waters. Can.
Bull. Fish. Aquat. Sci. 224:165-190.
9. Perttila, M., O. Stenman, H. Pyysalo, and K. Wickstrom. 1986. Heavy metals and organochlorine
compounds in seals in the Gulf of Finland. Mar. Environ. Res. 18:43-59.
10. Harkey, G.A., P.P. Landrum, and SJ. Klaine. 1994. Comparison of whole-sediment, elutriate, and
pore-water exposures for use in assessing sediment-associated organic contaminants in bioassays.
Environ. Toxicol. Chem. 13:1315-1329.
176
-------
BIOACCUMULATION SUMMARY CHLORDANE
11. Wilcock, R.J., R.D. Pridmore, G.L. Northcott, J.E. Hewitt, S.F. Thrush, and V.J. Cummings. 1994.
Uptake of chlordane by a deposit-feeding bivalve: Does the depth of sediment contamination make
a difference. Environ. Toxicol Chem. 13:1535-1541.
12. Wilcock, R.J., TJ. Smith, R.D. Pridmore, S.F. Thrush, V.J. Cummings, and J.E. Hewitt. 1993.
Bio accumulation and elimination of chlordane by selected intertidal benthic fauna. Environ.
Toxicol. Chem. 12:733-742.
13. Gooch, J.W., F. Matsumura, and MJ. Zabik. 1990. Chlordane residues in Great Lakes lake trout:
Acute toxicity and interaction at the gaba receptor of rat and lake trout brain. Chemosphere 21:393-
406.
14. Arruda, J.A., M.S. Cringan, D. Gilliland, S.G. Haslouer, J.E. Fry, R. Broxterman, and K.L.
Brunson. 1987. Correspondence between urban areas and the concentrations of chlordane in fish
from the Kansas River. Bull. Environ. Contam. Toxicol. 39:563-570.
15. Schmitt, C.J., L. Zajicek, and P.H. Peterman. 1990. National Contaminant Biomonitoring
Program: Residues of organochlorine chemicals in U.S. freshwater fish, 1976-1984. Arch. Environ.
Contam. Toxicol 19:748-781.
16. Elliott, J.E., R.J. Norstrom, and J.A. Keith. 1988. Organochlorines and eggshell thinning in
northern gannets (Sula bassanus) from eastern Canada, 1968-1984. Environ. Pollut. 52:81-102.
17. Boer, J.D., and P. Wester. 1991. Chlorobiphenyls and organochlorine pesticides in various
subantarctic organisms. Mar. Pollut. Bull. 22:441-447.
18. Parkerton, T.F., J.P. Connolly, R.V. Thomann, and C.G. Uchrin. 1993. Do aquatic effects or
human health end points govern the development of sediment-quality criteria for nonionic organic
chemicals? Environ. Toxicol. Chem. 12:507-523.
19. Smith, V.E., J.M. Spurr, J.C. Filkins, and J.J. Jones. 1985. Organochlorine contaminants of
wintering ducks foraging on Detroit River sediments. /. Great Lakes Res. 11:231-246.
20. Oliver, E.G., and A.J. Niimi. 1988. Trophodynamic analysis of polychlorinated biphenyl
congeners and other chlorinated hydrocarbons in the Lake Ontario ecosystem. Environ. Sci.
Technol 22:388-397.
21. Columbo, J.C., M.F. Khahl, M. Arnac, and A.C. Horth. 1990. Distribution of chlorinated
pesticides and individual polychlorinated biphenyls in biotic and abiotic compartments of the Rio
de la Plata, Argentina. Environ. Sci. Technol. 24:498-505.
22. Schimmel, S.C., J.M. Patrick, and J. Forester. 1976. Heptachlor: Toxicity to and uptake by several
estuarine organisms. /. Toxicol Environ. Health 1:955-965.
23. Parrish, P.R., S.C. Schimmel, D.J. Hansen, J.M. Patrick, and J. Forester. 1976. Chlordane: Effects
on several estuarine organisms. Toxicol Environ. Health 1:485-494.
177
-------
BIOACCUMULATION SUMMARY CHLORDANE
24. Tate, C.M., and J.S. Heiny. 1996. Organochlorine compounds in bed sediment and fish tissue in
the South Platte River basin, USA, 1992-1993. Arch. Environ. Contain. Toxicol 30:62-78.
25. USEPA. 1995. Great Lakes Water Quality Initiative Technical Support Document for the
procedure to determine bio accumulation factors. EPA-820-B-95-005. U.S. Environmental
Protection Agency, Office of Water, Washington, DC.
26. USEPA. 1998. Ambient water quality criteria derivation methodology: Human health. Technical
Support Document. EPA-822-B-98-005. U.S. Environmental Protection Agency, Office of Water,
Washington, DC.
178
-------
BIOACCUMULATION SUMMARY CHLORPYRIFOS
Chemical Category: PESTICIDE (ORGANOPHOSPHATE)
Chemical Name (Common Synonyms): CHLORPYRIFOS CASRN: 2921-88-2
Chemical Characteristics
Solubility in Water: 0.7 ppm at 20°C [1] Half-Life: No data [2]
Log Kow: 5.26 [3] Log Koc: 5.17 L/kg organic carbon
Human Health
Oral RfD: 3 x 10~3 mg/kg/day [4] Confidence: Medium, uncertainty factor
=10[4]
Critical Effect: Decreased plasma cholinesterase activity after 9 days of 20-day human feeding study
Oral Slope Factor): No data [4] Carcinogenic Classification: No data [4],
D[5]
Wildlife
Partitioning Factors: Partitioning factors for chlorpyrifos in wildlife were not found in the literature.
Food Chain Multipliers: Food chain multipliers for chlorpyrifos in wildlife were not found in the
literature.
Aquatic Organisms
Partitioning Factors: The only partitioning factors for chlorpyrifos in aquatic organisms found in the
literature were log BCF of 3.23 for an isopod [14].
Food Chain Multipliers: Food chain multipliers for chlorpyrifos in aquatic organisms were not found
in the literature.
Toxicity/Bioaccumulation Assessment Profile
Chlorpyrifos or Dursban is an organophosphorus insecticide which is used to control both adult and larval
mosquitoes [6]. It is more toxic to nontarget organisms like cladocerans, amphipods, and other organisms
than to mosquito larvae, however. The increase of chlorpyrifos concentration in water proportionally
increased the bioconcentration factor in fish [7]. A low recovery (20 percent or lower) of chlorpyrifos
from C-18 columns was attributed to its high binding affinity [8]. Also, acidic or basic conditions were
179
-------
BIOACCUMULATION SUMMARY CHLORPYRIFOS
not effective in reducing its concentration in water [9]. Because of the binding capacity and the high Kow,
chlorpyrifos does not remain in aqueous solution or suspension but is bound to the organic and clay
fractions of sediments. The time for sediment-associated pesticides to degrade and reach nontoxic states
is much greater than for aqueous phases [10]. The responses to chlorpyrifos from single-species tests
were compared to responses observed in a field mesocosm [11]. The EC50 for seven species in the
mesocosms ranged from 0.1 to 3.4 ug/L and were within the same order of magnitude as the laboratory
data. Toxicity to the most sensitive test species, D. magna , at 1 |ig/L was representative of sensitive
indigenous species.
The results of toxicity tests exposing Chironomus tentans to sediments with differing organic carbon
content spiked with chlorpyrifos revealed that an organic carbon partitioning model can be reasonably
used to predict the toxicity of chlorpyrifos to benthic macroinvertebrates [12]. The TOC-normalized,
solid-phase concentration of chlorpyrifos was no better predictor of the toxicity of the pesticide to C.
tentans than the sediment dry-weight concentration of chlorpyrifos. The effects based on predicted pore-
water concentrations were accurate to within a factor of two of expected effects based on water-only
toxicity tests with the midge.
Distinct pulses of pesticides, including chlorpyrifos, were detected in the San Joaquin River and in the
Sacramento River following rainfall events [13]. The results of short-term chronic tests with
Ceriodaphnia dubia indicated that Sacramento River water at Rio Vista was acutely toxic for three
consecutive days, while San Joaquin River water at Vernalis was toxic for 12 consecutive days.
180
-------
Summary of Biological Effects Tissue Concentrations for Chlorpyrifos
Species: Concentration, Units in1:
Taxa Sediment Water
Invertebrates
Mytilus
galloprovincialis,
Mediterranean mussel
Aselliis aquaticus, 0.7 |j.g/L
Isopod 5.0 (j.g/L
Fishes
Pimephales promelas,
Fathead minnow
Tissue (Sample Type)
42 mg/kg
(whole body)4
4 mg/kg
(whole body)4
1 .9 mg/kg
(whole body)4
4 mg/kg
(whole body)4
140,000 ng/kg
260,000 ng/kg
2 mg/kg
(whole body)4
4.5 mg/kg
(whole body)4
4.5 mg/kg
(whole body)4
Toxicity: Ability to Accumulate2:
Log Log
Effects BCF BAF BSAF
Mortality,
ED50
Morphology,
LOED
Morphology,
NOED
Mortality, NOED
3.23
Growth,
LOED
Morphology,
LOED
Mortality, LOED
Source:
Reference
[19]
[19]
[19]
[19]
[14]
[21]
[21]
[21]
Comments3
L; estimated
from table 4
L; presence of
functional byssus
L; estimated
from table 4
F
L; significant
reduction in
growth
L; body
constriction
behind opercula,
shortening of
caudal peduncle
L; significant
reduction in
survival
-------
Summary of Biological Effects Tissue Concentrations for Chlorpyrifos
Species: Concentration, Units in1:
Taxa Sediment Water Tissue (Sample Type)
0.45 mg/kg
(whole body)4
4.5 mg/kg
(whole body)4
4.5 mg/kg
(whole body)4
2 mg/kg
(whole body)4
1.1 mg/kg
(whole body)4
1.1 mg/kg
(whole body)4
0.45 mg/kg
(whole body)4
0.2 mg/kg
(whole body)4
2 mg/kg
(whole body)4
1.1 mg/kg
(whole body)4
Toxicity: Ability to Accumulate2:
Log Log
Effects BCF BAF BSAF
Physiological,
LOED
Growth,
NA
Physiological,
NA
Physiological,
NA
Physiological,
NA
Growth,
NOED
Growth,
NOED
Growth,
NOED
Morphology,
NOED
Morphology,
NOED
Source:
Reference
[21]
[21]
[21]
[21]
[21]
[21]
[21]
[21]
[21]
[21]
Comments3
L; inhibition of
acetylcholinester
ase (ACHE)
activity
L; significant
reduction in
growth
L; inhibition of
acetylcholinester
ase (ACHE)
activity
L; inhibition of
acetylcholinester
ase (ACHE)
activity
L; inhibition of
acetylcholinester
ase (ACHE)
activity
L; no effect on
growth
L; no effect on
growth
L; no effect on
growth
L; no effect on
appearance or
development
L; no effect on
appearance or
development
-------
Summary of Biological Effects Tissue Concentrations for Chlorpyrifos
Species: Concentration, Units in1:
Taxa Sediment Water Tissue (Sample Type)
0.45 mg/kg
(whole body)4
0.2 mg/kg
(whole body)4
2 mg/kg
(whole body)4
1.1 mg/kg
(whole body)4
0.45 mg/kg
(whole body)4
0.2 mg/kg
(whole body)4
0.2 mg/kg
(whole body)4
Toxicity: Ability to Accumulate2:
Log Log
Effects BCF BAF BSAF
Morphology,
NOED
Morphology,
NOED
Mortality, NOED
Mortality, NOED
Mortality, NOED
Mortality, NOED
Physiological,
NOED
Source:
Reference
[21]
[21]
[21]
[21]
[21]
[21]
[21]
Comments3
L; no effect on
appearance or
development
L; no effect on
appearance or
development
L; no effect on
survival
L; no effect on
survival
L; no effect on
survival
L; no effect on
survival
L; inhibition of
acetylcholinester
ase (ACHE)
activity
Gambusia affinis,
Mosquito fish
0.0352 mg/kg
(whole body)4
Mortality, NOED
[22]
L; no effect on
survivorship
after 3 days
Poecilia reticulata,
Guppy
0.9 |ig/L
1.9|ig/L
3.9 ng/L
10|ig/L
19|ig/L
6 (ig/glipid
33 |ig/g lipid
66 |ig/g lipid
350 |ig/g lipid
710 |ig/g lipid
2,100 |ig/g lipid
[15]
-------
Summary of Biological Effects Tissue Concentrations for Chlorpyrifos
Species: Concentration, Units in1: Toxicity: Ability to Accumulate2: Source:
Log Log
Taxa Sediment Water Tissue (Sample Type) Effects BCF BAF BSAF Reference Comments3
Poecilia reticulata,
Guppy
Gasterosteus
aculeatus, Three-
spined stickleback
Cyprinodon
variegatus,
Sheepshead minnow
Cyprinodon
variegatus,
Sheepshead minnow
0.12 |ig/L
0.46 ng/L
l.Ong/L
series 1
0.78|ig/L
1.7 \ig/L
3.0 |ig/L
6.8 |ig/L
series 1
0.78|ig/L
1.7 ng/L
3.0 |ig/L
6.8 |ig/L
series 1
0.78|ig/L
1.7 ng/L
3.0 ng/L
6.8 |ig/L
series 2
3.1 ng/L
7.2 ng/L
14 |ig/L
26 |ig/L
52 ng/L
2,810mg/kg Mortality,
(whole body)4 ED 100
8.1 |ig/glipid
31.2|ig/glipid
125 |ig/g lipid
0.033 ng/g
0.22 |ig/g
0.45 |ig/g
4.8 |ig/g
0.054 ng/g
0.12 |ig/g
0.78 |ig/g
2.9 |ig/g
0.66 |ig/g
0.19 |ig/g
2.9 |ig/g
7.3 ng/g
0.67 |ig/g
1.8 |ig/g
4.3 |ig/g
17 M-g/g
34 |ig/g
[18] L; lifestage: 2-3
months
[16] L
[17] L (low feeding:
20 Artemia/fish/
feeding )
[17] L (medium
feeding: 110
Artemia/fish/
feeding )
[17] L (high feeding:
550 Artemial
fish/feeding )
[17] L (low feeding:
20 Artemia/fish/
feeding )
-------
Summary of Biological Effects Tissue Concentrations for Chlorpyrifos
Species: Concentration, Units in1:
Taxa Sediment Water
series 2
3.1 ng/L
7.2 ng/L
14|ig/L
26 \iglL
52ng/L
series 2
3.1 ng/L
7.2 ng/L
14|ig/L
26|ig/L
52ng/L
Leuresthes tenuis,
California grunion
Tissue (Sample Type)
0.82 |ig/g
2.9 |ig/g
5.5 |ig/g
15.9 |ig/g
52 ng/g
2.2 Hg/g
5.3 |ig/g
13.9 ng/g
37 |ig/g
95 |ig/g
0.21 mg/kg
(whole body)4
0.038 mg/kg
(whole body)4
0.21 mg/kg
(whole body)4
0.21 mg/kg
(whole body)4
0.58 mg/kg
(whole body)4
0.39 mg/kg
(whole body)4
Toxicity:
Effects
Behavior,
LOED
Growth,
LOED
Growth,
LOED
Morphology,
LOED
Mortality,
LOED
Mortality,
LOED
Ability to Accumulate2: Source:
Log Log
BCF BAF BSAF Reference
[17]
[17]
[23]
[23]
[23]
[23]
[23]
[23]
Comments3
L (medium
feeding: 110
Artemia/fish/
feeding)
L (high feeding:
550 Artemial
fish/feeding)
L; reduced
activity
L; significant
reduction in
weight of fry
L; significant
reduction in
mean fish weight
L; fish appeared
darker, abnormal
lateral flexure of
the back
L; nearly 40%
reduction in fry
survival
L; 38% reduction
in fry survival
-------
oo
ON
Summary of Biological Effects Tissue Concentrations for Chlorpyrifos
Species:
Taxa
Opsaniis beta,
Gulf toadfish
Concentration, Units in1:
Sediment Water Tissue (Sample Type)
0.58 mg/kg
(whole body)4
0.15 mg/kg
(whole body)4
0.0 15 mg/kg
(whole body)4
0.15 mg/kg
(whole body)4
0.15 mg/kg
(whole body)4
0.0 15 mg/kg
(whole body)4
0.15 mg/kg
(whole body)4
0.038 mg/kg
(whole body)4
0.21 mg/kg
(whole body)4
770 mg/kg
(whole body)4
12 mg/kg
(whole body)4
175 mg/kg
(whole body)4
Toxicity: Ability to Accumulate2:
Log Log
Effects BCF BAF BSAF
Growth, NA
Behavior,
NOED
Growth,
NOED
Growth,
NOED
Morphology,
NOED
Mortality,
NOED
Mortality,
NOED
Mortality,
NOED
Mortality,
NOED
Development,
ED25
Growth,
ED25
Growth,
ED50
Source:
Reference
[23]
[23]
[23]
[23]
[23]
[23]
[23]
[23]
[23]
[20]
[20]
[20]
Comments3
L; significant
reduction in
weight of fry
L; no effect on
behavior
L; no effect on
weight of fry
L; no effect on
growth
L; no effect on
morphology
L; no effect on
fry mortality
L; no effect on
fry survival
L; no effect on
fry mortality
L; no effect on
fry survival
L; delayed
development of
25% of sac fry
L; 25% reduction
in average
weight of fry
L; 50% reduction
in average
weight of fry
-------
Summary of Biological Effects Tissue Concentrations for Chlorpyrifos
00
-J
Species: Concentration, Units in1:
Taxa Sediment Water Tissue (Sample Type)
770 mg/kg
(whole body)4
0.95 mg/kg
(whole body)4
770 mg/kg
(whole body)4
2.2 mg/kg
(whole body)4
4.7 mg/kg
(whole body)4
15 mg/kg
(whole body)4
30 mg/kg
(whole body)4
9.9 mg/kg
(whole body)4
45 mg/kg
(whole body)4
770 mg/kg
(whole body)4
0.14 mg/kg
(whole body)4
12 mg/kg
(whole body)4
9.9 mg/kg
(whole body)4
Toxicity:
Effects
Behavior,
LOED
Growth,
LOED
Mortality,
LOED
Growth, NA
Growth, NA
Growth, NA
Growth, NA
Growth, NA
Growth, NA
Growth, NA
Growth,
NOED
Mortality,
NOED
Mortality,
NOED
Ability to Accumulate2: Source:
Log Log
BCF BAF BSAF Reference
[20]
[20]
[20]
[20]
[20]
[20]
[20]
[20]
[20]
[20]
[20]
[20]
[20]
Comments3
L; hyperactivity,
hyperventilation
L; 9% reduction
in fry weight
L; significant
increase in fry
mortality
L; 19% reduction
in fry weight
L; 21% reduction
in fry weight
L; 37% reduction
in fry weight
L; 42% reduction
in fry weight
L; 21% reduction
in average
weight of fry
L; 35% reduction
in average
weight of fry
L; 62% reduction
in average
weight of fry
L; no effect on
growth
L; no effect on
fry mortality
L; no effect on
fry mortality
-------
00
oo
Summary of Biological Effects Tissue Concentrations for Chlorpyrifos
Species:
Taxa
Concentration, Units in1:
Sediment Water Tissue (Sample Type)
45 mg/kg
(whole body)4
175 mg/kg
(whole body)4
Toxicity:
Effects
Mortality,
NOED
Mortality,
NOED
Ability
Log
BCF
to Accumulate2:
Log
BAF BSAF
Source:
Reference
[20]
[20]
Comments3
L; no effect on
fry mortality
L; no effect on
fry mortality
Concentration units based on wet weight unless otherwise noted.
BCF = bioconcentration factor, BAF = bioaccumulation factor, BSAF = biota-sediment accumulation factor.
L = laboratory study, spiked sediment, single chemical; F = field study, multiple chemical exposure; other unusual study conditions or observations noted.
This entry was excerpted directly from the Environmental Residue-Effects Database (ERED, www.wes.army.mil/el/ered, U.S. Army Corps of Engineers and U.S.
Environmental Protection Agency). The original publication was not reviewed, and the reader is strongly urged to consult the publication to confirm the information
presented here.
-------
BIOACCUMULATION SUMMARY CHLORPYRIFOS
References
1. MacKay, D., and Shin Wy; J. Chem Eng Data 22:399 (1977). (Cited in: USEPA. 1995. Hazardous
Substances Data Bank (HSDB). National Library of Medicine online (TOXNET). U.S.
Environmental Protection Agency, Office of Health and Environmental Assessment, Environmental
Criteria and Assessment Office, Cincinnati, OH. September.)
2. USEPA. 1989. Chemical fate rate constants for SARA section 313 chemicals and Superfund Health
Manual chemicals. Draft. Prepared by Chemical Hazard Assessment Division, Syracuse Research
Corporation, for U.S. Environmental Protection Agency, Office of Toxic Substances, Exposure
Evaluation Division, Washington, DC, and Environmental Criteria and Assessment Office,
Cincinnati, OH. August 11.
3. Karickhoff, S.W., and J.M. Long. 1995. Internal report on summary of measured, calculated, and
recommended log Kow values. Draft. Prepared by U.S. Environmental Protection Agency, Office
of Research and Development, Environmental Research Laboratory-Athens, for E. Southerland,
Office of Water, Office of Science and Technology, Standards and Applied Science Division,
Washington, DC. April 10.
4. USEPA. 1997. Integrated Risk Information System (IRIS). National Library of Medicine online
(TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental
Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. January.
5. USEPA. 1992. Classification list of chemicals evaluated for carcinogenicity potential - U.S.
Environmental Protection Agency, Office of Pesticide Programs, Washington, DC.
6. Mull, M.S., G. Majori, and A.A. Arata. 1979. Impact of biological and chemical mosquito control
agents on nontarget biota in aquatic ecosystems. In Mosquito control agents in aquatic ecosystems,
pp. 121-173. Springer-Verlag, New York, NY.
7. Weling, W., and J.W. de Vries. 1992. Bioconcentration kinetics of the organophosphorus
insecticide chlorpyrifos in guppies (Poecilia reticulatd). Ecotoxicol. Environ. Saf. 23:64-75.
8. Racke, K.D. 1993. The environmental fate of chlorpyrifos. In Reviews of environmental
contamination and toxicology, ed. G.W. Ware, Vol. 131, pp. 234-276. Springer-Verlag, New
York, NY.
9. Bailey, H.C., C. DiGiorgio, K. Kroll, J.L. MiUer, D.E. Hinton, and G. Starrett. 1996. Development
of procedures for indentifying pesticide toxicity in ambient waters: Carbofutran, diazinon,
chlorpyrifos. Environ. Toxicol. Chem. 15:837-845.
10. Green, A.S., G.T. Chandler, and W.W. Piegorsch. 1996. Life-stage-specific toxicity of sediment-
associated chlorpyrifos to a marine, infaunal copepod. Environ. Toxicol. Chem. 15:1182-1185.
189
-------
BIOACCUMULATION SUMMARY CHLORPYRIFOS
11. Wijngaarden van, R.P.A., PJ. van den Brink, SJ.H. Crum, J.H.O. Voshaar, T.C.M. Brock, and
P. Leeuwangh. 1996. Effects of the insecticide Dursban 4E (active ingredient chlorpyrifos) in
outdoor experimental ditches: I. Comparison of short-term toxicity between the laboratory and the
field. Environ. Toxicol. Chem. 15:1133-1142.
12. Ankley, G.T., DJ. CaU, J.S. Cox, M.D. Kahl, R.A. Hoke, and P.A. Kosian. 1994. Organic carbon
partitioning as a basis for predicting the toxicity of chlorpyrifos in sediments. Environ. Toxicol.
Chem. 13:621-626.
13. Kuivila, K.M., and C.G. Foe. 1995. Concentrations, transport and biological effects of dormant
spray pesticides in the San Francisco estuary, California. Environ. Toxicol. Chem.l4:ll4l-ll50.
14. Montanes, C.J.F., Bert van Hattum, and J. Deneer. 1995. Bioconcentration of chlorpyrifos by the
freshwater isopod Asellus aquaticus (L.) in outdoor experimental ditches. Environ. Pollut.
88:137-146.
15. Deneer, J.W. 1993. Uptake and elimination of chlorpyrifos in the guppy at sublethal and lethal
aqueous concentrations. Chemosphere 26:1607-1616.
16. Deneer, J.W. 1994. Bioconcentration of chlorpyrifos by the three-spined stickleback under
laboratory and field conditions. Chemosphere 29:1561-1575.
17. Cripe, G.M., DJ. Hansen, S.F. Macauley, and J. Forester. 1986. Effects of diet quantity on
sheepshead minnows (Cyprinodon variegatus) during early life-stage exposures to chlorpyrifos.
In Aquatic toxicology and environmental fate, ASTM STP 921, ed. T.M. Poston and R. Purdy, pp.
450-460. American Society for Testing and Materials, Philadelphia, PA.
18. Ohayo-mitoko, G.J.A., and J.W. Deneer. 1993. Lethal body burdens of four organophosphorus
pesticides in the guppy (Poecilia reticulata). Science Total Environ. 559-565.
19. Serrano, R., F. Hernandez, J.B. Pena, V. Dosda, and J. Canales. 1995. Toxicity and
bioconcentration of selected organophosphorus pesticides in Mytilus galloprovincialis and Venus
gallina. Arch. Environ. Contain. Toxicol. 29: 284-290.
20. Hansen, D.J., L.R. Goodman, G.M. Cripe, and S.F. Macauley. 1986. Early life-stage toxicity test
methods for guff toadfish (Opsanus beta) and results using chlorpyrifos. Ecotoxicol. Environ. Saf.
11:15-22.
21. Jarvinen, A.W., B.R. Nordling, and M.E. Henry. 1983. Chronic toxicity of Dursban (chlorpyrifos)
to the fathead minnow (Pimephales promelas) and the resultant acetylcholinesterase inhibition.
Ecotoxicol. Environ. Saf. 7:423-434.
22. Metcalf, R.L. 1974. A laboratory model ecosystem to evaluate compounds producing biological
magnification. In Essays in Toxicology, ed. W.J. Hayes, Vol. 5, pp. 17-38. Academic Press, New
York, NY.
190
-------
BIOACCUMULATION SUMMARY CHLORPYRIFOS
23. Goodman, L.R., DJ. Hansen, G.M. Cripe, D.P. Middaugh, and J.C. Moore. 1985. A new early life-
stage toxicity test using the California grunion (Leuresthes tenuis) and results with chlorpyrifos.
Ecotoxicol Environ. Saf. 10:12-21.
191
-------
192
-------
BIOACCUMULATION SUMMARY CHROMIUM
Chemical Category: METAL
Chemical Name (Common Synonyms): CHROMIUM (hexavalent) CASRN: 18540-29-9
Chemical Characteristics
Solubility in Water: Insoluble [1] Half-Life: Not applicable, stable [1]
LogKow: - LogKoc: -
Human Health
Oral RfD: 5 x 10~3 mg/kg/day [2] Confidence: Low, uncertainty factor = 500
Critical Effect: No effects observed (Currently under review by RfD/RfC Work Group)
Oral Slope Factor: Not available [2] Carcinogenic Classification: A [2]
Wildlife
Partitioning Factors: Partitioning factors for chromium in wildlife were not found in the literature.
Food Chain Multipliers: Food chain multipliers for chromium in wildlife were not found in the
literature.
Aquatic Organisms
Partitioning Factors: In aqueous solutions, within a pH range of 6 to 8, hexavalent chromium is
distributed between two species: monovalent hydrochromate anion and divalent chromate anion.
Hexavalent chromium may account for 75 to 85 percent of the dissolved chromium while trivalent
chromium is generally below detection limits in most oxic surface waters [3]. In some surface waters,
as much as 10 to 15 percent of the dissolved chromium may be present in the colloidal/organic form. A
log BCF of 2.74 was reported for Daphia magna [9].
Food Chain Multipliers: Little evidence exists for the bioaccumulation/biomagnification of chromium
in aquatic food webs, although sediments frequently contain elevated concentrations of trivalent
chromium [4].
Toxicity/Bioaccumulation Assessment Profile
Chromium appears to have limited mobility under typical conditions in most aquatic habitats because the
trivalent form tends to bind to sediments. Plants can, however, bioaccumulate and reduce chromium.
193
-------
BIOACCUMULATION SUMMARY CHROMIUM
Tissue residue-toxicity relationships can also be variable because organisms might sequester metal in
various forms that might be analytically measurable as tissue residue but are actually stored in unavailable
forms within the organism as a form of detoxification [5]. Whole body residues might also not be
indicative of effects concentrations at the organ level because concentrations in target organs, such as the
kidneys and liver, may be 20 times more than whole body residues [6]. The application of "clean"
chemical analytical and sample preparation techniques is critical for the accurate measurement of metal
tissue residues [7]. Accumulation of hexavalent chromium in the gills of rainbow trout was significantly
higher at pH 6.5 than at 8.1 and is directly coupled with oxygen transfer, irrespective of exposure time
or concentration [8]. The authors of that study suggested that chromium uptake might be related to the
HCr04 to Cr04 ratio, whereby the monovalent hydrochromate anion is taken up more readily by the gill
tissue.
194
-------
Summary of Biological Effects Tissue Concentrations for Chromium
Species:
Taxa
Concentration, Units in1:
Sediment Water
Toxicity:
Tissue (Sample Type) Effects
Ability to Accumulate2:
Log Log
BCF
BAF
BSAF
Source:
Reference Comments3
Invertebrates
Mytilus
galloprovincialis,
Mussel
0.73-1. 04 mg/kg
0.018
[13]
Daphnia magna,
Cladoceran
Day 21:
1.1 mmol/kg
10% mortality 2.74
[9]
Xantho hydrophilus,
Mud crab
1 |ig/L 0.2 |ig/g (whole body)
0.2 |ig/g
(hepatopancreas)
0.4 ng/g (gill)
0.05 |ig/g (muscle)
[12]
Fishes
Oncorhynchus mykiss
(Salmo gairdneri),
Rainbow trout
1.5 mg/L
Day 22:
171 |ig/g (skin)
187 |ig/g (muscle)
132 |ig/g (gastro-
intestinal)
49.8 |ig/g (bone)
75.4 |ig/g (kidney)
77.2 |ig/g (blood)
16.9 |ig/g (fat)
27.3 |ig/g (liver)
10.0 |ig/L 133.6 |ig/g
1.3|ig/L 16.6 |ig/g
[10]
[11]
-------
Summary of Biological Effects Tissue Concentrations for Chromium
Species:
Taxa
Concentration, Units in1:
Sediment Water
Toxicity:
Tissue (Sample Type) Effects
Ability to Accumulate2:
Log Log
BCF
BAF
BSAF
Source:
Reference Comments3
Oncorhynchus mykiss
Salmo gairdneri),
Rainbow trout
LO mg/L
LO mg/L
5.0 mg/L
5.0 mg/L
16.5 mg/L
2.0 |ig/g (whole body)
31.7ng/g(gill)
6.2 |ig/g
(digestive tract)
2.0 |ig/g (liver)
6.7 |ig/g (kidney)
0.9 |ig/g (whole body)
5.1 ng/g (gill)
7.4 |ig/g
(digestive tract)
3.4 |ig/g (liver)
8.5 |ig/g (kidney)
5.5 |ig/g (whole body)
51.8ng/g(gill)
9.5 ng/g
(digestive tract)
3.8 |ig/g (liver)
10.7 |ig/g (kidney)
2.3 |ig/g (whole body)
10.6 ng/g (gill)
100% survival
[8]
L; pH = 6.5
100% survival
[8]
L; pH = 7.8
100% survival
[8]
L; pH = 6.5
100% survival
[8]
L; pH = 7.8
(digestive tract)
5.1 |ig/g (liver)
12.2 |ig/g (kidney)
8.7 |ig/g (whole body) 25% survival
139 |ig/g (gill)
23.4 |ig/g
(digestive tract)
24.8 |ig/g (liver)
43.2 |ig/g (kidney)
[8]
L; pH = 6.5
-------
Summary of Biological Effects Tissue Concentrations for Chromium
Species:
Taxa
Concentration, Units in1:
Sediment Water
Toxicity:
Tissue (Sample Type) Effects
Ability to Accumulate2:
Log Log
BCF BAF BSAF
Source:
Reference Comments3
Oncorhynchus mykiss
(Salmo gairdneri),
Rainbow trout
16.5 mg/L 8.9 |ig/g (whole body) 63% survival
35.3 ng/g (gill)
22.6 |ig/g
(digestive tract)
25.9 |ig/g (liver)
24.6 |ig/g (kidney)
50 mg/L 0% survival
50 mg/L 10.5 |ig/g (whole body) 50% survival
37.6 ng/g (gill)
45.0 |ig/g
(digestive tract)
84.6 |ig/g (liver)
70.3 |ig/g (kidney)
[8]
[8]
[8]
L; pH = 7.8
L; pH = 6.5
L; pH = 7.8
Oncorhynchus
mykiss, Rainbow
trout
45 mg/kg Mortality,
(digestive tract)4 ED50
37.6 mg/kg (gill)4 Mortality,
ED50
70.3 mg/kg (kidney)4 Mortality,
ED50
85.6 mg/kg (liver)4 Mortality,
ED50
[14] L;pH7.8;
increased
mortality relative
to control
[14] L;pH7.8;
increased
mortality relative
to control
[14] L;pH7.8;
increased
mortality relative
to control
[14] L;pH7.8;
increased
mortality relative
to control
-------
Summary of Biological Effects Tissue Concentrations for Chromium
Species:
Taxa
Concentration, Units in1:
Sediment Water Tissue (Sample Type)
10.5 mg/kg
(whole body)4
23.4 mg/kg
(digestive tract)4
139 mg/kg (gill)4
Toxicity:
Effects
Mortality,
ED50
Mortality,
ED75
Mortality,
ED75
Ability to Accumulate2: Source:
Log Log
BCF BAF BSAF Reference
[14]
[14]
[14]
Comments3
L;pH7.8;
increased
mortality relative
to control
L;pH6.5;
increased
mortality relative
to control
L; pH 6.5;
increased
mortality relative
to control
43.1 mg/kg (kidney)4 Mortality,
ED75
24.8 mg/kg (liver)4 Mortality,
ED75
8.7 mg/kg
(whole body)4
22.6 mg/kg
(digestive tract)4
Mortality,
ED75
Mortality, NA
35.3 mg/kg (gill)4 Mortality, NA
[14] L;pH6.5;
increased
mortality relative
to control
[14] L;pH6.5;
increased
mortality relative
to control
[14] L;pH6.5;
increased
mortality relative
to control
[14] L;pH7.8;
increased
mortality relative
to control
[14] L;pH7.8;
increased
mortality relative
to control
-------
Summary of Biological Effects Tissue Concentrations for Chromium
Species: Concentration, Units in1:
Taxa Sediment Water Tissue (Sample Type)
24.6 mg/kg (kidney)4
25.9 mg/kg (liver)4
8.9 mg/kg
(whole body)4
9.5 mg/kg
(digestive tract)4
11. 2 mg/kg
(digestive tract)4
Toxicity: Ability to Accumulate2:
Log Log
Effects BCF BAF BSAF
Mortality, NA
Mortality, NA
Mortality, NA
Mortality, NOED
Mortality, NOED
Source:
Reference
[14]
[14]
[14]
[14]
[14]
Comments3
L;pH7.8;
increased
mortality relative
to control
L;pH7.8;
increased
mortality relative
to control
L;pH7.8;
increased
mortality relative
to control
L; pH 6.5; no
increased
mortality relative
to control
L;pH7.8;no
increased
51.8 mg/kg (gill)4
Mortality, NOED
10.6 mg/kg (gill)4 Mortality, NOED
10.7 mg/kg (kidney)4 Mortality, NOED
mortality relative
to control
[14] L; pH 6.5; no
increased
mortality relative
to control
[14] L;pH7.8;no
increased
mortality relative
to control
[14] L; pH 6.5; no
increased
mortality relative
to control
-------
Summary of Biological Effects Tissue Concentrations for Chromium
Species:
Taxa
Concentration, Units in1: Toxicity: Ability to Accumulate2:
Log Log
Sediment Water Tissue (Sample Type) Effects BCF BAF BSAF
Source:
Reference Comments3
12.2 mg/kg (kidney)4 Mortality, NOED
3.8 mg/kg (liver)4
5.1 mg/kg (liver)4
5.5 mg/kg
(whole body)4
2.3 mg/kg
(whole body)4
Mortality, NOED
Mortality, NOED
Mortality, NOED
Mortality, NOED
[14] L; ph 7.8; no
increased
mortality relative
to control
[14] L; pH 6.5; no
increased
mortality relative
to control
[14] L;pH7.8;no
increased
mortality relative
to control
[14] L; pH 6.5; no
increased
mortality relative
to control
[14] L;pH7.8;no
increased
mortality relative
to control
Concentration units based on wet weight unless otherwise noted.
BCF = bioconcentration factor, BAF = bioaccumulation factor, BSAF = biota-sediment accumulation factor.
L = laboratory study, spiked sediment, single chemical; F = field study, multiple chemical exposure; other unusual study conditions or observations noted.
This entry was excerpted directly from the Environmental Residue-Effects Database (ERED, www.wes.army.mil/el/ered, U.S. Army Corps of Engineers and U.S.
Environmental Protection Agency). The original publication was not reviewed and the reader is strongly urged to consult the publication to confirm the information
presented here.
-------
BIOACCUMULATION SUMMARY CHROMIUM
References
1. Sax. Hawley's condensed chemical dictionary, 11th ed., 1987, p. 280. (Cited in: USEPA. 1995.
Hazardous Substances Data Bank (HSDB). National Library of Medicine online (TOXNET).
U.S. Environmental Protection Agency, Office of Health and Environmental Assessment,
Environmental Criteria and Assessment Office, Cincinnati, OH. September.)
2. USEPA. 1995. Integrated Risk Information System (IRIS). National Library of Medicine online
(TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental
Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. September.
3. Beaubien, S., J. Nriagu, D. Blowes, and G. Lawson. 1994. Chromium speciation and distribution
in the Great Lakes. Environ. Sci. Technol. 28:730-736.
4. Weis, J.S., and P. Weis. 1993. Trophic transfer of contaminants from organisms living by
chromated-copper-arsenate (CCA)-treated wood to their predators. /. Exp. Mar. Biol. Ecol
168:25-34.
5. Klerks, P.L., and P.R. Bartholomew. 1991. Cadmium accumulation and detoxification in a Cd-
resistant population of the oligochaete Limnodrilus hoffmeisteri. Aquatic Toxicol. 19:97-112.
6. McKinney, J. 1993. Metals bioavailability and disposition kinetics research needs workshop. July
18-19, 1990. Toxicol. Environ. Chem. 38:1-71.
7. Schmitt, C.J., and S.E. Finger. 1987. The effects of sample preparation on measured
concentrations of eight elements in edible tissues of fish from streams contaminated by lead
mining. Arch. Environ. Contam. Toxicol. 16:185-207.
8. Van der Putte, I., and P. Part. 1982. Oxygen and chromium transfer in perfused gills of rainbow
trout (Salmo gairdneri) exposed to hexavalent chromium at two different pH levels. Aquat.
Toxicol. 2:31-45.
9. Enserink, E.L., J.L. Maas-Diepeveen, and CJ. van Leeuwen. 1991. Combined effects of metals:
An ecotoxicological evaluation. Water Res. 25:679-687.
10. Buhler, D.R., R.M. Stokes, and R.S. Caldwell. 1977. Tissue accumulation and enzymatic effects
of hexavalent chromium in rainbow trout (Salmo gairdneri). J. Fish. Res. Board Can. 34:9-18.
11. Fromm, P.O., and R.M. Stokes. 1962. Assimilation and metabolism of chromium by trout. /.
Water Poll. Control. Fed. 34:1151-1155.
12. Peternac, B., and T. Legovic. 1986. Uptake, distribution and loss of Cr in the crab Xantho
hydrophilus. Mar. Biol. 91:467-471.
13. Houkal, D., B. Rummel, and B. Shephard. 1996. Results of an in situ mussel bioassay in the Puget
Sound. Abstract, 17th Annual Meeting Society of Environmental Toxicology and Chemistry,
Washington, DC, November 17-21, 1996.
201
-------
BIOACCUMULATION SUMMARY CHROMIUM
14. Van De Putte, L., J. Lubbers, and Z. Kolar, 1981. Effect of pH on uptake, tissue distribution and
retention of hexavelent chromium in rainbow trout (Salmo gairdneri). Aquatic Toxicol. 1: 3-18.
202
-------
BIOACCUMULATION SUMMARY CHRYSENE
Chemical Category: POLYNUCLEAR AROMATIC HYDROCARBON (high molecular weight)
Chemical Name (Common Synonyms): CHRYSENE CASRN: 218-01-9
Chemical Characteristics
Solubility in Water: 0.0020 mg/L at 25°C [1] Half-Life: 1.02 yrs - 2.72 yrs based on aerobic
soil die-away test data. [2]
Log Kow: 5.70 [3] Log Koc: 5.60 L/kg organic carbon
Human Health
Oral RfD: No data [4] Confidence: —
Critical Effect: —
Oral Slope Factor (Reference): Not available [4] Carcinogenic Classification: B2 [4]
Wildlife
Partitioning Factors: Partitioning factors for chrysene in wildlife were not found in the literature.
Food Chain Multipliers: Food chain multipliers for chrysene in wildlife were not found in the literature.
Aquatic Organisms
Partitioning Factors: Partitioning factors for chrysene in aquatic organisms were not found in the
literature.
Food Chain Multipliers: Food chain multipliers for chrysene in aquatic organisms were not found in the
literature. Log BAF values found in the literature ranged from -0.68 for the clam Macoma nasuta [7]
to 4.31 for the amphipod Pontoporeia hoyi [9].
Toxicity/Bioaccumulation Assessment Profile
The results from the laboratory experiments performed by Harkey [5] indicated that accumulation of
chrysene from elutriates was significantly lower than that from whole sediment, and the elutriate-sediment
accumulations followed a downward curve over time. A similar curve was observed for pore water-to-
sediment accumulation ratios. The concentrations of chrysene in whole sediment and pore water were
34.2 ng/g and 0.305 mg/mL, respectively [5]. Uptake rate coefficients for Diporeia spp. were highest in
pore water (244.3 ug/goc/h) and lowest in elutriate (55.2 |ig/goc/h). The authors concluded that aqueous
203
-------
BIOACCUMULATION SUMMARY CHRYSENE
extracts of whole sediment did not accurately represent the exposure observed in whole sediment [5].
The aqueous extracts of whole sediment underexposed organisms, compared to whole sediment, even
after adjusting accumulation to the fraction of organic carbon contained in the test media. While the total
chrysene concentration in the sediment stayed constant, total concentration decreased appreciably in pore
water and elutriate over the course of the exposure, and it is likely that the bioavailability concentrations
in these media also decreased. Benthic amphipods, Gammarus pulex, exposed to sediments containing
polynuclear aromatic hydrocarbons (PAHs) and water spiked with sediment extract from PAH-
contaminated sediment, accumulated chrysene in direct proportion to exposure concentrations [6].
204
-------
Summary of Biological Effects Tissue Concentrations for Chrysene
Species:
Taxa
Invertebrates
Macoma nasuta,
Clam
Diporeia spp.,
Amphipod
Diporeia spp.,
Amphipod
Pontoporeia hoyi,
Amphipod
Concentration, Units in1:
Sediment Water
7.4 ng/g
5.9 ng/g
50 ng/g
41 ng/g
174 ng/g
249 ng/g
15 nmol/g
50 ng/g 7 ng/mL
30 ng/g 1.5 ng/mL
Toxicity:
Tissue (Sample Type) Effects
29 ng/g
8.1 ng/g
29.8 ng/g
30 ng/g
88 ng/g
72 ng/g
213 nmol/g
2.6 mg/kg Mortality,
(whole body)4 NOED
600 ng/g
180 ng/g
Ability to Accumulate2:
Log Log
BCF BAF BSAF
-0.21
-0.68
-0.40
-0.28
-0.33
-0.41
4.31
Source:
Reference
[7]
[7]
[7]
[7]
[7]
[7]
[8]
[5]
[9]
[9]
Comments3
F
F
F
F
F
F
L
L; no increase in
mortality in 96 hours
L
L
-------
to
o
o\
Summary of Biological Effects Tissue Concentrations for Chrysene
Species:
Taxa
Concentration, Units in1:
Toxicity:
Ability to Accumulate2:
Log Log
Sediment Water Tissue (Sample Type) Effects BCF BAF BSAF
Source:
Reference Comments3
Fishes
Oncorhynchus
mykiss,
Rainbow trout
30 mg/kg
(whole body)4
Physiological,
LOED
[11] L; induction of
hepatic mixed
function oxidases
Cyprinus carpio,
Common carp
109 mg/kg (liver)4
Physiological,
NA
[10] L; significant
increase in EROD
enzyme and P450 la
protein content
Concentration units based on wet weight unless otherwise noted.
BCF = bioconcentration factor, BAF = bioaccumulation factor, BSAF = biota-sediment accumulation factor.
L = laboratory study, spiked sediment, single chemical; F = field study, multiple chemical exposure; other unusual study conditions or observations noted.
This entry was excerpted directly from the Environmental Residue-Effects Database (ERED, www.wes.army.mil/el/ered, U.S. Army Corps of Engineers and U.S.
Environmental Protection Agency). The original publication was not reviewed, and the reader is strongly urged to consult the publication to confirm the information
presented here.
-------
BIOACCUMULATION SUMMARY CHRYSENE
References
1. Mackay, D., and Shin Wy; J. Chem. Eng. Data 22:399 (1977). (Cited in: USEPA. 1995.
Hazardous Substances Data Bank (HSDB). National Library of Medicine online (TOXNET). U.S.
Environmental Protection Agency, Office of Health and Environmental Assessment,
Environmental Criteria and Assessment Office, Cincinnati, OH. September.)
2. USEPA. 1989. Chemical fate rate constants for SARA section 313 chemicals and Superfund
Health Manual chemicals. Prepared by Chemical Hazard Assessment Division, Syracuse
Research Corporation, for U.S. Environmental Protection Agency, Office of Toxic Substances,
Exposure Evaluation Division, Washington, DC, and Environmental Criteria and Assessment
Office, Cincinnati, OH. August 11.
3. Karickhoff, S.W., and J.M. Long. 1995. Internal report on summary of measured, calculated, and
recommended log Kow values. Draft. Prepared by U.S. Environmental Protection Agency, Office
of Research and Development, Environmental Research Laboratory-Athens, for E. Southerland,
Office of Water, Office of Science and Technology, Standards and Applied Science Division,
Washington, DC. April 10.
4. USEPA. 1997. Integrated Risk Information System (IRIS). National Library of Medicine online
(TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental
Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. January.
5. Harkey, G.A., P.F. Landrum, and SJ. Klaine. 1994. Comparison of whole-sediment, elutriate and
pore-water exposures for use in assessing sediment-associated organic contaminants in bioassays.
Environ. Toxicol. Chem. 13:1315-1329.
6. Maltby, L., A.B.A. Boxall, D.M. Forrow, P. Calow, and C.I. Betton. 1995. The effects of
motorway runoff on freshwater ecosystems: 2. Identifying major toxicants. Environ. Toxicol.
Chem. 14:1093-1101.
7. Ferraro, S.P., H. Lee II, R.J. Ozretich, and D.T. Specht. 1990. Predicting bioaccumulation
potential: A test of a fugacity-based model. Arch. Environ. Contam. Toxicol. 19:386-394.
8. Landrum, P.F., BJ. Eadie, and W.R. Faust. 1992. Variation in the bioavailability of polycyclic
aromatic hydrocarbons to the amphipod Diporeia (spp.) with sediment aging. Environ. Toxicol.
Chem. 11:1197-1208.
9. Eadie, B.J., P.F. Landrum, and W. Faust. 1982. Polycyclic aromatic hydrocarbons in sediments,
pore water and the amphipod Pontoporeia hoyi from Lake Michigan. Chemosphere 11:847-858.
10. Van Der Weidern, M.E.J., F.H.M Hanegraaf, M.L Eggens, M. Celander, W. Seinen, and M. Ven
Den Berg. 1994. Temporal induction of cytochrome P450 la in the mirror carp (Cyprinus carpio)
after administration of several polycyclic aromatic hydrocarbons. Environ. Toxicol. Chem. 13:
797-802.
11. Gerhart, E.H., and R.H. Carlson. 1978. Hepatic mixed-function oxidase activity in rainbow trout
exposed to several polycyclic aromatic hydrocarbons. Environ. Res. 17:284-295.
207
-------
208
-------
BIOACCUMULATION SUMMARY
COPPER
Chemical Category: METAL
Chemical Name (Common Synonyms): COPPER
CASRN: 7440-50-8
Chemical Characteristics
Solubility in Water: Insoluble [1]
Log Kow: —
Half-Life: Not applicable, stable [1]
Log Koc: —
Human Health
Oral RfD: Not available [2]
Critical Effect: —
Oral Slope Factor: No data [2]
Confidence:
Carcinogenic Classification: D [2]
Wildlife
Partitioning Factors: Partitioning factors for copper in wildlife were not found in the literature.
Food Chain Multipliers: Food chain multipliers for copper in wildlife were not found in the literature.
Aquatic Organisms
Partitioning Factors: Up to 29 different species of copper can be present in aqueous solution in the pH
range from 6 to 9. Aqueous copper speciation and toxicity depend on the ionic strength of the water. The
hydroxide species and free copper ions are mostly responsible for toxicity, while copper complexes
consisting of carbonates, phosphates, nitrates, ammonia, and sulfates are weakly toxic or nontoxic.
Copper in the aquatic environment can partition to dissolved and particulate organic carbon. The
bioavailability of copper also can be influenced to some extent by total water hardness. Bioavailability
of copper in sediments is controlled by the acid-volatile sulfide (AVS) concentration [12]. A log BCF of
3.77 was reported for the midge [4].
Food Chain Multipliers: Little evidence exists to support the general occurrence of biomagnification
of copper in the aquatic environment [3]. Copper is taken up by aquatic organisms primarily through
dietary exposure.
209
-------
BIOACCUMULATION SUMMARY COPPER
Toxicity/Bioaccumulation Assessment Profile
The free copper ions are the most bioavailable inorganic forms, although they might account for only a
minor proportion of the total dissolved metal. The concentration of copper found in interstitial water is
usually much lower than that in surface water. The amount of bioavailable copper in sediment is
controlled in large part by the concentration of AVS and organic matter. A considerable number of
aquatic species are sensitive to dissolved concentrations of copper in the range of 1-10 |ig/L. Metal
metabolism by aquatic biota has significant affects on metal accumulation, distribution in tissues, and
toxic effects. Concentration of copper in benthic organisms from contaminated areas can be one to two
orders of magnitude higher than normal. Copper is accumulated by aquatic organisms primarily through
dietary exposure [3]. However, most organisms retain only a small proportion of the heavy metals
ingested with their diet.
Rule and Alden [13] studied the relationship between uptake of cadmium and copper from the sediment
by blue mussel (Mytilus edulis), grass shrimp (Palaemonetes pugio), and hard clam (Mercenaria
mercenarid). The uptake of copper by all organisms was related only to copper concentration in
sediment.
210
-------
Summary of Biological Effects Tissue Concentrations for Copper
Species: Concentration, Units in1:
Taxa Sediment Water
Plants
Eichhornia crassipes,
Water Hyacinth
Tissue (Sample Type)
11.4mg/kg(leaf)
549 mg/kg (root)
37.8 mg/kg (stem)
11. 4 mg/kg (leaf)
549 mg/kg (root)
Toxicity: Ability to Accumulate2:
Log Log
Effects BCF BAF BSAF
Growth, LOED
Growth, LOED
Growth, LOED
Morphology,
LOED
Morphology,
LOED
Source:
Reference
[22]
[22]
[22]
[22]
[22]
Comments3
L; reduced growth
rate, chlorosis
L; reduced growth
rate, chlorosis
L; reduced growth
rate, chlorosis
L; chlorosis,
browning,
necrosis,
waterlogging of
tissues
L; chlorosis,
browning,
37.8 mg/kg (stem) Morphology,
LOED
13.8 mg/kg (leaf) Growth, NA
1,750 mg/kg (root) Growth, NA
74.4 mg/kg (stem) Growth, NA
necrosis,
waterlogging of
tissues
[22] L; chlorosis,
browning,
necrosis,
waterlogging of
tissues
[22] L; reduced growth
rate, chlorosis
[22] L; reduced growth
rate, chlorosis
[22] L; reduced growth
rate, chlorosis
-------
Summary of Biological Effects Tissue Concentrations for Copper
Species: Concentration, Units in1:
Taxa Sediment Water Tissue (Sample Type)
13.8 mg/kg (leaf)
1,750 mg/kg (root)
74.4 mg/kg (stem)
4.6 mg/kg (leaf)
7.8 mg/kg (leaf)
20.8 mg/kg (root)
82.8 mg/kg (root)
10 mg/kg (stem)
15.2 mg/kg (stem)
4.6 mg/kg (leaf)
Toxicity: Ability to Accumulate2:
Log Log
Effects BCF BAF BSAF
Morphology, NA
Morphology, NA
Morphology, NA
Growth, NOED
Growth, NOED
Growth, NOED
Growth, NOED
Growth, NOED
Growth, NOED
Morphology,
NOED
Source:
Reference
[22]
[22]
[22]
[22]
[22]
[22]
[22]
[22]
[22]
[22]
Comments3
L; chlorosis,
browning,
necrosis,
waterlogging of
tissues
L; chlorosis,
browning,
necrosis,
waterlogging of
tissues
L; chlorosis,
browning,
necrosis,
waterlogging of
tissues
L; no effect on
growth
L; no effect on
growth
L; no effect on
growth
L; no effect on
growth
L; no effect on
growth
L; no effect on
growth
L; no effect on
plant appearance
-------
Summary of Biological Effects Tissue Concentrations for Copper
Species:
Taxa
Concentration, Units in1:
Sediment Water Tissue (Sample Type)
7.8 mg/kg (leaf)
20.8 mg/kg (root)
82.8 mg/kg (root)
10 mg/kg (stem)
15.2 mg/kg (stem)
Toxicity:
Effects
Morphology,
NOED
Morphology,
NOED
Morphology,
NOED
Morphology,
NOED
Morphology,
NOED
Ability to Accumulate2: Source:
Log Log
BCF BAF BSAF Reference
[22]
[22]
[22]
[22]
[22]
Comments3
L; no effect on
plant appearance
L; no effect on
plant appearance
L; no effect on
plant appearance
L; no effect on
plant appearance
L; no effect on
plant appearance
Invertebrates
Invertebrates
field-collected
Tubificidae
Total SEM Filt Nonfilt
|ig/g |ig/g |ig/L |ig/L
Body
7,820 6
583
480
478
128
16
172 ng/g
185 |ig/g
175 |ig/g
125 n-g/g
130 |ig/g
,971
325
287
251
77
<12
79
36
16
9
9
2
11,080 l,382|ig/g
698 122 |ig/g
274 181 |ig/g
184 266 ng/g
58 48 |ig/g
35 26 |ig/g
17.14 mg/g
10.23 mg/g
16.11 mg/g
20. 12 mg/g
14.73 mg/g
[10]
[9]
-------
Summary of Biological Effects Tissue Concentrations for Copper
Species: Concentration, Units in1:
Taxa Sediment Water
Nereis diversicolor, 41 jj.g/g
Polychaete worm 44 |ig/g
52 |ig/g
436 |ig/g
591 |ig/g
3,020 |ig/g
Meretrix casta,
Marine clam
Mytilus edulis,
Mussel
Toxicity: Ability to Accumulate2:
Log Log
Tissue (Sample Type) Effects BCF BAF BSAF
28 |ig/g
22 |ig/g
33 ng/g
31 |ig/g
106 |ig/g
257 |ig/g
1,142 ng/g
201 mg/kg Mortality, ED50
(whole body)4
67.4 mg/kg Mortality, ED50
(whole body)4
67.4 mg/kg Behavior, LOED
(whole body)4
80 mg/kg Mortality, ED 100
(whole body)4
3 6 mg/kg Mortality, ED 1 00
(whole body)4
23 mg/kg Mortality, ED 1 00
(whole body)4
1 5 mg/kg Mortality, ED 1 00
(whole body)4
Source:
Reference
[5]
[25]
[21]
[21]
[26]
[26]
[26]
[26]
Comments3
L
L; lethal body
burden
L; lethal body
burden after
7 - 8 days
L; total valve
closure, increased
mucus
production,
reduced byssus
production
L; lethal body
burden
L; lethal body
burden
L; lethal body
burden
L; lethal body
burden
-------
Summary of Biological Effects Tissue Concentrations for Copper
Species:
Taxa
Concentration, Units in1:
Toxicity:
Ability to Accumulate2:
Log Log
Sediment Water Tissue (Sample Type) Effects BCF BAF BSAF
Source:
Reference Comments3
12 mg/kg
(whole body)4
12 mg/kg
(whole body)4
12 mg/kg
(whole body)4
56 mg/kg
(whole body)4
Mortality, ED 100
Mortality, ED 100
Mortality, ED 100
Mortality, ED 100
[26]
[26]
[26]
[26]
L; lethal body
burden
L; lethal body
burden
L; lethal body
burden
L; lethal body
burden
Mytilus
galloprovincialis,
Mussel
1.9-3.1 mg/kg
0.04
[14]
Dreissena
polymorpha,
Zebra mussel
8.1 mg/kg
(whole body)4
2.7 mg/kg
(whole body)4
Physiological;
LOED
Physiological,
NOED
[24]
[24]
L; indicative of
breakdown of
internal Cu
regulatory
process
L; no effect on
internal Cu
regulatory
process
-------
to
ON
Summary of Biological Effects Tissue Concentrations for Copper
Species:
Taxa
Concentration, Units in1: Toxicity: Ability to Accumulate2:
Log Log
Sediment Water Tissue (Sample Type) Effects BCF BAF BSAF
Source:
Reference Comments3
Elliptic complanata, 0.1-23.7 |ig/g
Freshwater mussel
5.4 jj,g/g (foot)
2.4 jj.g/g (muscle)
8.5 (j.g/g (visceral)
29.0 ng/g
(hepatopancreas)
29.5 |ig/g (gill)
17.6 (j.g/g (mantle)
[11]
0.1-40.7 |ig/g
5.4 |ig/g (foot)
2.7 (j.g/g (muscle)
10.5 (j.g/g (visceral)
28.8 |ig/g
(hepatopancreas)
27.8 ng/g (gill)
11.8 (j,g/g (mantle)
0.2-106 |ig/g
12.7 |ig/g (foot)
11.7 (j.g/g (muscle)
16.5 (j.g/g (visceral)
44.5 |ig/g
(hepatopancreas)
214 ng/g (gill)
94 jj.g/g (mantle)
-------
Summary of Biological Effects Tissue Concentrations for Copper
Species:
Taxa
Concentration, Units in1:
Toxicity:
Ability to Accumulate2:
Log Log
Sediment Water Tissue (Sample Type) Effects BCF BAF BSAF
Source:
Reference Comments3
Elliptio complanata, 0.3-142 jj.g/g
Freshwater mussel
13.1 ng/g (foot)
10.7 (j.g/g (muscle)
16.1 (j.g/g (visceral)
72.9 |ig/g
(hepatopancreas)
132 ng/g (gill)
81.7 |ig/g (mantle)
Unto pictorum,
Freshwater mussel
6.5 mg/kg
(digestive gland)4
10 mg/kg (gill)4
2.7 mg/kg
(digestive gland)4
Physiological;
LOED
Physiological;
LOED
[24]
4.6 mg/kg (mantle)4 Physiological;
LOED
Physiological;
NOED
[24]
[24]
[24]
L; indicative of
breakdown of
internal Cu
regulatory
process
L; indicative of
breakdown of
internal Cu
regulatory
process
L; indicative of
breakdown of
internal Cu
regulatory
process
L; no effect on
internal Cu
regulatory
process
-------
Summary of Biological Effects Tissue Concentrations for Copper
Species: Concentration, Units in1: Toxicity: Ability to Accumulate2:
Log Log
Taxa Sediment Water Tissue (Sample Type) Effects BCF BAF BSAF
1 .9 mg/kg (gill)4 Physiological;
NOED
1 .7 mg/kg (gonad)4 Physiological;
NOED
4 mg/kg (gonad)4 Physiological;
NOED
2 mg/kg (kidney)4 Physiological;
NOED
3.7 mg/kg (kidney)4 Physiological;
NOED
1.1 mg/kg (mantle)4 Physiological;
NOED
Source:
Reference Comments3
[24] L; no effect on
internal Cu
regulatory
process
[24] L; no effect on
internal Cu
regulatory
process
[24] L; no effect on
internal Cu
regulatory
process
[24] L; no effect on
internal Cu
regulatory
process
[24] L; no effect on
internal Cu
regulatory
process
[24] L; no effect on
internal Cu
regulatory
process
-------
Summary of Biological Effects Tissue Concentrations for
Species:
Taxa
Daphnia magna,
Cladoceran
Hyalella azteca,
Amphipod
Hyalella azteca,
Amphipod
Copper
Concentration, Units in1: Toxicity: Ability to Accumulate2: Source:
Log Log
Sediment Water Tissue (Sample Type) Effects BCF BAF BSAF Reference Comments3
7.7 ng/L
10.7 |ig/L
16.7 |ig/L
25.4 |ig/L
43.8 |ig/L
81.3 |ig/L
Total SEM Filt Nonfilt
|ig/g |ig/g |ig/L |ig/L
7,820 6,971 79 11,080
583 325 36 698
480 287 16 274
478 251 9 184
128 77 9 58
16 <12 2 35
5.8 mg/kg Reproduction,
(whole body)4 ED 10
68 mg/kg Mortality, ED50
(whole body)4
91 |ig/g 54% survival
92 |ig/g 50% survival
95 |ig/g 40% survival
88 |ig/g 29% survival
80 |ig/g 6% survival
— 0% survival
Body;
249 |ig/g
87 |ig/g
124 |ig/g
127 |ig/g
124 |ig/g
84 ug/g
[7] L; 10% reduction
in number of
offspring
[7] L; lethal body
burden after 21
day exposure
[6] L
[10] F
-------
to
0
Summary of Biological Effects Tissue Concentrations for Copper
Species: Concentration, Units in1:
Taxa Sediment Water Tissue (Sample Type)
Corophiumvolutator, 16.9 mg/kg
Amphipod (whole body)4
Balanus crenatus, 80 mg/kg
Barnacle (whole body)4
Orconectes rusticus, 24 mg/kg (abdomen)4
Crayfish
26 mg/kg (abdomen)4
32 mg/kg (abdomen)4
42 mg/kg (abdomen)4
52 mg/kg (abdomen)4
17.8 mg/kg (claw)4
24 mg/kg (claw)4
24 mg/kg (claw)4
30 mg/kg (claw)4
Toxicity: Ability to Accumulate2:
Log Log
Effects BCF BAF BSAF
NA, LOED
Behavior, NOED
Mortality, NOED
Mortality, NOED
Mortality, NOED
Mortality, NOED
Mortality, NOED
Mortality, NOED
Mortality, NOED
Mortality, NOED
Mortality, NOED
Source:
Reference
[18]
[29]
[19]
[19]
[19]
[19]
[19]
[19]
[19]
[19]
[19]
Comments3
L; 100%
dissolved oxygen
saturation during
test
L; regulation of
metals endpoint-
summer
experiment
L; no effect on
survivorship
L; no effect on
survivorship
L; no effect on
survivorship
L; no effect on
survivorship
L; no effect on
survivorship
L; no effect on
survivorship
L; no effect on
survivorship
L; no effect on
survivorship
L; no effect on
survivorship
-------
Summary of Biological Effects Tissue Concentrations for Copper
Species: Concentration, Units in1:
Taxa Sediment Water Tissue (Sample Type)
34 mg/kg (claw)4
42 mg/kg (thorax)4
50 mg/kg (thorax)4
56 mg/kg (thorax)4
60 mg/kg (thorax)4
70 mg/kg (thorax)4
2 mg/kg
(whole body)4
9 mg/kg
(whole body)4
11. 2 mg/kg
(whole body)4
19.2 mg/kg
(whole body)4
26 mg/kg
(whole body)4
Toxicity: Ability to Accumulate2:
Log Log
Effects BCF BAF BSAF
Mortality, NOED
Mortality, NOED
Mortality, NOED
Mortality, NOED
Mortality, NOED
Mortality, NOED
Mortality, NOED
Mortality, NOED
Mortality, NOED
Mortality, NOED
Mortality, NOED
Source:
Reference
[19]
[19]
[19]
[19]
[19]
[19]
[19]
[19]
[19]
[19]
[19]
Comments3
L; no effect on
survivorship
L; no effect on
survivorship
L; no effect on
survivorship
L; no effect on
survivorship
L; no effect on
survivorship
L; no effect on
survivorship
L; no effect on
survivorship
L; no effect on
survivorship
L; no effect on
survivorship
L; no effect on
survivorship
L; no effect on
survivorship
-------
Summary of Biological Effects Tissue Concentrations for Copper
Species: Concentration, Units in1:
Taxa Sediment Water
Chironomiis riparius, 0.087 mg/L
Midge
Chironomiis thummi, 12.55 mg/kg
Midge
Chironomiis decorus,
Midge
Tissue (Sample Type)
500 ng/g
35.7 mg/kg
39.7 mg/kg
1,000 mg/kg
(whole body)4
142 mg/kg
(whole body)4
107 mg/kg
(whole body)4
126 mg/kg
(whole body)4
86.2 mg/kg
(whole body)4
130 mg/kg
(pupal exuviae)4
18 mg/kg
(whole body)4
14.8 mg/kg
(pupal exuviae)4
Toxicity: Ability to Accumulate2:
Log Log
Effects BCF BAF BSAF
3.77
Normal larvae
Deformed larvae
Mortality, ED 100
Mortality, ED50
Mortality, LOED
Mortality, LOED
Mortality, NOED
Development,
LOED
Development,
LOED
Development,
NOED
Source:
Reference
[4]
[8]
[23]
[23]
[23]
[23]
[23]
[23]
[23]
[23]
Comments3
F
F
L; 100% mortality
L; ED50
L; significant
mortality
L; significant
mortality
L; no effect on
mortality
L; increased time
to adult
emergence by 10
days
L; increased time
to adult
emergence by 10
days
L; no effect on
time to adult
emergence
-------
Summary of Biological Effects Tissue Concentrations for Copper
Species:
Taxa
Fishes
Oncorhynchus
mykiss,
Rainbow trout
Concentration, Units in1:
Sediment Water Tissue (Sample Type)
75.6 mg/kg
(pupal exuviae)4
2.28 mg/kg
(whole body)4
7.2 mg/kg
(whole body)4
13 mg/kg
(whole body)4
7.14 mg/kg
(whole body)4
40 mg/kg
(whole body)4
1.6 mg/kg
(whole body)4
6.8 mg/kg
(whole body)4
2.22 mg/kg
(whole body)4
Toxicity: Ability to Accumulate2:
Log Log
Effects BCF BAF BSAF
Development,
NOED
Development,
NOED
Development,
NOED
Development,
NOED
Morphology,
NOED
Physiological;
LOED
Mortality, ED 100
Physiological,
LOED
Mortality, LOED
Source:
Reference
[23]
[23]
[23]
[23]
[8]
[16]
[17]
[17]
[20]
Comments3
L; no effect on
time to adult
emergence
L; no effect on
time to adult
emergence
L; no effect on
time to adult
emergence
L; no effect on
time to adult
emergence
L; 4th instar larvae
L; induction of
metallothionein
L; 100% mortality
in non-metallo-
thionein-induced
fish
L; induction of
metallothionein
L; 50% mortality
in 7 hours
-------
Summary of Biological Effects Tissue Concentrations for Copper
Species:
Taxa
Pimephales
promelas,
Fathead minnow
Cypriniis carpio,
Common carp
Concentration, Units in1: Toxicity: Ability to Accumulate2:
Log Log
Sediment Water Tissue (Sample Type) Effects BCF BAF BSAF
4.48 mg/kg Survival, LOED
(whole body)4
3.92 mg/kg Not applicable,
(whole body)4 NOED
78.9 |ig/g 10.28 mg/g
H0|ig/g 9.32 mg/g
125 |ig/g 9.13 mg/g
130 |ig/g 9.70 mg/g
130 |ig/g 9.86 mg/g
172 |ig/g 6.92 mg/g
175 |ig/g 7.28 mg/g
175 |ig/g 10.96 mg/g
185 |ig/g 9.37 mg/g
12.1 mg/kg Morphology,
(whole body)4 LOED
12.1 mg/kg Morphology,
(whole body)4 LOED
12.1 mg/kg Mortality, LOED
(whole body)4
Source:
Reference Comments3
[27] L
[27] L
[9] F
[29] L; larval
deformation, pH
6.3, body burden
from graph
[29] L; larval
deformation, pH
7.6, body burden
from graph
[29] L; larval
mortality, pH 6.3,
body burden from
graph
-------
Summary of Biological Effects Tissue Concentrations for Copper
Species:
Taxa
Lepomis
macrochirus,
Bluegill
Concentration, Units in1:
Sediment Water Tissue (Sample Type)
12.1 mg/kg
(whole body)4
24.1 mg/kg
(whole body)4
7.62 mg/kg
(whole body)4
7.62 mg/kg
(whole body)4
12.1 mg/kg
(whole body)4
12.1 mg/kg
(whole body)4
13 mg/kg (gill)4
Toxicity: Ability to Accumulate2:
Log Log
Effects BCF BAF BSAF
Mortality, LOED
Reproduction,
LOED
Morphology,
NOED
Mortality, NOED
Reproduction,
NOED
Reproduction,
NOED
Growth, LOED
Source:
Reference
[29]
[29]
[29]
[29]
[29]
[29]
[15]
Comments3
L; larval
mortality, pH 7.6,
body burden from
graph
L; egg mortality,
pH 6.3, body
burden from
graph
L; larval
deformation, pH
7.6, body burden
from graph
L; larval
mortality, pH 7.6,
body burden from
graph
L; egg mortality,
pH 7.6, body
burden from
graph
L; egg mortality,
pH 6.3, body
burden from
graph
L; duration = 22
months or 660
days
-------
Summary of Biological Effects Tissue Concentrations for Copper
Species: Concentration, Units in1:
Taxa Sediment Water Tissue (Sample Type)
44 mg/kg (kidney)4
480 mg/kg (liver)4
13 mg/kg (gill)4
44 mg/kg (kidney)4
480 mg/kg (liver)4
13 mg/kg (gill)4
44 mg/kg (kidney)4
480 mg/kg (liver)4
6 mg/kg (gill)4
12 mg/kg (kidney)4
Toxicity: Ability to Accumulate2:
Log Log
Effects BCF BAF BSAF
Growth, LOED
Growth, LOED
Mortality, LOED
Mortality, LOED
Mortality, LOED
Reproduction,
LOED
Reproduction,
LOED
Reproduction,
LOED
Growth, NOED
Growth, NOED
Source:
Reference
[15]
[15]
[15]
[15]
[15]
[15]
[15]
[15]
[15]
[15]
Comments3
L; duration = 22
months or 660
days
L; duration = 22
months or 660
days
L; duration = 22
months or 660
days
L; duration = 22
months or 660
days
L; duration = 22
months or 660
days
L; duration = 22
months or 660
days
L; duration = 22
months or 660
days
L; duration = 22
months or 660
days
L; duration = 22
months or 660
days
L; duration = 22
months or 660
days
-------
Summary of Biological Effects Tissue Concentrations for Copper
Species: Concentration, Units in1:
Taxa Sediment Water Tissue (Sample Type)
57 mg/kg (liver)4
6 mg/kg (gill)4
12 mg/kg (kidney)4
57 mg/kg (liver)4
6 mg/kg (gill)4
12 mg/kg (kidney)4
57 mg/kg (liver)4
Toxicity: Ability to Accumulate2:
Log Log
Effects BCF BAF BSAF
Growth, NOED
Mortality, NOED
Mortality, NOED
Mortality, NOED
Reproduction,
NOED
Reproduction,
NOED
Reproduction,
NOED
Source:
Reference
[15]
[15]
[15]
[15]
[15]
[15]
[15]
Comments3
L; duration = 22
months or 660
days
L; duration = 22
months or 660
days
L; duration = 22
months or 660
days
L; duration = 22
months or 660
days
L; duration = 22
months or 660
days
L; duration = 22
months or 660
days
L; duration = 22
months or 660
days
1 Concentration units based on wet weight unless otherwise noted.
2 BCF = bioconcentration factor, BAF = bioaccumulation factor, BSAF = biota-sediment accumulation factor.
L = laboratory study, spiked sediment, single chemical; F = field study, multiple chemical exposure; other unusual study conditions or observations noted.
This entry was excerpted directly from the Environmental Residue-Effects Database (ERED, www.wes.army.mil/el/ered, U.S. Army Corps of Engineers and U.S.
Environmental Protection Agency). The original publication was not reviewed, and the reader is strongly urged to consult the publication to confirm the information
presented here.
-------
BIOACCUMULATION SUMMARY COPPER
References
1. Weast handbook of chemistry andphysics, 68th edition, 1987-1988, B-88. (Cited in: USEPA. 1995.
Hazardous Substances Data Bank (HSDB). National Library of Medicine online (TOXNET). U.S.
Environmental Protection Agency, Office of Health and Environmental Assessment, Environmental
Criteria and Assessment Office, Cincinnati, OH. September.)
2. USEPA. 1995. Integrated Risk Information System (IRIS). National Library of Medicine online
(TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental
Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. September.
3. Woodward, D.F., W.G. Brumbaugh, A.J. DeLonay, E.E. Little, and C.E. Smith. 1994. Effects on
rainbow trout fry of a metals-contaminated diet of benthic invertebrates from the Clark Fork River,
Montana. Tran. Amer. Fish. Soc. 123:51-62.
4. Timmermans, K.R., E. Spijkerman, and M. Tonkes. 1992. Cadmium and zinc uptake by two
species of aquatic invertebrate predators from dietary and aqueous sources. Can. J. Fish. Aquat. Sci.
49: 655-662.
5. Bryan, G.W., and L.G. Hummerstone. 1971. Adaptation of the polychaete Nereis diversicolor to
estuarine sediments containing high concentrations of heavy metals. /. Mar. Biol. Ass. U.K. 51:845-
863.
6. Borgmann, U., W.P. Norwood, and C. Clarke. 1993. Accumulation, regulation and toxicity of
copper, zinc, lead and mercury in Hyalella azteca. Hydrobiologia 259:79-89.
7. Enserink, E.L., J.L. Mass-Diepeveen, and CJ. Van Leeuwen. 1991. Combined effects of metals:
An ecotoxicological evaluation. Water Res. 25:679-687.
8. Janssens De Bisthoven, L.G., K.R. Timmermans, and F. Ollevier. 1992. The concentration of
cadmium, lead, copper, and zinc in Chironomus gr. tummi larvae (Diptera, Chironomidae) with
deformed versus normal antennae. Hydrobiologia 239:141-149.
9. Krantzberg, G. 1994. Spatial and temporal variability in metal bioavailability and toxicity of
sediment from Hamilton Harbour, Lake Ontario. Environ. Toxicol. Chem. 13:1685-1698.
10. Ingersoll; C.G., W.G. Brumbaugh, FJ. Dwuer, and N. E. Kemble. 1994. Bioaccumulation of metals
by Hyalella azteca exposed to contaminated sediments from the Upper Clark Fork River, Montana.
Environ. Toxicol. Chem. 13:2013-2020.
11. Tessier, A., P.G.C. Campbell, J.C. Auclair, and M. Bisson. 1984. Relationships between the
partitioning of trace metals in sediments and their accumulation in the tissues of the freshwater
mollusc Elliptio complanata in a mining area. Can. J. Fish. Aquat. Sci. 41:1463-1472.
12. Di Toro, D.M., J.D. Mahony, D.J. Hansen, K.J. Scott, M.B. Hicks, S.M. Mayr, and M.S. Redmond.
1990. Toxicity of cadmium in sediments: The role of acid volatile sulfide. Environ. Toxicol. Chem.
9:1487-1502.
228
-------
BIOACCUMULATION SUMMARY COPPER
13. Rule J.H., and R.W. Alden III. 1996. Interactions of Cd and Cu in anaerobic estuarine sediments.
II. Bioavailability, body burdens and respiration effects as related to geochemical partitioning.
Environ. Toxicol Chem. 15:466-471.
14. Houkal, D., B. Rummel, and B. Shephard. 1996. Results of an in situ mussel bioassay in the Puget
Sound. Abstract, 17th Annual Meeting Society of Environmental Toxicology and Chemistry,
Washington, DC, November 17-21, 1996.
15. Benoit, D.A. 1975. Chronic effects of copper on survival; growth, and reproduction of the bluegill
(Lepomis macrochirus). Trans. Am. Fish. Soc. 104(2):353-358
16. Bonham, K., M. Zararullah, and L. Gedamu. 1987. The rainbow trout metailothioneins: Molecular
cloning and characterization of two distinct cDNA sequences. DNA 6:519-528.
17. Dixon, D.G.,and J.B. Sprague. 1981. Copper bioaccumulation and hepatoprotein synthesis during
acclimation to copper by juvenile rainbow trout. Aquat. Toxicol. 1:69-81.
18. Ericksson, S.P., and J.M. Weeks. 1994. Effects of copper and hypoxia on two populations of the
benthic amphipod Corophium volutator (Pallas). Aquat. Toxicol. 29:73-81
19. Evans, M.L. 1980. Copper accumulation in the crayfish (Orconectes rusticus). Bull. Environ.
Contain. Toxicol. 24:916-920.
20. Handy, R.D. 1992. The assessment of episodic metal pollution. I. Uses and limitations of tissue
contaminant analysis in rainbow trout (Oncorhynchus mykiss) after short waterborne exposure to
cadmium or copper. Arch. Environ. Contam. Toxicol. 22:74-81.
21. Hvilsom, M.M. 1983. Copper induced differential mortality in the mussel Mytilus edulis. Mar. Biol.
76:291-295.
22. Kay, S.H., W.T. Haller, and L.A. Garrard. 1984. Effects of heavy metals on water hyacinths
(Eichhornia crassipes (mart.) Solms). Aquat. Toxicol. 5:117-128.
23. Kosalwat, P., and A.W. Knight. 1987. Acute toxicity of aqueous and substrate bound copper to the
midge, Chironomus decorus. Arch. Environ. Contam. Toxicol. 16:275-282.
24. Kraak, M.H.S., M. Toussaint, E.A.J. Bleeker, and D. Lavy. 1993. Metal regulation in two species
of freshwater bivalves. In Ecotoxicology of metals in invertebrates, ed., R. Dallinger and P.S.
Rainbow, pp. 175-186. Society of Environmental Toxicology and Chemistry Special Pub. Ser.,
Pensacola, FL.
25. Kumaraguru, A.K., D. Selvi, and V.K. Venugopalan. 1980. Copper toxicity to an estuarine clam
(Meretrix casta). Bull. Environ. Contam. Toxicol. 24:853-857.
26. Martin, J.L.M. 1979. Schema of lethal action of copper on mussels. Bull. Environ. Contam. Toxicol.
21:808-814.
229
-------
BIOACCUMULATION SUMMARY COPPER
27. Mount, D.R., A.K. Earth, T.D.Garrison, K.A. Barten, and J.R. Hockett. 1994. Dietary and
waterborne exposure of rainbow trout (Oncorhynchus mykiss) to copper, cadmium, lead and zinc
using a live diet. Environ. Toxicol. Chem. 13(12):2031-2041.
28. Powell; M.I., K.N. White. 1990. Heavy metal accumulation by barnacles and its implications for
their use as biological monitors. Mar. Environ. Res. 30:91-118.
29. Stouthart, J.H.X., J.L.M. Haans, R.A.C. Lock, and S.E.W. Bonga. 1996. Effects of water pH on
copper toxicity to early life stages on the common carp (Cyprinus carpio). Environ. Toxicol. Chem.
15(3):376-383.
230
-------
BIOACCUMULATION SUMMARY
1,2,3,4,6,7,8-HeptaCDD
Chemical Category: POLYCHLORINATED DIBENZO-p-DIOXINS
Chemical Name (Common Synonyms):
1,2,3,4,6,7,8-HEPTACHLORODIBENZO-p-DIOXIN
CASRN: 35822-46-9
Chemical Characteristics
Solubility in Water: No data [1], 2.4 mg/L [2]
Log Kow: No data [4], 8.00 [2]
Half-Life: No data [2,3]
Log Koc: 7.86 L/kg organic carbon
Human Health
Oral RfD: No data [5]
Critical Effect: —
Oral Slope Factor: No data [5]
Confidence:
Carcinogenic Classification:
Wildlife
Partitioning Factors: Partitioning factors for 1,2,3,4,6,7,8-heptaCDD in wildlife were not found in the
studies reviewed.
Food Chain Multipliers: Limited information was found on specific biomagnification factors of
PCDDs and PCDFs through terrestrial wildlife. Due to the toxicity, high K,,w values, and highly persistent
nature of the PCDDs and PCDFs, they possess a high potential to bioaccumulate and biomagnify through
the food web. PCDDs and PCDFs have been identified in fish and wildlife throughout the global aquatic
and marine environments [6]. Studies conducted in Lake Ontario indicated that biomagnification of
2,3,7,8-tetrachlorodibenzo-p-dioxin (2,3,7,8-TCDD) appears to be significant between fish and fish-
eating birds but not between fish and their food. When calculated for older predaceous fish such as lake-
trout-eating young smelt, the biomagnification factor (BMF) can equal 3. The log BMP from ale wife
to herring gulls in Lake Ontario was 1.51 for 2,3,7,8-TCDD [7]. Log BMFs of 1.18 to 1.70 were
determined for mink fed 1,2,3,4,6,7,8-Hepta CDD in the diet [18].
EPA has developed risk-based concentrations of 2,3,7,8-TCDD in different media that present low and
high risk to fish, mammalian, and avian wildlife. These concentrations were developed based on toxic
effects of 2,3,7,8-TCDD and its propensity to bioaccumulate in fish, mammals, and birds.
231
-------
BIOACCUMULATION SUMMARY
1,2,3,4,6,7,8-HeptaCDD
Environmental Concentrations Associated With 2,3,7,8-TCDD Risk to Aquatic Life and Associated
Wildlife [8]
Organism
Fish Concentration
(Pg/g)
Sediment
Concentration
(pg/g dry wt.)
Water Concentration (pg/L)
POC=0.2
POC=1.0
Low Risk
Fish
Mammalian Wildlife
Avian Wildlife
50
0.7
6
60
2.5
21
0.6
0.008
0.07
3.1
0.04
0.35
High Risk to Sensitive Species
Fish
Mammalian Wildlife
Avian Wildlife
80
7
60
100
25
210
1.0
0.08
0.7
5
0.4
3.5
Note: POC - Paniculate organic carbon
Fish lipid of 8% and sediment organic carbon of 3% assumed where needed.
For risk to fish, BSAF of 0.3 used; for risk to wildlife, BSAF of 0.1 used.
Low risk concentrations are derived from no-effects thresholds for reproductive effects (mortality in embryos and
young) in sensitive species.
High risk concentrations are derived from TCDD doses expected to cause 50 to 100% mortality in embryos and
young of sensitive species.
Aquatic Organisms
Partitioning Factors: In one study, the BSAF for carp collected from a reservoir in central Wisconsin
was 0.0048. In a laboratory study, log BCFs for fathead minnow, rainbow trout, and goldfish exposed
to 1,2,3,4,6,7,8-HeptaCDD were 2.71, 3.15, and 4.28, respectively.
Food Chain Multipliers: No specific food chain multipliers were identified for 1,2,3,4,6,7,8-heptaCDD.
Food chain multiplier information was only available for 2,3,7,8-TCDD. Biomagnification of 2,3,7,8-
TCDD does not appear to be significant between fish and their prey. Limited data for the base of the
Lake Ontario lake trout food chain indicated little or no biomagnification between zooplankton and
forage fish. BMFs based on fish consuming invertebrate species are probably close to 1.0 because of
the 2,3,7,8-TCDD biotransformation by forage fish. BMFs greater than 1.0 may exist between some
zooplankton species and their prey due to the lack of 2,3,7,8-TCDD biotransformation in
invertebrates [8].
Toxicity/Bioaccumulation Assessment Profile
The polychlorinated dibenzo-p-dioxins (PCDDs) and polychlorinated dibenzofurans (PCDFs) each
consist of 75 isomers that differ in the number and position of attached chlorine atoms. The PCDDs and
PCDFs are polyhalogenated aromatic compounds and exhibit several properties common to this group
of compounds. These compounds tend to be highly lipophilic and the degree of lipophilicity is increased
with increasing ring chlorination [6]. In general, the PCDDs and PCDFs exhibit relative inertness to
acids, bases, oxidation, reduction, and heat, increasing in environmental persistence and chemical
232
-------
BIOACCUMULATION SUMMARY
1,2,3,4,6,7,8-HeptaCDD
stability with increasing chlorination [9,6]. Because of their lipophilic nature, the PCDDs and PCDFs
have been detected in fish, wildlife, and human adipose tissue, milk, and serum [6].
Each isomer has its own unique chemical and lexicological properties. The most toxic of the PCDD and
PCDF isomers is 2,3,7,8-TCDD, one of the 22 possible congeners of tetrachlorodibenzo-j?-dioxin [9].
Toxicity equivalency factors (TEFs) have been developed by EPA relating the toxicities of other PCDD
and PCDF isomers to that of 2,3,7,8-TCDD [10]. The biochemical mechanisms leading to the toxic
response resulting from exposure to PCDDs and PCDFs are not known in detail, but experimental data
suggest that an important role in the development of systemic toxicity resulting from exposure to these
chemicals is played by an intracellular protein, the Ah receptor. This receptor binds halogenated
polycyclic aromatic molecules, including PCDDs and PCDFs. In several mouse strains, the expression
of toxicity of 2,3,7,8-TCDD-related compounds, including cleft palate formation, liver damage, effects
on body weight gain, thymic involution, and chloracnegenic response, has been correlated with their
binding affinity for the Ah receptor, and with their ability to induce several enzyme systems [10].
Toxicity Equivalency Factors (TEF) for PCDD and PCDF Isomers [10]
Isomer
Total TetraCDD
2,3,7,8-TCDD
Other TCDDs
Total PentaCDDs
2,3,7,8-PentaCDDs
Other PentaCDDs
Total HexaCDDs
2,3,7,8-HexaCDDs
Other HexaCDDs
Total HeptaCDDs
2,3,7,8-HeptaCDDs
Other HeptaCDDs
Total TetraCDFs
2,3,7,8-TetraCDF
Other TetraCDFs
Total PentaCDFs
2,3,7,8-PentaCDFs
Other PentaCDFs
Total HexaCDFs
2,3,7,8-HexaCDFs
Other HexaCDFs
Total HeptaCDFs
2,3,7,8-HeptaCDFs
Other HeptaCDFs
TEF
1
1
0.01
0.5
0.5
0.005
0.04
0.04
0.0004
0.001
0.001
0.00001
0.1
0.1
0.001
0.1
0.1
0.001
0.01
0.01
0.0001
0.001
0.001
0.00001
233
-------
BIOACCUMULATION SUMMARY 1,2,3,4,6,7,8-HeptaCDD
In natural systems, PCDDs and PCDFs are typically associated with sediments, biota, and the organic
carbon fraction of ambient waters [8]. Congener-specific analyses have shown that the 2,3,7,8-
substituted PCDDs and PCDFs were the major compounds present in most sample extracts [6]. Results
from limited epidemiology studies are consistent with laboratory-derived threshold levels to 2,3,7,8-
TCDD impairment of reproduction in avian wildlife. Population declines in herring gulls (Larus
argentatus) on Lake Ontario during the early 1970s coincided with egg concentrations of 2,3,7,8-TCDD
and related chemicals expected to cause reproductive failure based on laboratory experiments (2,3,7,8-
TCDD concentrations in excess of 1,000 pg/g). Improvements in herring gull reproduction through the
mid-1980s were correlated with declining 2,3,7,8-TCDD concentrations in eggs and lake sediments [8].
Based on limited information on isomer-specific analysis from animals at different trophic levels, it
appears that at higher trophic levels, i.e., fish-eating birds and fish, there is a selection of the planar
congeners with the 2,3,7,8-substituted positions [11].
PCDDs and PCDFs are accumulated by aquatic organisms through exposure routes that are determined
by the habitat and physiology of each species. With log K,,w>5, exposure through ingestion of
contaminated food becomes an important route for uptake in comparison to respiration of water [8]. The
relative contributions of water, sediment, and food to uptake of 2,3,7,8-TCDD by lake trout in Lake
Ontario were examined by exposing yearling lake trout to Lake Ontario smelt and sediment from Lake
Ontario along with water at a 2,3,7,8-TCDD concentration simulated to be at equilibrium with the
sediments. Food ingestion was found to contribute approximately 75 percent of total 2,3,7,8-TCDD [8].
There have been a number of bioconcentration studies of 2,3,7,8-TCDD using model ecosystem and
single species exposure. Although there is variation in the actual BCF values, in general, the algae and
plants have the lowest BCF values, on the order of a few thousand. A log BCF value of 4.38 has been
reported for the snail Physa sp. Crustacea and insect larvae appear to have the next highest BCF values,
followed by several species of fish, with the highest log BCF value of 4.79 [11].
Exposure of juvenile rainbow trout to 2,3,7,8-TCDD and -TCDF in water for 28 days resulted in adverse
effects on survival, growth, and behavior at extremely low concentrations. A no-observed-effects
concentration (NOEC) for 2,3,7,8-TCDD could not be determined because the exposure to the lowest
dose of 0.038 ng/1 resulted in significant mortality [12]. A number of biological effects have been
reported in fish following exposure to 2,3,7,8-TCDD including enzyme induction, immunological
effects, wasting syndrome, dermatological effects, hepatic effects, hematological effects, developmental
effects, and cardiovascular effects [11].
234
-------
Summary of Biological Effects Tissue Concentrations for 1,2,3,4,6,7,8-HeptaCDD
Species:
Taxa
Fishes
Salmonids
Oncorhynchus
miikiss (Salmo
gairderni),
Rainbow trout
Oncorhynchus
mukiss (Salmo
gairderni),
Rainbow trout
Cypriniis carpio,
Carp
Concentration, Units in1: Toxicity: Ability to Accumulate2: Source:
Log Log
Sediment Water Tissue (Sample Type) Effects BCF BAF BSAF Reference Comments3
0.0031 [20] F
Exposure 3.15 [16] L
water ± 2.35
ll-55ng/L
0.000035 mg/kg Biochemical, [19] L; significant
(liver)4 LOED increase in liver
ethoxyresorufin
O-deethylase
(EROD)
2,190 pg/g5 27pg/g5 0.0048 [13] F; Petenwell
Reservoir, central
Wisconsin; BSAF
based on 8%
tissue lipid
content and 3.1%
sediment organic
carbon
-------
to
u>
o\
Summary of Biological Effects Tissue Concentrations for 1,2,3,4,6,7,8-HeptaCDD
Species:
Taxa
Concentration, Units in1:
Toxicity:
Ability to Accumulate2:
Source:
Log Log
Sediment Water Tissue (Sample Type) Effects BCF BAF BSAF Reference Comments3
Carassius auratus,
Goldfish
1.91/2.2 ng/g5
(whole body)
4.28
[15] L; fish were
exposed for 120
hr; exposure
water contained
fly ash extract;
concentrations
were measured in
water, but data
were not
presented
Pimephales
promelas,
Fathead minnow
Exposure
water
8-39 ng/L
2.71 ±
2.03
[16]
L
Platycephalus
caemlopiinctatiis
and Platycephalus
bassensis,
Flathead
Sillago bassensis,
School whiting
0.356 pg/g,
dw
558 pg/kg
0.356 pg/g,
dw
375 pg/kg
[14] F; unimpacted
coastal site;
surface sediment
composite; most
other dioxin
congeners
were below
detection.
Wildlife
Falco peregrinus,
Peregrine falcon
0.7 ng/g (eggs)
(n = 6)
11.4% eggshell
thinning
[17] F; Kola
Peninsula, Russia
-------
Summary of Biological Effects Tissue Concentrations for 1,2,3,4,6,7,8-HeptaCDD
Species: Concentration, Units in1: Toxicity: Ability to Accumulate2:
Log Log
Taxa Sediment Water Tissue (Sample Type) Effects BCF BAF BSAF
Mustela vison, Diet:
Mink 5pg/g5 1 15 pg/g5 (liver) NOAEL log BMP
= 1.18
7 pg/g5 330 pg/g5 (liver) LOAEL; log BMP
reduced kit = 1 .70
body weights
followed by
reduced
survival
6 pg/g5 290 pg/g5 (liver) Reduced kit log BMP
body weights = 1 .69
followed by
reduced
survival
13 pg/g5 380 pg/g5 (liver) Significant log BMP
decrease in =1 .66
number of live
kits whelped
per female
1 Concentration units based on wet weight unless otherwise noted.
2 BCF = bioconcentration factor, BAF = bioaccumulation factor, BSAF = biota-sediment accumulation factor.
T = 1 ahnratnrv ctiirlv cniVprl c^rlimpnt cinolp phpmiml1 P = fiplrl ctiirlv miiltinlf1 rhfmiral fvnriQiirf1' nthfr iimiQiial ctiirlv pnnrl
Source:
Reference Comments3
[18] L;BMF =
lipid-normalized
concentration
in the liver
divided by the
lipid-normalized
dietary
concentration
itinrw nr nh«prv9tinn« nnt^rl
4 This entry was excerpted directly from the Environmental Residue-Effects Database (ERED, www.wes.army.mil/el/ered, U.S. Army Corps of Engineers and U.S.
Environmental Protection Agency). The original publication was not reviewed, and the reader is strongly urged to consult the publication to confirm the information
presented here.
5 Not clear from reference if concentration is based on wet or dry weight.
-------
BIOACCUMULATION SUMMARY 1,2,3,4,6,7,8-HeptaCDD
References
1. USEPA. 1996. Hazardous Substances Data Bank (HSDB). National Library of Medicine
online (TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental
Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. February.
2. MacKay, D.M., W.Y. Shiw, and K.C. Ma. 1992. Illustrated handbook of physical-chemical
properties and environmental fate for organic chemicals. Vol. n, Polynuclear aromatic
hydrocarbons, poly chlorinated dioxins and dibenzofurans. Lewis Publishers, Boca Raton, FL.
3. USEPA. 1989. Chemical fate rate constants for SARA section 313 chemicals and Superfund
Health Evaluation Manual chemicals. Prepared by Chemical Hazard Assessment Division,
Syracuse Research Corporation, for U.S. Environmental Protection Agency, Office of Toxic
Substances, Exposure Evaluation Division, Washington, DC, and Environmental Criteria and
Assessment Office, Cincinnati, OH. August 11.
4. Karickhoff, S.W., and J.M. Long. 1995. Internal report on summary of measured, calculated
and recommended log Kow values. Draft. Prepared by U.S. Environmental Protection Agency,
Office of Research and Development, Environmental Research Laboratory-Athens, for E.
Southerland, Office of Water, Office of Science and Technology, Standards and Applied Science
Division, Washington, DC. April 10.
5. USEPA. 1996. Integrated Risk Information System (IRIS). National Library of Medicine online
(TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental
Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. September.
6. Safe, S. 1990. Polychlorinated biphenyls (PCBs), dibenzo-p-dioxins (PCDDs), dibenzofurans
(PCDFs), and related compounds: Environmental and mechanistic considerations which support
the development of toxicity equivalency factors (TEF). Crit. Rev. Toxicol. 21:51-88.
7. Braune, B.M., and RJ. Norstrom. 1989. Dynamics of organochlorine compounds in herring
gulls: HI. Tissue distribution and bioaccumulation in Lake Ontario gulls. Environ. Toxicol.
Chem. 8:957-968.
8. USEPA. 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. U.S. Environmental
Protection Agency, Office of Research and Development, Washington, DC.
9. Eisler, R. 1986. Dioxin hazards to fish, wildlife, and invertebrates: A synoptic review. U.S.
Fish Wildl. Ser. Biol. Rep. 85 (1.8). 37 pp.
10. USEPA. 1989. Interim procedures for estimating risks associated with exposure to mixtures of
chlorinated dibenzo-p-dioxins and -dibenzofurans (CDDs and CDFs) and 1989 update.
EPA/625/3-89/016. U.S. Environmental Protection Agency, Risk Assessment Forum,
Washington, DC.
238
-------
BIOACCUMULATION SUMMARY 1,2,3,4,6,7,8-HeptaCDD
11. Cooper, K.R. 1989. Effects of polychlorinated dibenzo-p-dioxins and polychlorinated
dibenzofurans on aquatic organisms. Rev. Aquat. Set 1:227-242.
12. Mehrle, P.M., D.R. Buckler, E.E. Little, L.M. Smith, J.D. Petty, P.M. Peterman, D.L. Stalling,
G.M. DeGraeve, JJ. Coyle, and WJ. Adams. 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.
13. Kuehl, D.W., P.M. Cook, A.R. Batterman, D. Lothenbach, and B.C. Butterworth. 1987.
Bioavailability of polychlorinated dibenzo-p-dioxins and dibenzofurans from contaminated
Wisconsin River sediment to carp. Chemosphere 16(4):667-679.
14. Mosse, P.R.L., and D. Haynes. 1993. Dioxin and furan concentrations in uncontaminated
waters, sediments and biota of the Ninety Mile Beach, Bass Strait, Australia. Marine Pollut. Bull.
26(8):465-468.
15. Sijm, D.T.H.M., H. Wever, and A. Opperhuizen. 1993. Congener-specific biotransformation
and bioaccumulation of PCDDs and PCDFs from fly ash in fish. Environ. Tax. Chem.
12:1895-1907.
16. 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 14(6/7):829-833.
17. Henny, C.J., S.A. Ganusevich, F.P. Ward, and T.R. Schwartz. 1994. Organochlorine pesticides,
chlorinated dioxins and furans, and PCBs in peregrine falcon Falco peregrinus eggs from the
Kola Penninsula, Russia. In Raptor conservation today, ed. B.U. Meyburg and R.D. Chancellor,
pp. 739-749. WWGPB/The Pica Press.
18. Tillitt, D.E., R.W. Gale, J.C. Meadows, J.L. Zajicek, P.M. Peterman, S.N. Heaton, P.O. Jones,
S.J. Bursian, TJ. Kubiak, J/P. Giesy, and RJ. Aulerich. 1996. Dietary exposure of mink to carp
from Saginaw Bay. 3. Characterization of dietary exposure to planar halogenated hydrocarbons,
dioxin equivalents, and biomagnification. Environ. Sci. Technol. 30:283-291.
19. Parrott, J.L., P.V. Hodson, M.R. Servos, S.L. Huestis, and G.D. Dixon. 1995. Relative potency
of polychlorinated dibenzo-p-dioxins and dibenzofurans for inducing mixed-function oxygenase
activity in rainbow trout. Environ. Toxicol. Chem. 14(6):1041-1050.
20. USEPA. 1995. Great Lakes Water Quality Initiative Technical Support Document for the
procedure to determine bioaccumulation factors. EPA-820-B-95-005. U.S. Environmental
Protection Agency, Office of Water, Washington, DC.
239
-------
240
-------
BIOACCUMULATION SUMMARY 1,2,3,4,7,8-HexaCDD
Chemical Category: POLYCHLORINATED DIBENZO-p-DIOXINS
Chemical Name (Common Synonyms): CASRN: 39227-28-6
1,2,3,4,7,8-HEXACHLORODIBENZO-p-DIOXIN
Chemical Characteristics
Solubility in Water: No data [1], Half-Life: No data [2,3]
8.25 xlO-6mg/L [1,2]
Log Kow: No data [4], 7.70 [2] Log Koc: 7.57 L/kg organic carbon
Human Health
Oral RfD: No data [5] Confidence: —
Critical Effect: —
Oral Slope Factor (Reference): No data [5] Carcinogenic Classification: —
Wildlife
Partitioning Factors: Partitioning factors for 1,2,3,4,7,8-hexaCDD in wildlife were not found in the
studies reviewed.
Food Chain Multipliers: Limited information was found reporting on specific biomagnification factors
of PCDDs and PCDFs through terrestrial wildlife. Due to the toxicity, high K,,w values, and highly
persistent nature of the PCDDs and PCDFs, they possess a high potential to bioaccumulate and
biomagnify through the food web. PCDDs and PCDFs have been identified in fish and wildlife
throughout the global aquatic and marine environments [6]. Studies conducted in Lake Ontario indicated
that biomagnification of 2,3,7,8-tetrachlorodibenzo-p-dioxin (2,3,7,8-TCDD) appears to be significant
between fish and fish-eating birds but not between fish and their food. When calculated for older
predaceous fish such as lake-trout-eating young smelt, the biomagnification factor (BMF) can equal 3.
The BMF from alewife to herring gulls in Lake Ontario was 32 for 2,3,7,8-TCDD [7]. A log BMF of
0.97 was reported for mink exposed to 1,2,3,4,7,8-hexaCDD in the diet. [14].
EPA has developed risk-based concentrations of 2,3,7,8-TCDD in different media that present low and
high risk to fish, mammalian, and avian wildlife. These concentrations were developed based on toxic
effects of 2,3,7,8-TCDD and its propensity to bioaccumulate in fish, mammals, and birds.
241
-------
BIOACCUMULATION SUMMARY
1,2,3,4,7,8-HexaCDD
Environmental Concentrations Associated With 2,3,7,8-TCDD Risk to Aquatic Life and Associated
Wildlife [8]
Organism
Fish Concentration
(Pg/g)
Sediment
Concentration
(pg/g dry wt.)
Water Concentration (pg/L)
POC=0.2
POC=1.0
Low Risk
Fish
Mammalian Wildlife
Avian Wildlife
50
0.7
6
60
2.5
21
0.6
0.008
0.07
3.1
0.04
0.35
High Risk to Sensitive Species
Fish
Mammalian Wildlife
Avian Wildlife
80
7
60
100
25
210
1.0
0.08
0.7
5
0.4
3.5
Note: POC - Paniculate organic carbon
Fish lipid of 8% and sediment organic carbon of 3% assumed where needed.
For risk to fish, BSAF of 0.3 used; for risk to wildlife, BSAF of 0.1 used.
Low risk concentrations are derived from no-effects thresholds for reproductive effects (mortality in embryos and
young) in sensitive species.
High risk concentrations are derived from TCDD doses expected to cause 50 to 100% mortality in embryos and
young of sensitive species.
Aquatic Organisms
Partitioning Factors: In a laboratory study, log BCFs for rainbow trout and fathead minnow exposed
to 1,2,3,4,7,8-HexaCDD were 3.73 and 4.00, respectively.
Food Chain Multipliers: No specific food chain multipliers were identified for 1,2,3,4,7,8-hexaCDD.
Food chain multiplier information was only available for 2,3,7,8-TCDD. Biomagnification of 2,3,7,8-
TCDD does not appear to be significant between fish and their prey. Limited data for the base of the
Lake Ontario lake trout food chain indicated little or no biomagnification between zooplankton and
forage fish. BMFs based on fish consuming invertebrate species are probably close to 1.0 because of the
2,3,7,8-TCDD biotransformation by forage fish. BMFs greater than 1.0 may exist between some
zooplankton species and their prey due to the lack of 2,3,7,8-TCDD biotransformation in invertebrates
[8].
Toxicity/Bioaccumulation Assessment Profile
The polychlorinated dibenzo-p-dioxins (PCDDs) and polychlorinated dibenzofurans (PCDFs) each
consist of 75 isomers that differ in the number and position of attached chlorine atoms. The PCDDs and
PCDFs are polyhalogenated aromatic compounds and exhibit several properties common to this group
of compounds. These compounds tend to be highly lipophilic and the degree of lipophilicity is increased
with increasing ring chlorination [6]. In general, the PCDDs and PCDFs exhibit relative inertness to
acids, bases, oxidation, reduction, and heat, increasing in environmental persistence and chemical
242
-------
BIOACCUMULATION SUMMARY
1,2,3,4,7,8-HexaCDD
stability with increasing chlorination [9,6]. Because of their lipophilic nature, the PCDDs and PCDFs
have been detected in fish, wildlife, and human adipose tissue, milk, and serum [6].
Each isomer has its own unique chemical and lexicological properties. The most toxic of the PCDD and
PCDF isomers is 2,3,7,8-TCDD, one of the 22 possible congeners of tetrachlorodibenzo-j?-dioxin [10].
Toxicity equivalency factors (TEFs) have been developed by EPA relating the toxicities of other PCDD
and PCDF isomers to that of 2,3,7,8-TCDD [9]. The biochemical mechanisms leading to the toxic
response resulting from exposure to PCDDs and PCDFs are not known in detail, but experimental data
suggest that an important role in the development of systemic toxicity resulting from exposure to these
chemicals is played by an intracellular protein, the Ah receptor. This receptor binds halogenated
polycyclic aromatic molecules, including PCDDs and PCDFs. In several mouse strains, the expression
of toxicity of 2,3,7,8-TCDD-related compounds, including cleft palate formation, liver damage, effects
on body weight gain, thymic involution, and chloracnegenic response, has been correlated with their
binding affinity for the Ah receptor, and with their ability to induce several enzyme systems [10].
Toxicity Equivalency Factors (TEF) for PCDD and PCDF Isomers [10]
Isomer
Total TetraCDD
2,3,7,8-TCDD
Other TCDDs
Total PentaCDDs
2,3,7,8-PentaCDDs
Other PentaCDDs
Total HexaCDDs
2,3,7,8-HexaCDDs
Other HexaCDDs
Total HeptaCDDs
2,3,7,8-HeptaCDDs
Other HeptaCDDs
Total TetraCDFs
2,3,7,8-TetraCDF
Other TetraCDFs
Total PentaCDFs
2,3,7,8-PentaCDFs
Other PentaCDFs
Total HexaCDFs
2,3,7,8-HexaCDFs
Other HexaCDFs
Total HeptaCDFs
2,3,7,8-HeptaCDFs
Other HeptaCDFs
TEF
1
1
0.01
0.5
0.5
0.005
0.04
0.04
0.0004
0.001
0.001
0.00001
0.1
0.1
0.001
0.1
0.1
0.001
0.01
0.01
0.0001
0.001
0.001
0.00001
243
-------
BIOACCUMULATION SUMMARY 1,2,3,4,7,8-HexaCDD
In natural systems, PCDDs and PCDFs are typically associated with sediments, biota, and the organic
carbon fraction of ambient waters [7]. Congener-specific analyses have shown that the 2,3,7,8-substituted
PCDDs and PCDFs were the major compounds present in most sample extracts [6]. Results from limited
epidemiology studies are consistent with laboratory-derived threshold levels to 2,3,7,8-TCDD
impairment of reproduction in avian wildlife. Population declines in herring gulls (Larus argentatus)
on Lake Ontario during the early 1970s coincided with egg concentrations of 2,3,7,8-TCDD and related
chemicals expected to cause reproductive failure based on laboratory experiments (2,3,7,8-TCDD
concentrations in excess of 1,000 pg/g). Improvements in herring gull reproduction through the mid-
1980s were correlated with declining 2,3,7,8-TCDD concentrations in eggs and lake sediments [8].
Based on limited information on isomer-specific analysis from animals at different trophic levels, it
appears that at higher trophic levels, i.e., fish-eating birds and fish, there is a selection of the planar
congeners with the 2,3,7,8-substituted positions [11].
PCDDs and PCDFs are accumulated by aquatic organisms through exposure routes that are determined
by the habitat and physiology of each species. With log K,,w>5, exposure through ingestion of
contaminated food becomes an important route for uptake in comparison to respiration of water [8]. The
relative contributions of water, sediment, and food to uptake of 2,3,7,8-TCDD by lake trout in Lake
Ontario were examined by exposing yearling lake trout to Lake Ontario smelt and sediment from Lake
Ontario along with water at a 2,3,7,8-TCDD concentration simulated to be at equilibrium with the
sediments. Food ingestion was found to contribute approximately 75 percent of total 2,3,7,8-TCDD [8].
There have been a number of bioconcentration studies of 2,3,7,8-TCDD using model ecosystem and
single species exposure. Although there is variation in the actual BCF values, in general, the algae and
plants have the lowest BCF values, on the order of a few thousand. A log BCF value of 4.38 has been
reported for the snail Physa sp. Crustacea and insect larvae appear to have the next highest BCF values,
followed by several species of fish, with the highest log BCF value of 4.79 [11].
Exposure of juvenile rainbow trout to 2,3,7,8-TCDD and -TCDF in water for 28 days resulted in adverse
effects on survival, growth, and behavior at extremely low concentrations. A no-observed-effects
concentration (NOEC) for 2,3,7,8-TCDD could not be determined because the exposure to the lowest
dose of 0.038 ng/1 resulted in significant mortality [12]. A number of biological effects have been
reported in fish following exposure to 2,3,7,8-TCDD including enzyme induction, immunological
effects, wasting syndrome, dermatological effects, hepatic effects, hematological effects, developmental
effects, and cardiovascular effects [11].
244
-------
Summary of Biological Effects Tissue Concentrations for 1,2,3,4,7,8-HexaCDD
Species:
Taxa
Fishes
Oncorhynchus
miikiss (Salmo
gairderni),
Rainbow trout
Oncorhynchus
mukiss,
Rainbow trout
Concentration, Units in1: Toxicity:
Sediment Water Tissue (Sample Type) Effects
Exposure
water
10-47 ng/L
0.0000395 mg/kg Biochemical,
(liver)4 LOED
Ability to Accumulate2: Source:
Log Log
BCF BAF BSAF Reference Comments3
3.73 [11] L
[15] L; significant
increase in liver
ethoxyresorufin
O-deethylase
(EROD)
Pimephales
promelas,
Fathead minnow
Exposure
water
10-47 ng/L
4.00
[11]
Wildlife
Falco peregrinits,
Peregrine falcon
3.3 ng/g (eggs) (n = 6)
11.4% eggshell
thinning
[13] F; Kola Peninsula,
Russia
-------
Summary of Biological Effects Tissue Concentrations for 1,2,3,4,7,8-HexaCDD
Species: Concentration, Units in1:
Taxa Sediment Water
Mustela vison, Diet:
Mink 2 pg/g5
1 Pg/g5
3 Pg/g5
Tissue (Sample Type)
6 pg/g5 (liver)
77 pg/g5 (liver)
15 pg/g5 (liver)
1 Concentration units based on wet weight unless otherwise noted.
2 BCF = bioconcentration factor, BAF = bioaccumulation factor, BSAF =
3 L = laboratory study, spiked sediment, single chemical; F = field study,
^ Thic f»ntri7 \x/9c fYpfrntfrl rHr^rtl-u frnm thf» THniHrnnm^nt^l Rfcirhif-TH ffi
Toxicity: Ability
Log
Effects BCF
LOAEL; reduced
kit body weights
followed by
reduced survival
Reduced kit body
weights followed
by reduced survival
Significant
decrease in number
of live kits whelped
per female
to Accumulate2: Source:
Log
BAF BSAF Reference
[14]
No
BMP
reported
No
BMP
reported
Log
BMF =
0.97
= biota-sediment accumulation factor.
multiple chemical exposure; other unusual study conditions or obi
^rtc PiQt^h^cf1 ^THPTHPI w/w/w/ w/i^c 9rrm7 mil /f^l/^r^rl TT *\ Arrm? f^nr
Comments3
L; BMP =
biomagnification
factor = v/vd
V[ = lipid-
normalized tissue
concentration,
vd = lipid-
normalized dietary
concentration.
nervations noted.
•nc nf THfminf^rc 9nH TT *\
Pnvironmental Protection Agency). The original publication was not reviewed, and the reader is strongly urged to consult the publication to confirm the information
presented here.
Not clear from reference if concentration is based on wet or dry weight.
-------
BIOACCUMULATION SUMMARY 1,2,3,4,7,8-HexaCDD
References
1. USEPA. 1996. Hazardous Substances Data Bank (HSDB). National Library of Medicine online
(TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental
Assessment, Environmental Criteria and Assessment Office, Cinncinati, OH. February.
2. MacKay, D.M., W.Y. Shiw, and K.C. Ma. 1992. Illustrated handbook of physical-chemical
properties and environmental fate for organic chemicals. Vol. n, Polynuclear aromatic
hydrocarbons, polychlorinated dioxins and dibenzofurans. Lewis Publishers, Boca Raton, FL.
3. USEPA. 1989. Chemical fate rate constants for SARA section 313 chemicals and Superfund
Health Evaluation Manual chemicals. Prepared by Chemical Hazard Assessment Division,
Syracuse Research Corporation, for U.S. Environmental Protection Agency, Office of Toxic
Substances, Exposure Evaluation Division, Washington, DC, and Environmental Criteria and
Assessment Office, Cincinnati, OH. August 11.
4. Karickhoff, S.W., and J.M. Long. 1995. Internal report on summary of measured, calculated and
recommended log Kow values. Draft. Prepared by U.S. Environmental Protection Agency, Office
of Research and Development, Environmental Research Laboratory-Athens, for E. Southerland,
Office of Water, Office of Science and Technology, Standards and Applied Science Division,
Washington, DC. April 10.
5. USEPA. 1996. Integrated Risk Information System (IRIS). National Library of Medicine online
(TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental
Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. September.
6. Safe, S. 1990. Polychlorinated biphenyls (PCBs), dibenzo-j?-dioxins (PCDDs), dibenzofurans
(PCDFs), and related compounds: Environmental and mechanistic considerations which support the
development of toxicity equivalency factors (TEF). Crit. Rev. Toxicol. 21:51-88.
7. Braune, B.M., and RJ. Norstrom. 1989. Dynamics of organochlorine compounds in herring gulls:
HI. Tissue distribution and bioaccumulation in Lake Ontario gulls. Environ. Toxicol. Chem. 8:957-
968.
8. USEPA. 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. U.S. Environmental
Protection Agency, Office of Research and Development, Washington, DC.
9. Eisler, R. 1986. Dioxin hazards to fish, wildlife, and invertebrates: A synoptic review. U.S. Fish
Wildl. Serv. Biol. Rep. 85(1.8). 37pp.
10. USEPA. 1989. Interim procedures for estimating risks associated with exposure to mixtures of
chlorinated dibenzo-p-dioxins and dibenzofurans (CDDs and CDFs) and 1989 update. EPA/625/3-
89/016. U.S. Environmental Protection Agency, Risk Assessment Forum, Washington, DC.
11. Cooper, K.R. 1989. Effects of polychlorinated dibenzo-p-dioxins and polychlorinated
dibenzofurans on aquatic organisms. Rev. Aquat. Sci. 1:227-242.
247
-------
BIOACCUMULATION SUMMARY 1,2,3,4,7,8-HexaCDD
12. Mehrle, P.M., D.R. Buckler, E.E. Little, L.M. Smith, J.D. Petty, P.M. Peterman, D.L. StaUing, G.M.
DeGraeve, JJ. Coyle, and WJ. Adams. 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.
13. Henny, C.J., S.A. Ganusevich, P.P. Ward, and T.R. Schwartz. 1994. Organochlorine pesticides,
chlorinated dioxins and furans, and PCBs in peregrine falcon Falco peregrinus eggs from the Kola
Penninsula, Russia. In Raptor conservation today, ed. B.U. Meyburg and R.D. Chancellor, pp. 739-
749. WWGPB/The Pica Press.
14. Tillitt, D.E., R.W. Gale, J.C. Meadows, J.L. Zajicek, P.M. Peterman, S.N. Heaton, P.O. Jones, S.J.
Bursian, TJ. Kubiak, J/P. Giesy, and RJ. Aulerich. 1996. Dietary exposure of mink to carp from
Saginaw Bay. 3. Characterization of dietary exposure to planar halogenated hydrocarbons, dioxin
equivalents, and biomagnification. Environ. Sci. Technol. 30:283-291.
15. Parrott, J.L., P.V. Hodson, M.R. Servos, S.L. Huestis, and G.D. Dixon. 1995. Relative potency of
polychlorinated dibenzo-p-dioxins and dibenzofurans for inducing mixed-function oxygenase
activity in rainbow trout. Environ. Toxicol. Chem. 14(6):1041-1050.
16. USEPA. 1995. Great Lakes Water Quality Initiative technical support document for the procedure
to determine bioaccumulation factors. EPA-820-B-95-005. U.S. Environmental Protection Agency,
Office of Water, Washington, DC.
248
-------
BIOACCUMULATION SUMMARY 1,2,3,6,7,8-HexaCDD
Chemical Category: POLYCHLORINATED DIBENZO-p-DIOXINS
Chemical Name (Common Synonyms): CASRN: 57653-85-7
1,2,3,6,7,8-HEXACHLORODIBENZO-p-DIOXIN
Chemical Characteristics
Solubility in Water: No data [1,2] Half-Life: No data [2,3]
Log Kow: No data [2,4] Log Koc: —
Human Health
Oral RfD: No data [5] Confidence: —
Critical Effect: Hepatic tumors in mice and rats
Oral Slope Factor: 6.2 x 10+3 per (mg/kg)/day [5] Carcinogenic Classification: B2 [5]
Wildlife
Partitioning Factors: Partitioning factors for 1,2,3,6,7,8-hexaCDD in wildlife were not found in the
studies reviewed.
Food Chain Multipliers: Limited information was found reporting on specific biomagnification factors
of PCDDs and PCDFs through terrestrial wildlife. Due to the toxicity, high Kow values, and highly
persistent nature of the PCDDs and PCDFs, they possess a high potential to bioaccumulate and
biomagnify through the food web. PCDDs and PCDFs have been identified in fish and wildlife
throughout the global aquatic and marine environments [6]. Studies conducted in Lake Ontario indicated
that biomagnification of 2,3,7,8-tetrachlorodibenzo-p-dioxin (2,3,7,8-TCDD) appears to be significant
between fish and fish-eating birds but not between fish and their food. When calculated for older
predaceous fish such as lake-trout-eating young smelt, the biomagnification factor (BMF) can equal 3.
The BMF from alewife to herring gulls in Lake Ontario was 32 for 2,3,7,8-TCDD [7]. Log BMFs of 1.42
and 1.43 were reported for mink exposed to 1,2,3,6,7,8-hexaCDD in the diet [18].
EPA has developed risk-based concentrations of 2,3,7,8-TCDD in different media that present low and
high risk to fish, mammalian, and avian wildlife. These concentrations were developed based on toxic
effects of 2,3,7,8-TCDD and its propensity to bioaccumulate in fish, mammals, and birds.
249
-------
BIOACCUMULATION SUMMARY
1,2,3,6,7,8-HexaCDD
Environmental Concentrations Associated With 2,3,7,8-TCDD Risk to Aquatic Life and Associated
Wildlife [8]
Organism
Fish Concentration
(Pg/g)
Sediment
Concentration
(pg/g dry wt.)
Water Concentration (pg/L)
POC=0.2
POC=1.0
Low Risk
Fish
Mammalian Wildlife
Avian Wildlife
50
0.7
6
60
2.5
21
0.6
0.008
0.07
3.1
0.04
0.35
High Risk to Sensitive Species
Fish
Mammalian Wildlife
Avian Wildlife
80
7
60
100
25
210
1.0
0.08
0.7
5
0.4
3.5
Note: POC - Paniculate organic carbon
Fish lipid of 8% and sediment organic carbon of 3% assumed where needed.
For risk to fish, BSAF of 0.3 used; for risk to wildlife, BSAF of 0.1 used.
Low risk concentrations are derived from no-effects thresholds for reproductive effects (mortality in embryos and
young) in sensitive species.
High risk concentrations are derived from TCDD doses expected to cause 50 to 100% mortality in embryos and
young of sensitive species.
Aquatic Organisms
Partitioning Factors: In one study, the BSAF for carp collected from a reservoir in central Wisconsin
was 0.035. The log BCF for goldfish during a laboratory exposure for 120 hours was 4.61.
Food Chain Multipliers: No specific food chain multipliers were identified for 1,2,3,6,7,8-hexaCDD.
Food chain multiplier information was only available for 2,3,7,8-TCDD. Biomagnification of 2,3,7,8-
TCDD does not appear to be significant between fish and their prey. Limited data for the base of the
Lake Ontario lake trout food chain indicated little or no biomagnification between zooplankton and
forage fish. BMFs based on fish consuming invertebrate species are probably close to 1.0 because of the
2,3,7,8-TCDD biotansformation by forage fish. BMFs greater than 1.0 may exist between some
zooplankton species and their prey due to the lack of 2,3,7,8-TCDD biotransformation in
invertebrates[8].
Toxicity/Bioaccumulation Assessment Profile
The polychlorinated dibenzo-p-dioxins (PCDDs) and polychlorinated dibenzofurans (PCDFs) each
consist of 75 isomers that differ in the number and position of attached chlorine atoms. The PCDDs and
PCDFs are polyhalogenated aromatic compounds and exhibit several properties common to this group
of compounds. These compounds tend to be highly lipophilic and the degree of lipophilicity is increased
with increasing ring chlorination [6]. In general, the PCDDs and PCDFs exhibit relative inertness to
acids, bases, oxidation, reduction, and heat, increasing in environmental persistence and chemical
250
-------
BIOACCUMULATION SUMMARY
1,2,3,6,7,8-HexaCDD
stability with increasing chlorination [9,6]. Because of their lipophilic nature, the PCDDs and PCDFs
have been detected in fish, wildlife, and human adipose tissue, milk, and serum [6].
Each isomer has its own unique chemical and lexicological properties. The most toxic of the PCDD and
PCDF isomers is 2,3,7,8 TCDD, one of the 22 possible congeners of tetrachlorodibenzo-j?-dioxin [9].
Toxicity equivalency factors (TEFs) have been developed by EPA relating the toxicities of other PCDD
and PCDF isomers to that of 2,3,7,8-TCDD [10]. The biochemical mechanisms leading to the toxic
response resulting from exposure to PCDDs and PCDFs are not known in detail, but experimental data
suggest that an important role in the development of systemic toxicity resulting from exposure to these
chemicals is played by an intracellular protein, the Ah receptor. This receptor binds halogenated
polycyclic aromatic molecules, including PCDDs and PCDFs. In several mouse strains, the expression
of toxicity of 2,3,7,8-TCDD-related compounds, including cleft palate formation, liver damage, effects
on body weight gain, thymic involution, and chloracnegenic response, has been correlated with their
binding affinity for the Ah receptor, and with their ability to induce several enzyme systems [10].
Toxicity Equivalency Factors (TEF) for PCDD and PCDF Isomers [10]
Isomer
Total TetraCDD
2,3,7,8-TCDD
Other TCDDs
Total PentaCDDs
2,3,7,8-PentaCDDs
Other PentaCDDs
Total HexaCDDs
2,3,7,8-HexaCDDs
Other HexaCDDs
Total HeptaCDDs
2,3,7,8-HeptaCDDs
Other HeptaCDDs
Total TetraCDFs
2,3,7,8-TetraCDF
Other TetraCDFs
Total PentaCDFs
2,3,7,8-PentaCDFs
Other PentaCDFs
Total HexaCDFs
2,3,7,8-HexaCDFs
Other HexaCDFs
Total HeptaCDFs
2,3,7,8-HeptaCDFs
Other HeptaCDFs
TEF
1
1
0.01
0.5
0.5
0.005
0.04
0.04
0.0004
0.001
0.001
0.00001
0.1
0.1
0.001
0.1
0.1
0.001
0.01
0.01
0.0001
0.001
0.001
0.00001
251
-------
BIOACCUMULATION SUMMARY 1,2,3,6,7,8-HexaCDD
In natural systems, PCDDs and PCDFs are typically associated with sediments, biota, and the organic
carbon fraction of ambient waters [7]. Congener-specific analyses have shown that the 2,3,7,8-
substituted PCDDs and PCDFs were the major compounds present in most sample extracts [6]. Results
from limited epidemiology studies are consistent with laboratory-derived threshold levels to 2,3,7,8-
TCDD impairment of reproduction in avian wildlife. Population declines in herring gulls (Larus
argentatus) on Lake Ontario during the early 1970s coincided with egg concentrations of 2,3,7,8-TCDD
and related chemicals expected to cause reproductive failure based on laboratory experiments (2,3,7,8-
TCDD concentrations in excess of 1,000 pg/g). Improvements in herring gull reproduction through the
mid-1980s were correlated with declining 2,3,7,8-TCDD concentrations in eggs and lake sediments [8].
Based on limited information on isomer-specific analysis from animals at different trophic levels, it
appears that at higher trophic levels, i.e., fish-eating birds and fish, there is a selection of the planar
congeners with the 2,3,7,8-substituted positions [11].
PCDDs and PCDFs are accumulated by aquatic organisms through exposure routes that are determined
by the habitat and physiology of each species. With log K^S, exposure through ingestion of
contaminated food becomes an important route for uptake in comparison to respiration of water [8]. The
relative contributions of water, sediment, and food to uptake of 2,3,7,8-TCDD by lake trout in Lake
Ontario were examined by exposing yearling lake trout to Lake Ontario smelt and sediment from Lake
Ontario along with water at a 2,3,7,8-TCDD concentration simulated to be at equilibrium with the
sediments. Food ingestion was found to contribute approximately 75 percent of total 2,3,7,8-TCDD [8].
There have been a number of bioconcentration studies of 2,3,7,8-TCDD using model ecosystem and
single species exposure. Although there is variation in the actual BCF values, in general, the algae and
plants have the lowest BCF values, on the order of a few thousand. A log value of 4.38 has been
reported for the snail Physa sp. Crustacea and insect larvae appear to have the next highest BCF values,
followed by several species of fish, with the highest log BCF value of 4.79 [11].
Exposure of juvenile rainbow trout to 2,3,7,8-TCDD and -TCDF in water for 28 days resulted in adverse
effects on survival, growth, and behavior at extremely low concentrations. A no-observed-effects
concentration (NOEC) for 2,3,7,8-TCDD could not be determined because the exposure to the lowest
dose of 0.038 ng/1 resulted in significant mortality [12]. A number of biological effects have been
reported in fish following exposure to 2,3,7,8-TCDD including enzyme induction, immunological
effects, wasting syndrome, dermatological effects, hepatic effects, hematological effects, developmental
effects, and cardiovascular effects [11].
252
-------
Summary of Biological Effects Tissue Concentrations for 1,2,3,6,7,8-HexaCDD
Species:
Taxa
Concentration, Units in1:
Toxicity:
Ability to Accumulate2:
Source:
Log Log
Sediment Water Tissue (Sample Type) Effects BCF BAF BSAF Reference Comments3
Fishes
Carassius auratus,
Goldfish
0.79 ng/g4
(whole body)
4.61
[14] L; fish were exposed
for 120 hr; exposure
water contained fly
ash extract; concen-
trations were
measured in water,
but data were not
presented
Cypriniis carpio, 180pg/g4
Carp
16pg/g4
0.035 [13]
F; Petenwell
Reservoir, central
Wisconsin; BSAF
based on 8% tissue
lipid content and
3.1% sediment
organic carbon
Salmonids
0.0073 [19]
-------
Summary of Biological Effects Tissue Concentrations for 1,2,3,6,7,8-HexaCDD
Species:
Taxa
Wildlife
Falco peregrinus,
Peregrine falcon
Haliaeetus
leiicocephaliis,
Bald eagle
chicks
Concentration, Units in1: Toxicity: Ability to Accumulate2: Source:
Log Log
Sediment Water Tissue (Sample Type) Effects BCF BAF BSAF Reference Comments3
7.2 ng/g (eggs) (n = 6) 1 1.4% eggshell [17] F; Kola Peninsula,
thinning Russia
Powell River site: A hepatic [15] F; southern coast of
-9,000 ng/kg lipid cytochrome British Columbia;
weight basis (yolk sac) P4501A cross- eggs were collected
reactive protein from nests and
Reference site: -500 (CYP1A) was hatched in the lab; -
ng/kg lipid weight induced nearly indicates value was
basis (yolk sac) 6-fold in chicks taken from a figure
from Powell
River site
compared to the
reference
(p < 0.05).
No significant
concentration-
related effects
were found for
morphological,
physiological,
or histological
parameters.
-------
Summary of Biological Effects Tissue Concentrations for 1,2,3,6,7,8-HexaCDD
Species:
Taxa
Ardea herodias,
Great blue heron
chicks
Concentration, Units in1:
Sediment Water Tissue (Sample Type)
Nicomekl site: 10±3.4
ng/kg (egg)(n=ll)
Vancouver site:
89±45.4 ng/kg (egg)
(n=12)
Crofton site:
430±105.9 ng/kg
(egg) (n=6)
Toxicity:
Effects
Depression of
growth
compared to
Nicomekl site.
Presence of
edema.
Depression of
growth
compared to
Nicomekl site.
Presence of
edema.
Ability to Accumulate2: Source:
Log Log
BCF BAF BSAF Reference Comments3
[16] L; eggs were
collected from three
British Columbia
colonies with
different levels of
contamination and
incubated in the
laboratory
-------
Summary of Biological Effects Tissue Concentrations for 1,2,3,6,7,8-HexaCDD
Species:
Taxa
Mustela vison,
Mink
Concentration, Units in1: Toxicity:
Sediment Water Tissue (Sample Type) Effects
Diet:
lpg/g4 54pg/g4 (liver) LOAEL;
reduced kit
body weights
followed by
reduced
survival
3pg/g4 77pg/g4 (liver) Reduced kit
body weights
followed by
reduced
survival
6pg/g4 130pg/g4 (liver) Significant
decrease in
number of live
kits whelped
per female
Ability to Accumulate2:
Log Log
BCF BAF BSAF
No BMP
reported
log BMP
= 1.42
log BMP
= 1.53
Source:
Reference Comments3
[18] L;BMF =
biomagnification
factor = v/vd,
V[ = lipid-
normalized tissue
concentration,
vd = lipid-
normalized dietary
concentration.
1 Concentration units based on wet weight unless otherwise noted.
2 BCF = bioconcentration factor, BAF = bioaccumulation factor, BSAF = biota-sediment accumulation factor.
3 L = laboratory study, spiked sediment, single chemical; F = field study, multiple chemical exposure; other unusual study conditions or observations noted.
4 Not clear from reference if concentration is based on wet or dry weight.
-------
BIOACCUMULATION SUMMARY 1,2,3,6,7,8-HexaCDD
References
1. USEPA. 1996. Hazardous Substances Data Bank (HSDB). National Library of Medicine
online (TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental
Assessment, Environmental Criteria and Assessment Office, Cinncinati, OH. February.
2. MacKay, D.M., W.Y. Shiw, and K.C. Ma. 1992. Illustrated handbook of physical-chemical
properties and environmental fate for organic chemicals. Vol. n, Polynuclear aromatic
hydrocarbons, poly chlorinated dioxins and dibenzofurans. Lewis Publishers, Boca Raton, FL.
3. USEPA. 1989. Chemical fate rate constants for SARA section 313 chemicals and Superfund
Health Evaluation Manual chemicals. Prepared by Chemical Hazard Assessment Division,
Syracuse Research Corporation, for U.S. Environmental Protection Agency, Office of Toxic
Substances, Exposure Evaluation Division, Washington, DC, and Environmental Criteria and
Assessment Office, Cincinnati, OH. August 11.
4. Karickhoff, S.W., and J.M. Long. 1995. Internal report on summary of measured, calculated and
recommended log Kow values. Draft. Prepared by U.S. Environmental Protection Agency, Office
of Research and Development, Environmental Research Laboratory-Athens, for E. Southerland,
Office of Water, Office of Science and Technology, Standards and Applied Science Division,
Washington, DC. April 10.
5. USEPA. 1996. Integrated Risk Information System (IRIS). National Library of Medicine online
(TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental
Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. September.
6. Safe, S. 1990. Polychlorinated biphenyls (PCBs), dibenzo-/?-dioxins (PCDDs), dibenzofurans
(PCDFs), and related compounds: Environmental and mechanistic considerations which support
the development of toxicity equivalency factors (TEF). Crit. Rev. Toxicol. 21:51-88.
7. Braune, B.M., and RJ. Norstrom. 1989. Dynamics of organochlorine compounds in herring
gulls: HI. Tissue distribution and bioaccumulation in Lake Ontario gulls. Environ. Toxicol.
Chem. 8:957-968.
8. USEPA. 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. U.S. Environmental
Protection Agency, Office of Research and Development, Washington, DC.
9. Eisler, R. 1986. Dioxin hazards to fish, wildlife, and invertebrates: A synoptic review. U.S. Fish
Wildl. Serv. Biol. Rep. 85 (1.8). p. 37.
10. USEPA. 1989. Interim procedures for estimating risks associated with exposure to mixtures
of chlorinated dibenzo-p-dioxins and -dibenzofurans (CDDs and CDFs) and 1989 update.
EPA/625/3-89/016. U.S. Environmental Protection Agency, Risk Assessment Forum,
Washington, DC.
11. Cooper, K.R. 1989. Effects of polychlorinated dibenzo-p-dioxins and polychlorinated
dibenzofurans on aquatic organisms. Rev. Aquat. Sci. 1:227-242.
257
-------
BIOACCUMULATION SUMMARY 1,2,3,6,7,8-HexaCDD
12. Mehrle, P.M., D.R. Buckler, E.E. Little, L.M. Smith, J.D. Petty, P.M. Peterman, D.L. Stalling,
G.M. DeGraeve, JJ. Coyle, and WJ. Adams. 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.
13. Kuehl, D.W., P.M. Cook, A.R. Batterman, D. Lothenbach, and B.C. Butterworth. 1987.
Bioavailability of polychlorinated dibenzo-p-dioxins and dibenzofurans from contaminated
Wisconsin River sediment to carp. Chemosphere 16(4):667-679.
14. Sijm, D.T.H.M., H. Wever, and A. Opperhuizen. 1993. Congener-specific biotransformation
and bioaccumulation of PCDDs and PCDFs from fly ash in fish. Environ. Toxicol. Chem.
12:1895-1907.
15. Elliott, J.E., R.J. Norstrom, A. Lorenzen, L.E. Hart, H. Philibert, S.W. Kennedy, JJ. Stegeman,
G.D. Bellward, and K.M. Cheng. 1996. Biological effects of polychlorinated dibenzo-p-dioxins,
dibenzofurans, and biphenyls in bald eagle (Haliaeetus leucocephalus) chicks. Environ. Toxicol
Chem. 15(5): 782-793.
16. Hart, L.E., K.M. Cheng, P.E. Whitehead, R.M. Shah, RJ. Lewis, S.R. Ruschkowski, R.W. Blair,
D.C. Bennett, S.M. Bandiera, RJ.Norstrom, and G.D. Bellward. 1991. Dioxin contamination
and growth and development in great blue heron embryos. /. Toxicol. Environ. Health 32:331-
344.
17. Henny, C.J., S.A. Ganusevich, F.P. Ward, and T.R. Schwartz. 1994. Organochlorine pesticides,
chlorinated dioxins and furans, and PCBs in peregrine falcon Falco peregrinus eggs from the
Kola Penninsula, Russia. In Raptor conservation today, ed. B.U. Meyburg and R.D. Chancellor,
pp. 739-749. WWGPB/The Pica Press.
18. Tillitt, D.E., R.W. Gale, J.C. Meadows, J.L. Zajicek, P.H. Peterman, S.N. Heaton, P.O. Jones,
S.J. Bursian, T.J. Kubiak, J.P. Giesy, and RJ. Aulerich. 1996. Dietary exposure of mink to carp
from Saginaw Bay. 3. Characterization of dietary exposure to planar halogenated hydrocarbons,
dioxin equivalents, and biomagnification. Environ. Sci. Technol. 30:283-291.
19. USEPA. 1995. Great Lakes Water Quality Initiative Technical Support Document for the
procedure to determine bioaccumulation factors. EPA-820-B-95-005. U.S. Environmental
Protection Agency, Office of Water, Washington, DC.
258
-------
BIOACCUMULATION SUMMARY
1,2,3,7,8-PentaCDD
Chemical Category: POLYCHLORINATED DIBENZO-p-DIOXINS
Chemical Name (Common Synonyms):
l,2,3,7,8-PENTACHLORODIBENOZ-/?-DIOXIN
CASRN: 40321-76-4
Chemical Characteristics
Solubility in Water: No data [1,3]
Log Kow: No data [3,4]
Half-Life: No data [2,3]
Log Koc: —
Human Health
Oral RfD: No data [5]
Critical Effect: —
Oral Slope Factor: No data [5]
Confidence:
Carcinogenic Classification:
Wildlife
Partitioning Factors: Partitioning factors for 1,2,3,7,8-pentaCDD in wildlife were not found in the
studies reviewed.
Food Chain Multipliers: Limited information was found reporting on specific biomagnification factors
of PCDDs and PCDFs through terrestrial wildlife; no information was available for 1,2,3,7,8-pentaCDD,
specifically. Due to the toxicity, high Kow values, and highly persistent nature of the PCDDs and PCDFs,
they possess a high potential to bioaccumulate and biomagnify through the food web. PCDDs and PCDFs
have been identified in fish and wildlife throughout the global aquatic and marine environments [6].
Studies conducted in Lake Ontario indicated that biomagnification of 2,3,7,8-tetrachlorodibenzo-p-dioxin
(2,3,7,8-TCDD) appears to be significant between fish and fish-eating birds but not between fish and
their food. When calculated for older predaceous fish such as lake-trout-eating young smelt, the log
biomagnification factor (BMF) can equal 0.48. The log BMP from alewife to herring gulls in Lake
Ontario was 1.51 for 2,3,7,8-TCDD [7].
EPA has developed risk-based concentrations of 2,3,7,8-TCDD in different media that present low and
high risk to fish, mammalian, and avian wildlife. These concentrations were developed based on toxic
effects of 2,3,7,8-TCDD and its propensity to bioaccumulate in fish, mammals, and birds.
259
-------
BIOACCUMULATION SUMMARY
1,2,3,7,8-PentaCDD
Environmental Concentrations Associated With 2,3,7,8-TCDD Risk to Aquatic Life and Associated
Wildlife [8]
Organism
Fish Concentration
(Pg/g)
Sediment
Concentration
(pg/g dry wt.)
Water Concentration (pg/L)
POC=0.2
POC=1.0
Low Risk
Fish
Mammalian Wildlife
Avian Wildlife
50
0.7
6
60
2.5
21
0.6
0.008
0.07
3.1
0.04
0.35
High Risk to Sensitive Species
Fish
Mammalian Wildlife
Avian Wildlife
80
7
60
100
25
210
1.0
0.08
0.7
5
0.4
3.5
Note: POC - Paniculate organic carbon
Fish lipid of 8% and sediment organic carbon of 3% assumed where needed.
For risk to fish, BSAF of 0.3 used; for risk to wildlife, BSAF of 0.1 used.
Low risk concentrations are derived from no-effects thresholds for reproductive effects (mortality in embryos and
young) in sensitive species.
High risk concentrations are derived from TCDD doses expected to cause 50 to 100% mortality in embryos and
young of sensitive species.
Aquatic Organisms
Partitioning Factors: Partitioning factors for 1,2,3,7,8-pentaCDF in aquatic organisms were not found
in the studies reviewed.
Food Chain Multipliers: No specific food chain multipliers were identified for 1,2,3,7,8-pentaCDD.
Food chain multiplier information was only available for 2,3,7,8-TCDD. Biomagnification of 2,3,7,8-
TCDD does not appear to be significant between fish and their prey. Limited data for the base of the
Lake Ontario lake trout food chain indicated little or no biomagnification between zooplankton and
forage fish. BMFs based on fish consuming invertebrate species are probably close to 1.0 because of
the 2,3,7,8-TCDD biotransformation by forage fish. BMFs greater than 1.0 might exist between some
zooplankton species and their prey due to the lack of 2,3,7,8-TCDD biotransformation in
invertebrates[8].
Toxicity/Bioaccumulation Assessment Profile
The polychlorinated dibenzo-p-dioxins (PCDDs) and polychlorinated dibenzofurans (PCDFs) each
consist of 75 isomers that differ in the number and position of attached chlorine atoms. The PCDDs and
PCDFs are polyhalogenated aromatic compounds and exhibit several properties common to this group
of compounds. These compounds tend to be highly lipophilic and the degree of lipophilicity is increased
with increasing ring chlorination [6]. In general, the PCDDs and PCDFs exhibit relative inertness to
acids, bases, oxidation, reduction, and heat, increasing in environmental persistence and chemical
stability with increasing chlorination [6,9]. Because of their lipophilic nature, the PCDDs and PCDFs
have been detected in fish, wildlife, and human adipose tissue, milk, and serum [6].
260
-------
BIOACCUMULATION SUMMARY
1,2,3,7,8-PentaCDD
Each isomer has its own unique chemical and lexicological properties. The most toxic of the PCDD and
PCDF isomers is 2,3,7,8-TCDD, one of the 22 possible congeners of tetrachlorodibenzo-j?-dioxin [9].
Toxicity equivalency factors (TEFs) have been developed by the U.S. EPA relating the toxicities of other
PCDD and PCDF isomers to that of 2,3,7,8-TCDD [10]. The biochemical mechanisms leading to the
toxic response resulting from exposure to PCDDs and PCDFs are not known in detail, but experimental
data suggest that an important role in the development of systemic toxicity resulting from exposure to
these chemicals is played by an intracellular protein, the Ah receptor. This receptor binds halogenated
polycyclic aromatic molecules, including PCDDs and PCDFs. In several mouse strains, the expression
of toxicity of 2,3,7,8-TCDD-related compounds, including cleft palate formation, liver damage, effects
on body weight gain, thymic involution, and chloracnegenic response, has been correlated with their
binding affinity for the Ah receptor, and with their ability to induce several enzyme systems [10].
Toxicity Equivalency Factors (TEF) for PCDD and PCDF Isomers [10]
Isomer
Total TetraCDD
2,3,7,8-TCDD
Other TCDDs
Total PentaCDDs
2,3,7,8-PentaCDDs
Other PentaCDDs
Total HexaCDDs
2,3,7,8-HexaCDDs
Other HexaCDDs
Total HeptaCDDs
2,3,7,8-HeptaCDDs
Other HeptaCDDs
Total TetraCDFs
2,3,7,8-TetraCDF
Other TetraCDFs
Total PentaCDFs
2,3,7,8-PentaCDFs
Other PentaCDFs
Total HexaCDFs
2,3,7,8-HexaCDFs
Other HexaCDFs
Total HeptaCDFs
2,3,7,8-HeptaCDFs
Other HeptaCDFs
TEF
1
1
0.01
0.5
0.5
0.005
0.04
0.04
0.0004
0.001
0.001
0.00001
0.1
0.1
0.001
0.1
0.1
0.001
0.01
0.01
0.0001
0.001
0.001
0.00001
In natural systems, PCDDs and PCDFs are typically associated with sediments, biota, and the organic
carbon fraction of ambient waters [8]. Congener-specific analyses have shown that the 2,3,7,8-
substituted PCDDs and PCDFs were the major compounds present in most sample extracts [6]. Results
261
-------
BIOACCUMULATION SUMMARY 1,2,3,7,8-PentaCDD
from limited epidemiology studies are consistent with laboratory-derived threshold levels to 2,3,7,8-
TCDD impairment of reproduction in avian wildlife. Population declines in herring gulls (Larus
argentatus) on Lake Ontario during the early 1970s coincided with egg concentrations of 2,3,7,8-TCDD
and related chemicals expected to cause reproductive failure based on laboratory experiments (2,3,7,8-
TCDD concentrations in excess of 1,000 pg/g). Improvements in herring gull reproduction through the
mid-1980s were correlated with declining 2,3,7,8-TCDD concentrations in eggs and lake sediments [8].
Based on limited information on isomer-specific analysis from animals at different trophic levels, it
appears that at higher trophic levels, i.e., fish-eating birds and fish, there is a selection of the planar
congeners with the 2,3,7,8-substituted positions [11].
PCDDs and PCDFs are accumulated by aquatic organisms through exposure routes that are determined
by the habitat and physiology of each species. With log K^S, exposure through ingestion of
contaminated food becomes an important route for uptake in comparison to respiration of water [8]. The
relative contributions of water, sediment, and food to uptake of 2,3,7,8-TCDD by lake trout in Lake
Ontario were examined by exposing yearling lake trout to Lake Ontario smelt and sediment from Lake
Ontario along with water at a 2,3,7,8-TCDD concentration simulated to be at equilibrium with the
sediments. Food ingestion was found to contribute approximately 75 percent of total 2,3,7,8-TCDD [8].
There have been a number of bioconcentration studies of 2,3,7,8-TCDD using model ecosystem and
single species exposure. Although there is variation in the actual log BCF values, in general, the algae
and plants have the lowest BCF values, on the order of a few thousand. A log BCF value of 4.38 has
been reported for the snail Physa sp. Crustacea and insect larvae appear to have the next highest BCF
values, followed by several species of fish, with the highest log BCF value of 4.78 [11].
Exposure of juvenile rainbow trout to 2,3,7,8-TCDD and -TCDF in water for 28 days resulted in adverse
effects on survival, growth, and behavior at extremely low concentrations. A no-observed-effects
concentration (NOEC) for 2,3,7,8-TCDD could not be determined because the exposure to the lowest
dose of 0.038 ng/1 resulted in significant mortality [12]. A number of biological effects have been
reported in fish following exposure to 2,3,7,8-TCDD including enzyme induction, immunological
effects, wasting syndrome, dermatological effects, hepatic effects, hematological effects, developmental
effects, and cardiovascular effects [11].
262
-------
Summary of Biological Effects Tissue Concentrations for 1,2,3,7,8-PentaCDD
Species:
Taxa
Concentration, Units in1: Toxicity:
Sediment Water Tissue (Sample Type) Effects
Ability to Accumulate2:
BSAF
Log
BCF
Log
BAF
Source:
Reference Comments3
Fishes
Carassius auratus,
Goldfish
1.59/2.61 ng/g4
(whole body)
16,982
[14] L; fish were
exposed for 120
hr; exposure
water contained
fly ash extract;
concentrations
were measured in
water, but data
were not
presented
Cyprinus carpio, 31 pg/g4
Carp
4.8 pg/g4
0.06
[13] F; Petenwell
Reservoir, central
Wisconsin; BSAF
based on 8%
tissue lipid
content and 3.1%
sediment organic
carbon
Salmonids
0.054
[18]
Wildlife
Falco peregrinus,
Peregrine falcon
11 ng/g (eggs)
(n = 6)
11.4% eggshell
thinning
[17] F; Kola
Peninsula, Russia
-------
Summary of Biological Effects Tissue Concentrations for 1,2,3,7,8-PentaCDD
Species:
Taxa
Haliaeetus
leiicocephaliis,
Bald eagle chicks
Concentration, Units in1: Toxicity: Ability to Accumulate2:
Log Log
Sediment Water Tissue (Sample Type) Effects BCF BAF BSAF
Powell River site: A hepatic
-2,800 ng/kg lipid cytochrome
weight basis (yolk sac) P4501A cross-
reactive protein
Reference site: (CYP1A) was
-500 ng/kg lipid induced nearly
weight basis (yolk sac) six-fold in
chicks from
Powell River
site compared
to the reference
(p<0.05). No
significant
concentration-
related effects
were found for
morphological,
physiological,
or histological
parameters.
Source:
Reference Comments3
[15] F; southern coast
of British
Columbia; eggs
were collected
from nests and
hatched in the
lab; - indicates
value was taken
from a figure.
-------
Summary of Biological Effects Tissue Concentrations for 1,2,3,7,8-PentaCDD
Species:
Taxa
Ardea herodias,
Great blue heron
chicks
Concentration, Units in1:
Sediment Water Tissue (Sample Type)
Nicomekl site:
6±2.2 ng/kg (egg)
(n = 11)
Vancouver site:
57±25.8 ng/kg (egg)
(n = 12)
Toxicity: Ability to Accumulate2:
Log Log
Effects BCF BAF BSAF
Depression of
growth
compared to
Nicomekl site.
Presence of
edema.
Source:
Reference Comments3
[16] L; eggs were
collected from
three British
Columbia
colonies with
different levels of
contamination
and incubated in
the laboratory
Crofton site: Depression of
263±69.9 ng/kg (egg) growth
(n = 6) compared to
Nicomekl site.
Presence of
edema.
1 Concentration units based on wet weight unless otherwise noted.
2 BCF = bioconcentration factor, BAF = bioaccumulation factor, BSAF = biota-sediment accumulation factor.
3 L = laboratory study, spiked sediment, single chemical; F = field study, multiple chemical exposure; other unusual study conditions or observations noted.
4 Not clear from reference if concentration is based on wet or dry weight.
-------
BIOACCUMULATION SUMMARY 1,2,3,7,8-PentaCDD
References
1. USEPA. 1996. Hazardous Substances Data Bank (HSDB). National Library of Medicine
online (TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental
Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. February.
2. USEPA. 1989. Chemical fate rate constants for SARA section 313 chemicals and Superfund
Health Evaluation Manual chemicals. Prepared by Chemical Hazard Assessment Division,
Syracuse Research Corporation, for U.S. Environmental Protection Agency, Office of Toxic
Substances, Exposure Evaluation Division, Washington, DC, and Environmental Criteria and
Assessment Office, Cincinnati, OH. August 11.
3. MacKay, D.M., W.Y. Shiw, and K.C. Ma. 1992. Illustrated handbook of physical-chemical
properties and environmental fate for organic chemicals. Vol. n, Polynuclear aromatic
hydrocarbons, poly chlorinated dioxins and dibenzofurans. Lewis Publishers, Boca Raton, FL.
4. Karickhoff, S.W., and J.M. Long. 1995. Internal report on summary of measured, calculated
and recommended log Kow values. Draft. Prepared by U.S. Environmental Protection Agency,
Office of Research and Development, Environmental Research Laboratory-Athens, for E.
Southerland, Office of Water, Office of Science and Technology, Standards and Applied
Science Division, Washington, DC. April 10.
5. USEPA. 1996. Integrated Risk Information System (IRIS). National Library of Medicine online
(TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental
Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. September.
6. Safe, S. 1990. Polychlorinated biphenyls (PCBs), dibenzo-/?-dioxins (PCDDs), dibenzofurans
(PCDFs), and related compounds: Environmental and mechanistic considerations which support
the development of toxicity equivalency factors (TEF). Crit. Rev. Toxicol. 21:51-88.
7. Braune, B.M. And RJ. Norstrom. 1989. Dynamics of organochlorine compounds in herring
gulls: HI. Tissue distribution and bioaccumulation in Lake Ontario gulls. Environ. Toxicol.
Chem. 8:957-968.
8. USEPA. 1993. Interim report on data and methods for assessment of 2,3,7,8-
tetrachlorodibenzo-^-dioxin risks to aquatic life and associated wildlife. EPA/600/R-93/055.
U.S. Environmental Protection Agency, Office of Research and Development, Washington, DC.
9. Eisler, R. 1986. Dioxin hazards to fish, wildlife, and invertebrates: A synoptic review. U.S.
Fish Wildl. Serv. Biol. Rep. 85(1.8). 37 pp.
10. USEPA. 1989. Interim procedures for estimating risks associated with exposure to mixtures of
chlorinated dibenzo-p-dioxins and -dibenzofurans (CDDs and CDFs) and 1989 update.
EPA/625/3-89/016. U.S. Environmental Protection Agency, Risk Assessment Forum,
Washington, DC.
11. Cooper, K.R. 1989. Effects of polychlorinated dibenzo-p-dioxins and polychlorinated
dibenzofurans on aquatic organisms. Rev. Aquat. Sci. 1:227-242.
266
-------
BIOACCUMULATION SUMMARY 1,2,3,7,8-PentaCDD
12. Mehrle, P.M., D.R. Buckler, E.E. Little, L.M. Smith, J.D. Petty, P.M. Peterman, D.L. Stalling,
G.M. DeGraeve, JJ. Coyle, and WJ. Adams. 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.
13. Kuehl, D.W., P.M. Cook, A.R. Batterman, D. Lothenbach, and B.C. Butterworth. 1987.
Bioavailability of polychlorinated dibenzo-p-dioxins and dibenzofurans from contaminated
Wisconsin River sediment to carp. Chemosphere 16(4):667-679.
14. Sijm, D.T.H.M., H. Wever, and A. Opperhuizen. 1993. Congener-specific biotransformation
and bioaccumulation of PCDDs and PCDFs from fly ash in fish. Environ. Toxicol. Chem. 12:
1895-1907.
15. Elliott, J.E., R.J. Norstrom, A. Lorenzen, L.E. Hart, H. Philibert, S.W. Kennedy, JJ. Stegeman,
G.D. Bellward, and K.M. Cheng. 1996. Biological effects of polychlorinated dibenzo-p-dioxins,
dibenzofurans, and biphenyls in bald eagle (Haliaeetus leucocephalus) chicks. Environ. Toxicol
Chem. 15(5):782-793.
16. Hart, L.E., K.M. Cheng, P.E. Whitehead, R.M. Shah, RJ. Lewis, S.R. Ruschkowski, R.W. Blair,
D.C. Bennett, S.M. Bandiera, RJ.Norstrom, and G.D. Bellward. 1991. Dioxin contamination
and growth and development in great blue heron embryos. /. Toxicol. Environ. Health 32:331-
344.
17. Henny, C.J., S.A. Ganusevich, F.P. Ward, and T.R. Schwartz. 1994. Organochlorine pesticides,
chlorinated dioxins and furans, and PCBs in Peregrine Falcon Falco peregrinus eggs from the
Kola Penninsula, Russia. In Raptor Conservation Today, ed. B.U. Meyburg and R.D.
Chancellor, pp. 739-749, WWGPB/The Pica Press.
18. USEPA. 1995. Great Lakes Water Quality Initiative Technical Support Document for the
procedure to determine bioaccumulation factors. EPA-820-B-95-005. U.S. Environmental
Protection Agency, Office of Water, Washington, DC.
267
-------
268
-------
BIOACCUMULATION SUMMARY
2,3,7,8-TCDD
Chemical Category: POLYCHLORINATED DIBENZO-p-DIOXINS
Chemical Name (Common Synonyms):
2,3,7,8-TETRACHLORODIBENZO-p-DIOXIN
CASRN: 1746-01-6
Chemical Characteristics
Solubility in Water: 19.3 ng/L [1]
Log Kow: 6.53 [3]
Half-Life: 1.1.15-1.62 years based on soil
die-away test and lake water and
sediment die-away test [2]
Log Koc: 6.42 L/kg organic carbon
Human Health
Oral RfD: No data [4] Confidence: —
Critical Effect: —
Oral Slope Factor: 1.5 x 10+5 per (mg/kg)/day [4] Carcinogenic Classification: B2 [4]
Wildlife
Partitioning Factors: Partitioning factors for 2,3,7,8-TCDD in wildlife were not found in the literature.
Food Chain Multipliers: Limited information was found reporting on specific biomagnification factors
of PCDDs and PCDFs through terrestrial wildlife. Due to the toxicity, high Kow values, and highly
persistent nature of the PCDDs and PCDFs, they possess a high potential to bioaccumulate and
biomagnify through the food web. PCDDs and PCDFs have been identified in fish and wildlife
throughout the global aquatic and marine environments [5]. Studies conducted in Lake Ontario
indicated that biomagnification of 2,3,7,8-tetrachlorodibenzo-p-dioxin (2,3,7,8-TCDD) appears to be
significant between fish and fish-eating birds but not between fish and their food. When calculated for
older predaceous fish such as lake-trout-eating young smelt, the biomagnification factor (BMP) can equal
3. The BMP from alewife to herring gulls in Lake Ontario was 32 for 2,3,7,8-TCDD [6].
EPA has developed risk-based concentrations of 2,3,7,8-TCDD in different media that present low and
high risk to fish, mammalian, and avian wildlife. These concentrations were developed based on toxic
effects of 2,3,7,8-TCDD and its propensity to bioaccumulate in fish, mammals, and birds.
269
-------
BIOACCUMULATION SUMMARY
2,3,7,8-TCDD
Environmental Concentrations Associated With 2,3,7,8-TCDD Risk to Aquatic Life and Associated
Wildlife [7]
Organism
Fish Concentration
(Pg/g)
Sediment
Concentration
(pg/g dry wt.)
Water Concentration (pg/L)
POC=0.2
POC=1.0
Low Risk
Fish
Mammalian Wildlife
Avian Wildlife
50
0.7
6
60
2.5
21
0.6
0.008
0.07
3.1
0.04
0.35
High Risk to Sensitive Species
Fish
Mammalian Wildlife
Avian Wildlife
80
7
60
100
25
210
1.0
0.08
0.7
5
0.4
3.5
Note: POC - Paniculate organic carbon
Fish lipid of 8% and sediment organic carbon of 3% assumed where needed.
For risk to fish, BSAF of 0.3 used; for risk to wildlife, BSAF of 0.1 used.
Low risk concentrations are derived from no-effects thresholds for reproductive effects (mortality in embryos and
young) in sensitive species.
High risk concentrations are derived from TCDD doses expected to cause 50 to 100% mortality in embryos and
young of sensitive species.
Aquatic Organisms
Partitioning Factors: Steady-state BSAFs for invertebrates exposed to 2,3,7,8-TCDD in the laboratory
ranged from about 0.5 to 0.9 [8]. The BSAF for carp collected from a reservoir in central Wisconsin was
0.27 [9].
Food Chain Multipliers: Biomagnification of 2,3,7,8-TCDD does not appear to be significant between
fish and their prey. Limited data for the base of the Lake Ontario lake trout food chain indicated little
or no biomagnification between zooplankton and forage fish. BMFs based on fish consuming
invertebrate species are probably close to 1.0 because of the 2,3,7,8-TCDD biotansformation by forage
fish. BMFs greater than 1.0 may exist between some zooplankton species and their prey due to the lack
of 2,3,7,8-TCDD biotransformation in invertebrates [7].
Toxicity/Bioaccumulation Assessment Profile
The polychlorinated dibenzo-/?-dioxins (PCDDs) and polychlorinated dibenzofurans (PCDFs) each
consist of 75 isomers that differ in the number and position of attached chlorine atoms. The PCDDs and
PCDFs are polyhalogenated aromatic compounds and exhibit several properties common to this group
of compounds. These compounds tend to be highly lipophilic and the degree of lipophilicity is increased
with increasing ring chlorination [5]. In general, the PCDDs and PCDFs exhibit relative inertness to
acids, bases, oxidation, reduction, and heat, increasing in environmental persistence and chemical
stability with increasing chlorination [10,5]. Because of their lipophilic nature, the PCDDs and PCDFs
have been detected in fish, wildlife, and human adipose tissue, milk, and serum [5].
270
-------
BIOACCUMULATION SUMMARY
2,3,7,8-TCDD
Each isomer has its own unique chemical and lexicological properties. The most toxic of the PCDD and
PCDF isomers is 2,3,7,8-tetrachlorodibenzo-/?-dioxin (2,3,7,8-TCDD), one of the 22 possible congeners
of tetrachlorodibenzo-p-dioxin [10]. Toxicity equivalency factors (TEFs) have been developed by the
EPA relating the toxicities of other PCDD and PCDF isomers to that of 2,3,7,8-TCDD [11]. The
biochemical mechanisms leading to the toxic response resulting from exposure to PCDDs and PCDFs
are not known in detail, but experimental data suggest that an important role in the development of
systemic toxicity resulting from exposure to these chemicals is played by an intracellular protein, the Ah
receptor. This receptor binds halogenated polycyclic aromatic molecules, including PCDDs and PCDFs.
In several mouse strains, the expression of toxicity of 2,3,7,8-TCDD-related compounds, including cleft
palate formation, liver damage, effects on body weight gain, thymic involution, and chloracnegenic
response, has been correlated with their binding affinity for the Ah receptor, and with their ability to
induce several enzyme systems [11].
Toxicity Equivalency Factors (TEF) for PCDD and PCDF Isomers [11]
Isomer
Total TetraCDD
2,3,7,8-TCDD
Other TCDDs
Total PentaCDDs
2,3,7,8-PentaCDDs
Other PentaCDDs
Total HexaCDDs
2,3,7,8-HexaCDDs
Other HexaCDDs
Total HeptaCDDs
2,3,7,8-HeptaCDDs
Other HeptaCDDs
Total TetraCDFs
2,3,7,8-TetraCDF
Other TetraCDFs
Total PentaCDFs
2,3,7,8-PentaCDFs
Other PentaCDFs
Total HexaCDFs
2,3,7,8-HexaCDFs
Other HexaCDFs
Total HeptaCDFs
2,3,7,8-HeptaCDFs
Other HeptaCDFs
TEF
1
1
0.01
0.5
0.5
0.005
0.04
0.04
0.0004
0.001
0.001
0.00001
0.1
0.1
0.001
0.1
0.1
0.001
0.01
0.01
0.0001
0.001
0.001
0.00001
In natural systems, PCDDs and PCDFs are typically associated with sediments, biota, and the organic
carbon fraction of ambient waters [7]. Congener-specific analyses have shown that the 2,3,7,8-
271
-------
BIOACCUMULATION SUMMARY 2,3,7,8-TCDD
substituted PCDDs and PCDFs were the major compounds present in most sample extracts [5]. Results
from limited epidemiology studies are consistent with laboratory-derived threshold levels to 2,3,7,8-
TCDD impairment of reproduction in avian wildlife. Population declines in herring gulls (Larus
argentatus) on Lake Ontario during the early 1970s coincided with egg concentrations of 2,3,7,8-TCDD
and related chemicals expected to cause reproductive failure based on laboratory experiments (2,3,7,8-
TCDD concentrations in excess of 1,000 pg/g). Improvements in herring gull reproduction through the
mid-1980s were correlated with declining 2,3,7,8-TCDD concentrations in eggs and lake sediments [7].
Based on limited information on isomer-specific analysis from animals at different trophic levels, it
appears that at higher trophic levels, i.e., fish-eating birds and fish, there is a selection of the planar
congeners with the 2,3,7,8-substituted positions [12].
PCDDs and PCDFs are accumulated by aquatic organisms through exposure routes that are determined
by the habitat and physiology of each species. With log K^S, exposure through ingestion of
contaminated food becomes an important route for uptake in comparison to respiration of water [7]. The
relative contributions of water, sediment, and food to uptake of 2,3,7,8-TCDD by lake trout in Lake
Ontario were examined by exposing yearling lake trout to Lake Ontario smelt and sediment from Lake
Ontario along with water at a 2,3,7,8-TCDD concentration simulated to be at equilibrium with the
sediments. Food ingestion was found to contribute approximately 75 percent of total 2,3,7,8-TCDD [7].
There have been a number of bioconcentration studies of 2,3,7,8-TCDD using model ecosystem and
single species exposure. Although there is variation in the actual BCF values, in general, the algae and
plants have the lowest BCF values, on the order of a few thousand. A log BCF value of 4.38 has been
reported for the snail Physa sp. Crustacea and insect larvae appear to have the next highest BCF values,
followed by several species of fish, with the highest log BCF value of 4.79 [12].
Exposure of juvenile rainbow trout to 2,3,7,8-TCDD and -TCDF in water for 28 days resulted in adverse
effects on survival, growth, and behavior at extremely low concentrations. A no-observed-effects
concentration (NOEC) for 2,3,7,8-TCDD could not be determined because the exposure to the lowest
dose of 0.038 ng/1 resulted in significant mortality [13]. A number of biological effects have been
reported in fish following exposure to 2,3,7,8-TCDD including enzyme induction, immunological
effects, wasting syndrome, dermatological effects, hepatic effects, hematological effects, developmental
effects, and cardiovascular effects [12].
272
-------
Invertebrates
Summary of Biological Effects Tissue Concentrations for 2,3,7,8-TCDD
Species:
Taxa
Concentration, Units in1:
Toxicity:
Ability to Accumulate2:
Source:
Log Log
Sediment Water Tissue (Sample Type) Effects BCF BAF BSAF Reference Comments3
Plants
Oedogonium
cardiacum,
Green algae
1.34mg/kg (whole
body)4
Growth, NOED
[35]
L; no effect on
growth
Lemna minor,
Duckweed
0.00614 mg/kg
(whole body)4
Growth, NOED
[35]
L; no observed
effect
Nereis virens,
Sandworm
656±97 pg/g
dw; (n = 6)
422±103 pg/g dw
(whole body)
-0.5 [8,14] L; 180-day
exposure; sediment
TOC was 57
mg/kg; ~ indicates
approximate value,
as numbers were
estimated from bar
graphs.
Physa sp.,
Snail
0.364 mg/kg
(whole body)4
Mortality,
NOED
[35]
L; no effect on
survival
-------
to
-J
Summary of Biological Effects Tissue Concentrations for 2,3,7,8-TCDD
Species: Concentration, Units in1: Toxicity:
Taxa Sediment Water Tissue (Sample Type) Effects
Macoma nasuta, 656±97 pg/g 142 ± 20 pg/g dw
Clam dw; (n = 6)
Daphnia magna, 2.08 mg/kg Mortality,
Cladaceran (whole body)4 NOED
Palaemonetes 656±97pg/g 138 ±20 pg/g dw
pugio, dw; (n = 6)
Grass shrimp
Pacifastacus 0.003 mg/kg Mortality,
leniusculus, (whole body)4 ED25
Crayfish
0.03 mg/kg Mortality,
(whole body)4 ED50
Ability to Accumulate2: Source:
Log Log
BCF BAF BSAF Reference Comments3
-0.9 [8,14] L; 120-day
exposure; sediment
TOC was 57
mg/kg; ~ indicates
approximate value,
as numbers were
estimated from bar
graphs.
[35] L; no effect on
survival
-0.7 [8,14] L; 28-day
exposure; sediment
TOC was 57 mg/kg
~ indicates
approximate value,
as numbers were
estimated from bar
graphs.
[31] L; 25% mortality
after 40 days
[31] L; lethargy, 50% to
66% increase in
mortality
-------
Summary of Biological Effects Tissue Concentrations for 2,3,7,8-TCDD
Species: Concentration, Units in1:
Taxa Sediment Water Tissue (Sample Type)
0.003 mg/kg
(whole body)4
0.003 mg/kg
(whole body)4
0.003 mg/kg
(whole body)4
0.1 mg/kg (whole
body)4
0.0003 mg/kg (whole
body)4
0.0003 mg/kg (whole
body)4
Callinectes sapidus, 32.2 ppt5 8.2 ppt5
Blue crab (TOC = 3.2%) (hepatopancreas)
(% lipid = 7.6)
52.8 ppt5
(TOC = 3.9%)
Toxicity: Ability to Accumulate2:
Log Log
Effects BCF BAF BSAF
Behavior,
LOED
Physiological,
LOED
Physiological,
LOED
Morphology,
NOED
Mortality,
NOED
Physiological,
NOED
-0.72 0.089
Source:
Reference
[31]
[31]
[31]
[31]
[31]
[31]
[15]
Comments3
L; lack of
avoidance response
L; significant
induction of
cytochrome P450
L; significant
induction of liver
enzymes
(cytochrome P450)
L; no significant
pathology at
highest dose
L; no effect on
mortality
L; no significant
induction of liver
enzymes
(cytochrome P450)
F; northeastern
Florida; bleach-
kraft paper mill
receiving stream;
BAF and BSAF
calculated using
mean of two
sediment
concentrations.
-------
to
-J
o\
Summary of Biological Effects Tissue Concentrations for 2,3,7,8-TCDD
Species:
Taxa
Chironomiis
tentans, Midge
Fishes
Oncorhynchiis
mykiss (Salmo
gairdneri),
Rainbow trout
Oncorhynchiis
mykiss,
Rainbow trout
Concentration, Units in1: Toxicity: Ability to Accumulate2:
Log Log
Sediment Water Tissue (Sample Type) Effects BCF BAF BSAF
0.47 mg/kg Growth, NOED
(whole body)
water 1.0|ig/kg5 28-day LOEC 4.41
exposure (survival,
0.038 ng/L growth)
water 10.95 ng/g5 (whole 4.46
exposure body)
0.382 ng/L
0.00388 mg/kg Growth, LOED
(extractable lipid)4
0.00371 mg/kg Growth, LOED
(liver)4
0.00026 mg/kg Growth, LOED
(muscle)4
Source:
Reference Comments3
[44] L; concentrations
are lipid
[13] L
L; 6-hour exposure
period
[32] L; reduced growth,
exposed fish
weighed 50 g vs.
130 g for controls
[32] L; reduced growth,
exposed fish
weighed 50 g vs.
130 g for controls
[32] L; reduced growth,
exposed fish
weighed 50 g vs.
130 g for controls
-------
Summary of Biological Effects Tissue Concentrations for 2,3,7,8-TCDD
Species: Concentration, Units in1:
Taxa Sediment Water Tissue (Sample Type)
0.00065 mg/kg
(whole body)4
0.00388 mg/kg
(etractable lipid)4
0.00371 mg/kg
(liver)4
0.00026 mg/kg
(muscle)4
0.00065 mg/kg
(whole body)4
0.00388 mg/kg
(extractable lipid)4
0.00371 mg/kg
(liver)4
0.00026 mg/kg
(muscle)4
Toxicity: Ability to Accumulate2:
Log Log
Effects BCF BAF BSAF
Growth, LOED
Morphology,
LOED
Morphology,
LOED
Morphology,
LOED
Morphology,
LOED
Mortality,
LOED
Mortality,
LOED
Mortality,
LOED
Source:
Reference
[32]
[32]
[32]
[32]
[32]
[32]
[32]
[32]
Comments3
L; reduced growth,
exposed fish
weighed 50 g vs.
130 g for controls
L; livers enlarged
to nearly twice the
size of control fish
livers, fin rot
L; livers enlarged
to nearly twice the
size of control fish
livers, fin rot
L; livers enlarged
to nearly twice the
size of control fish
livers, fin rot
L; livers enlarged
to nearly twice the
size of control fish
livers, fin rot
L; lethal to 7 of 90
fish over 139 days
L; lethal to 7 of 90
fish over 139 days
L; lethal to 7 of 90
fish over 139 days
-------
Summary of Biological Effects Tissue Concentrations for 2,3,7,8-TCDD
Species:
Taxa
Oncorhynchus
mykiss,
Rainbow trout
Oncorhynchus
mykiss,
Rainbow trout
Concentration, Units in1:
Sediment Water Tissue (Sample Type)
0.00065 mg/kg
(whole body)4
0.01 mg/kg
(whole body)4
0.001 mg/kg
(whole body)4
0.025 mg/kg
(whole body)4
0.0003 15 mg/kg
(carcass)4
0.000102 mg/kg
(gastrointestinal tract)4
0.000244 mg/kg
(gill)4
0.00007 mg/kg
(heart)4
0.000092 mg/kg
(kidney)4
0.000072 mg/kg
(liver)4
0.000355 mg/kg
(pyloric caeca)4
Toxicity: Ability to Accumulate2:
Log Log
Effects BCF BAF BSAF
Mortality,
LOED
Mortality,
ED50
Growth, LOED
Morphology,
LOED
Growth, NOED
Growth, NOED
Growth, NOED
Growth, NOED
Growth, NOED
Growth, NOED
Growth, NOED
Source:
Reference
[32]
[36]
[36]
[36]
[38]
[38]
[38]
[38]
[38]
[38]
[38]
Comments3
L; lethal to 7 of 90
fish over 139 days
L; 80-day LD50 for
mortality
L; reduction in
body weight
L; fin necrosis,
hyperpigmentation
L; no effect on
growth
L; no effect on
growth
L; no effect on
growth
L; no effect on
growth
L; no effect on
growth
L; no effect on
growth
L; no effect on
growth
-------
Summary of Biological Effects Tissue Concentrations for 2,3,7,8-TCDD
Species: Concentration, Units in1:
Taxa Sediment Water Tissue (Sample Type)
0.000029 mg/kg
(skeletal muscle)4
0.000201 mg/kg
(skin)4
0.000085 mg/kg
(spleen)4
0.00327 mg/kg
(visceral fat)4
0.00025 mg/kg
(whole body)4
0.0003 15 mg/kg
(carcass)4
0.000102 mg/kg
(gastrointestinal tract)4
0.000244 mg/kg
(gill)4
0.00007 mg/kg
(heart)4
0.000092 mg/kg
(kidney)4
Toxicity: Ability to Accumulate2:
Log Log
Effects BCF BAF BSAF
Growth, NOED
Growth, NOED
Growth, NOED
Growth, NOED
Growth, NOED
Morphology,
NOED
Morphology,
NOED
Morphology,
NOED
Morphology,
NOED
Morphology,
NOED
Source:
Reference
[38]
[38]
[38]
[38]
[38]
[38]
[38]
[38]
[38]
[38]
Comments3
L; no effect on
growth
L; no effect on
growth
L; no effect on
growth
L; no effect on
growth
L; no effect on
growth
L; no effect on fin
necrosis or
hemorrhage
L; no effect on fin
necrosis or
hemorrhage
L; no effect on fin
necrosis or
hemorrhage
L; no effect on fin
necrosis or
hemorrhage
L; no effect on fin
necrosis or
hemorrhage
-------
g Summary of Biological Effects
Species: Concentration, Units in1:
Taxa Sediment Water Tissue (Sample Type)
0.000072 mg/kg
(liver)4
0.000355 mg/kg
(pyloric caeca)4
0.000029 mg/kg
(skeletal muscle)4
0.000201 mg/kg
(skin)4
0.000085 mg/kg
(spleen)4
0.00327 mg/kg
(visceral fat)4
0.00025 mg/kg
(whole body)4
0.0003 15 mg/kg
(carcass)4
0.000102 mg/kg
(gastrointestinal tract)4
Tissue Concentrations for 2,3,7,8-TCDD
Toxicity: Ability to Accumulate2:
Log Log
Effects BCF BAF BSAF
Morphology,
NOED
Morphology,
NOED
Morphology,
NOED
Morphology,
NOED
Morphology,
NOED
Morphology,
NOED
Morphology,
NOED
Mortality,
NOED
Mortality,
NOED
Source:
Reference
[38]
[38]
[38]
[38]
[38]
[38]
[38]
[38]
[38]
Comments3
L; no effect on fin
necrosis or
hemorrhage
L; no effect on fin
necrosis or
hemorrhage
L; no effect on fin
necrosis or
hemorrhage
L; no effect on fin
necrosis or
hemorrhage
L; no effect on fin
necrosis or
hemorrhage
L; no effect on fin
necrosis or
hemorrhage
L; no effect on fin
necrosis or
hemorrhage
L; no effect on
mortality
L; no effect on
mortality
-------
Summary of Biological Effects Tissue Concentrations for 2,3,7,8-TCDD
Species: Concentration, Units in1:
Taxa Sediment Water Tissue (Sample Type)
0.000244 mg/kg
(gill)4
0.00007 mg/kg
(heart)4
0.000092 mg/kg
(kidney)4
0.000072 mg/kg
(liver)4
0.000355 mg/kg
(pyloric caeca)4
0.000029 mg/kg
(skeletal muscle)4
0.000201 mg/kg
(skin)4
0.000085 mg/kg
(spleen)4
0.00327 mg/kg
(visceral fat)4
0.00025 mg/kg
(whole body)4
0.00452 mg/kg
(whole body)4
Toxicity: Ability to Accumulate2:
Log Log
Effects BCF BAF BSAF
Mortality,
NOED
Mortality,
NOED
Mortality,
NOED
Mortality,
NOED
Mortality,
NOED
Mortality,
NOED
Mortality,
NOED
Mortality,
NOED
Mortality,
NOED
Mortality,
NOED
Survival, ED50
Source:
Reference
[38]
[38]
[38]
[38]
[38]
[38]
[38]
[38]
[38]
[38]
[13]
Comments3
L; no effect on
mortality
L; no effect on
mortality
L; no effect on
mortality
L; no effect on
mortality
L; no effect on
mortality
L; no effect on
mortality
L; no effect on
mortality
L; no effect on
mortality
L; no effect on
mortality
L; no effect on
mortality
L; exposure
concentration is the
mean of measured
TCDD
concentration
-------
Summary of Biological Effects Tissue Concentrations for 2,3,7,8-TCDD
Species:
Taxa
Concentration, Units in1:
Toxicity:
Ability to Accumulate2:
Source:
Log Log
Sediment Water Tissue (Sample Type) Effects BCF BAF BSAF Reference Comments3
Oncorhynchus
mykiss,
Rainbow trout
0.0000047 mg/kg Biochemical,
(liver)4 LOED
0.000038 mg/kg
(liver)4
0.000016 mg/kg
(liver)4
Biochemical,
LOED
Biochemical,
LOED
[40] L; significant
increase in liver
ethoxyresorufin O-
deethylase (EROD)
[40] L; significant
increase in liver
ethoxyresorufin O-
deethylase (EROD)
[40] L; significant
increase in liver
ethoxyresorufin O-
deethylase (EROD)
Oncorhynchus
mykiss,
Rainbow trout
0.000439 mg/kg
(whole body)4
Mortality,
ED50
[42] L; mortality from
fertilization to
swim-up; exposure
dose calculated
from text; residue
measured in egg at
5-days post
exposure; dosed for
48 hours and
endpoint measured
after approximately
24 days
-------
Summary of Biological Effects Tissue Concentrations for 2,3,7,8-TCDD
Species:
Taxa
Concentration, Units in1:
Toxicity:
Ability to Accumulate2:
Source:
Log Log
Sediment Water Tissue (Sample Type) Effects BCF BAF BSAF Reference Comments3
0.000421 mg/kg
(whole body)4
Mortality,
ED50
0.000279 mg/kg
(whole body)4
Mortality,
LOED
[42] L; mortality from
fertilization to
swim-up; liposome
used to carry dose;
93% of dose
retained in egg and
assumed to be in
swim-up fry, flow
rate = 8-12
[42] L; significant
increase in
mortality from
hatch to swim-up at
lowest exposure
concentration
tested; exposure
dose calculated
from text; residue
measured in egg at
5-days post
exposure; dosed for
48 hours and
endpoint measured
after approximately
24 days
-------
Summary of Biological Effects Tissue Concentrations for 2,3,7,8-TCDD
Species:
Taxa
Concentration, Units in1:
Sediment Water
Toxicity:
Tissue (Sample Type) Effects
Ability to Accumulate2:
Log
BCF
Log
BAF
BSAF
Source:
Reference Comments3
0.000437 mg/kg
(whole body)4
0.000291 mg/kg
(whole body)4
Mortality,
LOED
Mortality,
NOED
[42] L; significant
increase in
mortality from
hatch to swim-up;
liposome used to
carry dose; 93% of
dose retained in
egg and assumed to
be in swim-up fry,
flow rate = 8-12
[42] L; no significant
increase in
mortality from
hatch to swim-up;
liposome used to
carry dose; 93% of
dose retained in
egg and assumed to
be in swim-up fry,
flow rate = 8 to 12
Oncorhynchus
mykiss,
Rainbow trout
0.00017 mg/kg
(whole body)4
Mortality,
ED50
[43] L; estimated LDSOs
for 6 strains of
rainbow trout,
orig_con_wet
ranged from 170 to
488; used low
value; exposure
concentration =
170 to 488
-------
Summary of Biological Effects Tissue Concentrations for 2,3,7,8-TCDD
Species:
Taxa
Concentration, Units in1:
Toxicity:
Ability to Accumulate2:
Source:
Log Log
Sediment Water Tissue (Sample Type) Effects BCF BAF BSAF Reference Comments3
Salmo trutta,
Brown trout
5.2 pg/g5 (fillet)
4.25-4.45
[22] F; locations
throughout Maine;
a range of mean
BAFs is presented;
the values are
means for locations
throughout Maine,
and the range is for
BAFs calculated
using river
concentrations
from years prior to
the sampling date
to account for
declines in paper
mill discharges
Salvelinus
fontinalis,
Brook trout
0.0006 mg/kg
(whole body)4
Physiological
[33]
L; induction of
hepatic EROD
-------
to
-------
Summary of Biological Effects Tissue Concentrations for 2,3,7,8-TCDD
Species:
Taxa
Concentration, Units in1: Toxicity:
Sediment Water Tissue (Sample Type) Effects
Ability to Accumulate2:
BSAF
Log
BCF
Log
BAF
Source:
Reference Comments3
0.0006 mg/kg
(whole body)4
Reproduction,
NOED
[41] L; no delay in
spawning; TCDD-
spiked diet to
produce desired
body burden;
abstract with
minimal
information
Salvelinus
fontinalis,
Brook trout
0.0002 mg/kg
(whole body)4
Mortality,
ED50
[43]
L; estimated LD50
Amia calva,
Bowfm
11.2ppt5(liver)
(n=l)
18.6 ppt5 (liver)
(n=l)
46.1 ppt5 (ovary)
(n=l)
-0.59 0.180 [15]
-0.36 0.255
0.03 0.281
F; northeastern
Florida; bleached-
kraft paper mill
receiving stream;
BAF and BSAF
calculated using
mean of two
sediment concen-
trations.
BAF =
(pg TCDD/g tissue)
T- (pg TCDD /
g sediment);
BSAF =
(pg TCDD/g lipid)
T- (pg TCDD /
g TOC).
oo
-J
-------
Summary of Biological Effects Tissue Concentrations for 2,3,7,8-TCDD
Species:
Taxa
Oncorhynchiis
kisutch,
Coho salmon
Carp,
(scientific name
unknown)
Salvelinus
namaycush,
Lake trout,
(early life stage)
Concentration, Units in1:
Sediment Water Tissue (Sample Type)
0.000478 mg/kg
(whole body)4
0.000478 mg/kg
(whole body)4
0.00217 mg/kg
(whole body)4
0.00217 mg/kg
(whole body)4
0.000125 mg/kg
(whole body)4
0.000125 mg/kg
(whole body)4
water 2.2 |ig/kg5
exposure
62pg/L
water 0.055 |ig/kg5 (egg)
exposure
20ng/L
Toxicity: Ability to Accumulate2:
Log Log
Effects BCF BAF BSAF
Growth, LOED
Mortality,
LOED
Growth, NA
Mortality, NA
Behavior,
NOED
Growth, NOED
Death (71 days)
48-hour LOEC
(mortality)
Source:
Reference
[39]
[39]
[39]
[39]
[39]
[39]
[16]
[21]
Comments3
L; reduced growth
L; reduced survival
L; reduced growth
L; reduced survival
L; no effect on food
consumption or
feeding
L; no effect on
growth
L
L
-------
Summary of Biological Effects Tissue Concentrations for 2,3,7,8-TCDD
Species:
Taxa
Salvelinus
namaycush,
Lake trout
Salvelinus
namaycush,
Lake trout
Concentration, Units in1:
Sediment Water Tissue (Sample Type)
water 0.034 |ig/kg5 (egg)
exposure
lOng/L
water 0.226 |ig/kg5 (egg)
exposure
62ng/L
0.000065 mg/kg
(whole body)4
0.000055 mg/kg
(whole body)4
0.000226 mg/kg
(whole body)4
0.000035 mg/kg
(whole body)4
0.000044 mg/kg
(whole body)4
Toxicity: Ability to Accumulate2:
Log Log
Effects BCF BAF BSAF
48-hour NOEC
(mortality)
48-hour LOEC
(hatchability)
Mortality,
ED50
Mortality,
LOED
Reproduction,
L
Mortality,
NOED
Mortality,
ED50
Source:
Reference
[21]
[21]
[15]
[15]
[15]
[15]
[34]
Comments3
L
L
L; lethal to 50% of
sac fry
L; lowest
statistically
significant increase
in mortality of sac
fry
L; reduced
hatchability of eggs
L; no effect on
mortality of sac fry
L; LD50 for sac fry
mortality
-------
Summary of Biological Effects Tissue Concentrations for 2,3,7,8-TCDD
Species:
Taxa
Concentration, Units in1:
Toxicity:
Ability to Accumulate2:
Source:
Log Log
Sediment Water Tissue (Sample Type) Effects BCF BAF BSAF Reference Comments3
Salvelinus
namaycush,
Lake trout
0.000065 mg/kg
(whole body)4
Mortality,
ED50
0.000055 mg/kg
(whole body)4
Mortality,
LOED
[42] L; mortality from
fertilization to
swim-up; exposure
dose calculated
from text; residue
measured in egg at
5-days post
exposure; dosed for
48 hours and
endpoint measured
after approximately
24 days
[42] L; significant
increase in
mortality from
hatch to swim-up;
exposure dose
calculated from
text; residue
measured in egg at
5-days post
exposure; dosed for
48 hours and
endpoint measured
after approximately
24 days
-------
Summary of Biological Effects Tissue Concentrations for 2,3,7,8-TCDD
Species:
Taxa
Concentration, Units in1:
Toxicity:
Ability to Accumulate2:
Source:
Log Log
Sediment Water Tissue (Sample Type) Effects BCF BAF BSAF Reference Comments3
0.000058 mg/kg
(whole body)4
Mortality,
LOED
0.000034 mg/kg
(whole body)4
Mortality,
NOED
[42] L; significant
increase in
mortality from
hatch to swim-up;
high control
mortality; liposome
used to carry dose;
93% of dose
retained in egg and
assumed to be in
swim-up fry, flow
rate = 8-12
[42] L; no significant
increase in
mortality from
hatch to swim-up;
exposure dose
calculated from
text; residue
measured in egg at
5-days post
exposure; dosed for
48 hours and
endpoint measured
after approximately
24 days
-------
Summary of Biological Effects Tissue Concentrations for 2,3,7,8-TCDD
Species:
Taxa
Concentration, Units in1: Toxicity:
Sediment Water Tissue (Sample Type) Effects
Ability to Accumulate2:
BSAF
Log
BCF
Log
BAF
Source:
Reference Comments3
0.000044 mg/kg
(whole body)4
Mortality,
NOED
[42] L; no significant
increase in
mortality from
hatch to swim-up;
high control
mortality; liposome
used to carry dose;
93% of dose
retained in egg and
assumed to be in
swim-up fry, flow
rate = 8 to 12
Salvelinus
namaycush,
Lake trout
0.000065 mg/kg
(whole body)4
Mortality,
ED50
[43]
L; estimated LD50
Carassius auratus,
Goldfish
0.58-0.63 ng/g5
(whole body)
4.39
[18] L; fish were
exposed for 120 hr;
exposure water
contained fly ash
extract;
concentrations
were measured in
water, but data
were not presented
-------
Summary of Biological Effects Tissue Concentrations for 2,3,7,8-TCDD
Species:
Taxa
Cyprinus carpio,
Carp
Cyprinus carpio,
Carp
Cyprinus carpio,
Carp
Cyprinus carpio,
Carp
Concentration, Units in1:
Sediment Water Tissue (Sample Type)
170 pg/g5 120 pg/g5
0.0022 mg/kg
(whole body)4
0.0022 mg/kg
(whole body) 4
0.0022 mg/kg
(whole body)4
0.003 mg/kg
(whole body)4
0.0022 mg/kg
(whole body)4
Toxicity: Ability to Accumulate2:
Log Log
Effects BCF BAF BSAF
0.27
Behavior,
LOED
Cellular, LOED
Morphology,
LOED
Mortality,
ED50
Mortality,
LOED
Source:
Reference Comments3
[9] F; Petenwell
Reservoir, central
Wisconsin; BSAF
based on 8% tissue
lipid content and
3.1% sediment
organic carbon
[15] L; difficulty
swimming
[15] L; edema, body
wall ulcers
[15] L; fin erosion,
hemorrhage,
morphologically
resembling Blue
Sac Disease
[36] L; 80-day LD50 for
mortality
[15] L; increased
mortality
-------
Summary of Biological Effects Tissue Concentrations for 2,3,7,8-TCDD
Species:
Taxa
Danio rerio,
Zebrafish
Bracydanio rerio,
Zebrafish
Pimephales
promelas,
Fathead minnow
Concentration, Units in1:
Sediment Water Tissue (Sample Type)
2. 16 ng/g (egg)
2.43 ng/g (egg)
2.45 ng/g (egg)
8.3 |ig/kg5
8.3 ng/kg5
17-2,042 |ig/kg5
Toxicity: Ability to Accumulate2:
Log Log
Effects BCF BAF BSAF
ED50 (pericar-
dial edema)
ED50 (yolk
sac edema)
LD50
LOEC
(reproduction)
LOEC
(oogenesis)
LD100
Source:
Reference Comments3
[23] L; newly fertilized
eggs were exposed
for 1 hr to water
containing graded
concentrations of
TCDD
[24] L; food exposure
[24] L; food exposure
[17] L; food exposure
-------
Summary of Biological Effects Tissue Concentrations for 2,3,7,8-TCDD
Species:
Taxa
Catostomus
commerson,
White sucker
Concentration, Units in1: Toxicity:
Sediment Water Tissue (Sample Type) Effects
9.6 pg/g5
(whole body)
Ability to Accumulate2:
Log Log
BCF BAF BSAF
4.89-5.03
Source:
Reference
[22]
Comments3
F; locations
throughout Maine;
a range of mean
BAFs is presented;
the values are
means for locations
throughout Maine,
and the range is for
BAFs calculated
using river
concentrations
from years prior to
the sampling date
to account for
declines in paper
mill discharges
-------
Summary of Biological Effects Tissue Concentrations for 2,3,7,8-TCDD
Species: Concentration, Units in1:
Taxa Sediment Water
Ictalurus nebulosus, 32.2 -52.8
Brown bullhead ppt5
catfish (TOC = 3.2-
3.9%)
Ictalurus melas,
Black bullhead
Toxicity:
Tissue (Sample Type) Effects
1.8 ppt5 (liver)
(% lipid = 3.5)
2.6 ppt5 (liver)
(% lipid = 2.9)
2.8 ppt5 (liver)
(% lipid = 3.2)
0.005 mg/kg Mortality,
(whole body)4 ED50
0.025 mg/kg Morphology,
(whole body)4 LOED
Ability to Accumulate2: Source:
Log Log
BCF BAF BSAF Reference Comments3
-1.40 0.043 [15] F; northeastern
Florida; bleached-
kraft paper mill
-1.22 0.074 receiving stream;
BAF and BSAF
calculated using
-1.15 0.073 mean of two
sediment concen-
trations.
BAF =
(pg TCDD/g tissue)
•f (pg TCDD/
g sediment);
BSAF =
(pg TCDD/g lipid)
•f (pg TCDD /
g TOC).
[36] L; 80 day LD50 for
mortality
[36] L; fin necrosis,
hyperpigmentation
-------
Summary of Biological Effects Tissue Concentrations for 2,3,7,8-TCDD
Species:
Taxa
Concentration, Units in1: Toxicity:
Sediment Water Tissue (Sample Type) Effects
Ability to Accumulate2:
BSAF
Log
BCF
Log
BAF
Source:
Reference Comments3
Ictalums punctatus,
Channel catfish
0.0044 mg/kg
(whole body)4
Mortality,
ED10
[45] L; radiolabelled
compounds in
sediment,
compound leached
into water for
exposure; all fish
died between days
14 and 15; body
residues from dead
fish
Gambusia affinis,
Mosquito fish
0.0072 mg/kg
(whole body)4
Mortality,
ED10
[45] L; radiolabelled
compounds in
sediment,
compound leached
into water for
exposure; all fish
died between days
14 and 15; body
residues from dead
fish
Oryzias latipes,
Japanese medaka
Water
exposure
2.2 ng/L
0.24 |ig/kg5
(embryo)
Lesions in
embryos
[19]
L
-------
Summary of Biological Effects Tissue Concentrations for 2,3,7,8-TCDD
Species:
Taxa
Oryzias latipes,
Japanese medaka
(juveniles)
Concentration, Units in1:
Sediment Water
water
exposure
101 ±26
Pg/L
(n = 23)
Toxicity:
Tissue (Sample Type) Effects
2,408 ±241 pg/g Obvious signs
ofTCDD
toxicity such as
generalized
edema, fin
erosion, and
discoloration in
many of the
exposed fish
Ability to Accumulate2:
Log Log
BCF BAF BSAF
4.38
non-
steady
state
5.71
predicted
steady
state
Source:
Reference Comments3
[20] L; 12-day exposure
period;
lipid content 7.5%
Oryzias latipes,
Japanese medaka
0.24 mg/kg
(whole body)4
0.3 mg/kg
(whole body)4
0.1 mg/kg
(whole body)4
Lesions, ED50
Lesions, LOED
Lesions, NOED
[19] L; ten replicates per
treatment
[19] L; 50% of embryos
with lesions but no
statistical
significance
analyzed; ten
replicates per
treatment
[19] L; no significant
incidence of lesions
at lowest doseage
tested; 10 replicates
per treatment,
resd_conc_wet
value > 0.1
-------
Summary of Biological Effects Tissue Concentrations for 2,3,7,8-TCDD
Species:
Taxa
Concentration, Units in1:
Sediment Water
Toxicity:
Tissue (Sample Type) Effects
Ability to Accumulate2:
Source:
Log
BCF
Log
BAF
BSAF Reference Comments3
Morone americana,
White perch
1.2
[22] F; locations
throughout Maine;
a range of mean
BAFs is presented;
the values are
means for locations
throughout Maine,
and the range is for
BAFs calculated
using river
concentrations
from years prior to
the sampling date
to account for
declines in paper
mill discharges
Lepomis
macrochirus,
Bluegill
0.016 mg/kg
(whole body)4
0.005 mg/kg
(whole body)4
0.025 mg/kg
(whole body)4
Mortality,
ED50
Growth, LOED
Morphology,
LOED
[36] L; 80-day LD50 for
mortality
[36] L; reduction in
body weight
[36] L; fin necrosis,
hyperpigmentation
-------
o
o
Summary of Biological Effects Tissue Concentrations for 2,3,7,8-TCDD
Species: Concentration, Units in1: Toxicity:
Taxa Sediment Water Tissue (Sample Type) Effects
Microperus 3.4 pg/g5 (fillet)
dolomieu,
Smallmouth bass
Ability to Accumulate2:
Log Log
BCF BAF BSAF
4.06-4.39
Source:
Reference
[22]
Comments3
F; locations
throughout Maine;
a range of mean
BAFs is presented;
the values are
means for locations
throughout Maine,
and the range is for
BAFs calculated
using river
concentrations
from years prior to
the sampling date
to account for
declines in paper
mill discharges
-------
Summary of Biological Effects Tissue Concentrations for 2,3,7,8-TCDD
Species:
Taxa
Concentration, Units in1:
Toxicity:
Ability to Accumulate2:
Log Log
Sediment Water Tissue (Sample Type) Effects BCF BAF BSAF
Source:
Reference Comments3
Microptems 32.2 ppt5
samoides, (TOC=3.2%)
Largemouth bass
52.8 ppt5
(TOC=3.9%)
Microptems
salmoides,
Largemouth bass
1.8 ppt5 (liver)
(% lipid =3.9)
2.9 ppt5 (liver)
(% lipid =2.4)
8.8 ppt5 (ovary)
(% lipid =7.6)
0.011 mg/kg Mortality,
(whole body)4 ED50
0.025 mg/kg Morphology,
(whole body)4 LOED
-1.40 0.038 [15] F; northeastern
Florida; bleached
kraft paper mill
-1.15 0.100 receiving stream;
BAF and BSAF
calculated using
-0.68 0.096 mean of two
sediment concen-
trations.
BAF =
(pgTCDD/
g tissue) -=-
(pg TCDD/
g sediment);
BSAF =
(pg TCDD/g lipid)
4- (pg TCDD/
g TOC).
[36] L; 80-day LD50
For Mortality
[36] L; Fin Necrosis,
Hyperpigment-
ation
Percaflavescens,
Yellow perch
0.003 mg/kg
(whole body)4
0.005 mg/kg
(whole body)4
Mortality,
ED50
Growth, LOED
[36] L; 80-day LD50 for
mortality
[36] L; reduction in
body weight
-------
Summary of Biological Effects Tissue Concentrations for 2,3,7,8-TCDD
Species: Concentration, Units in1:
Taxa Sediment Water Tissue (Sample Type)
0.025 mg/kg
(whole body)4
0.000129 mg/kg
(carcass)4
0.000148 mg/kg
(gastrointestinal tract)4
0.000155 mg/kg
(gill)4
0.000077 mg/kg
(heart)4
0.0001 19 mg/kg
(kidney)4
0.000466 mg/kg
(liver)4
0.000143 mg/kg
(pyloric caeca)4
0.000009 mg/kg
(skeletal muscle)4
0.000041 mg/kg
(skin)4
0.000166 mg/kg
(spleen)4
0.00277 mg/kg
(visceral fat)4
Toxicity: Ability to Accumulate2:
Log Log
Effects BCF BAF BSAF
Morphology,
LOED
Growth, NOED
Growth, NOED
Growth, NOED
Growth, NOED
Growth, NOED
Growth, NOED
Growth, NOED
Growth, NOED
Growth, NOED
Growth, NOED
Growth, NOED
Source:
Reference
[36]
[37]
[37]
[37]
[37]
[37]
[37]
[37]
[37]
[37]
[37]
[37]
Comments3
L; fin necrosis,
hyperpigmentation
L; no effect on
growth
L; no effect on
growth
L; no effect on
growth
L; no effect on
growth
L; no effect on
growth
L; no effect on
growth
L; no effect on
growth
L; no effect on
growth
L; no effect on
growth
L; no effect on
growth
L; no effect on
growth
-------
Summary of Biological Effects Tissue Concentrations for 2,3,7,8-TCDD
Species: Concentration, Units in1:
Taxa Sediment Water Tissue (Sample Type)
0.000143 mg/kg
(whole body)4
0.000129 mg/kg
(carcass)4
0.000148 mg/kg
(gastrointestinal tract)4
0.000155 mg/kg
(gill)4
0.000077 mg/kg
(heart)4
0.0001 19 mg/kg
(kidney)4
0.000466 mg/kg
(liver)4
0.000143 mg/kg
(pyloric caeca)4
0.000009 mg/kg
(skeletal muscle)4
Toxicity: Ability to Accumulate2:
Log Log
Effects BCF BAF BSAF
Growth, NOED
Morphology,
NOED
Morphology,
NOED
Morphology,
NOED
Morphology,
NOED
Morphology,
NOED
Morphology,
NOED
Morphology,
NOED
Morphology,
NOED
Source:
Reference
[37]
[37]
[37]
[37]
[37]
[37]
[37]
[37]
[37]
Comments3
L; no effect on
growth
L; no effect on fin
necrosis or
hemorrhage
L; no effect on fin
necrosis or
hemorrhage
L; no effect on fin
necrosis or
hemorrhage
L; no effect on fin
necrosis or
hemorrhage
L; no effect on fin
necrosis or
hemorrhage
L; no effect on fin
necrosis or
hemorrhage
L; no effect on fin
necrosis or
hemorrhage
L; no effect on fin
necrosis or
hemorrhage
-------
o Summary of Biological Effects Tissue Concentrations for 2,3,7,8-TCDD
Species: Concentration, Units in1:
Taxa Sediment Water Tissue (Sample Type)
0.000041 mg/kg
(skin)4
0.000166 mg/kg
(spleen)4
0.00277 mg/kg
(visceral fat)4
0.000143 mg/kg
(whole body)4
0.000129 mg/kg
(carcass)4
0.000148 mg/kg
(gastrointestinal tract)4
0.000 155 mg/kg
(gill)4
0.000077 mg/kg
(heart)4
0.0001 19 mg/kg
(kidney)4
0.000466 mg/kg
(liver)4
Toxicity:
Effects
Morphology,
NOED
Morphology,
NOED
Morphology,
NOED
Morphology,
NOED
Mortality,
NOED
Mortality,
NOED
Mortality,
NOED
Mortality,
NOED
Mortality,
NOED
Mortality,
NOED
Ability to Accumulate2: Source:
Log Log
BCF BAF BSAF Reference
[37]
[37]
[37]
[37]
[37]
[37]
[37]
[37]
[37]
[37]
Comments3
L; no effect on fin
necrosis or
hemorrhage
L; no effect on fin
necrosis or
hemorrhage
L; no effect on fin
necrosis or
hemorrhage
L; no effect on fin
necrosis or
hemorrhage
L; no effect on
mortality
L; no effect on
mortality
L; no effect on
mortality
L; no effect on
mortality
L; no effect on
mortality
L; no effect on
mortality
-------
Summary of Biological Effects Tissue Concentrations for 2,3,7,8-TCDD
Species: Concentration, Units in1:
Taxa Sediment Water Tissue (Sample Type)
0.000143 mg/kg
(pyoric ceca)4
0.000009 mg/kg
(skeletal muscle)4
0.000041 mg/kg
(skin)4
0.000 166 mg/kg
(spleen)4
0.00277 mg/kg
(visceral fat)4
0.000143 mg/kg
(whole body)4
Toxicity:
Effects
Mortality,
NOED
Mortality,
NOED
Mortality,
NOED
Mortality,
NOED
Mortality,
NOED
Mortality,
NOED
Ability to Accumulate2: Source:
Log Log
BCF BAF BSAF Reference
[37]
[37]
[37]
[37]
[37]
[37]
Comments3
L; no effect on
mortality
L; no effect on
mortality
L; no effect on
mortality
L; no effect on
mortality
L; no effect on
mortality
L., no effect on
mortality
Salmonids
0.059
[46]
-------
o
ON
Summary of Biological Effects Tissue Concentrations for 2,3,7,8-TCDD
Species:
Taxa
Concentration, Units in1:
Toxicity:
Ability to Accumulate2:
Source:
Log Log
Sediment Water Tissue (Sample Type) Effects BCF BAF BSAF Reference Comments3
Wildlife
Aix sponsa,
Wood duck
pg/g (eggs):
Site 1 geometric
mean: 36 (1.6 to 482)
Site 2 geometric
mean: 14 (0.8-74)
Site 3 geometric
mean: 4.2 (<1 to 19)
Site 4 geometric
mean: 0.01 (<1 to 0.5)
% eggs hatched:
47% (9.7 SE)
62% (10.1 SE)
79% (3.8 SE)
93% (3.4 SE)
[29] F; central
Arkansas; egg
TEFs and hatching
success and
duckling
production were
negatively
correlated; clutch
size was similar
among wetland
Sites 1-3 which
were 9, 17, and 58
km downstream
from point source
of contamination.
respectively, and
Site 4 which was
111 km away on a
separate drainage;
duckling abnor-
malities were also
noted
Aix sponsa,
Wood duck
Threshold range of
reduced
productivity was
> 20-50 ppt TEF.
-------
Summary of Biological Effects Tissue Concentrations for 2,3,7,8-TCDD
Species:
Taxa
Falco peregrinus,
Peregrine falcon
Haliaeetiis
leucocephalus,
Bald eagle chicks
Concentration, Units in1:
Sediment Water Tissue (Sample Type)
1 1 ng/g (eggs)
(n=6)
Powell River site:
2,200 ng/kg lipid
weight basis
(yolk sac)
Reference site: 300
ng/kg lipid weight
basis (yolk sac)
Toxicity: Ability to Accumulate2:
Log Log
Effects BCF BAF BSAF
11. 4% eggshell
thinning
A nearly 6-fold
greater
incidence of an
hepatic
cytochrome
P4501 A cross-
reactive protein
was induced in
chicks from
Powell River
site as
compared to the
reference
(p < 0.05).
No significant
concentration-
related effects
were found for
morphological,
physiological,
or histological
parameters.
Source:
Reference Comments3
[26] F; Kola Peninsula,
Russia
[25] F; southern coast of
British Columbia;
eggs were collected
from nests and
hatched in the lab;
~ indicates value
was taken from a
figure.
o
-J
-------
o
oo
Summary of Biological Effects Tissue Concentrations for 2,3,7,8-TCDD
Species:
Taxa
Sterna forsteri,
Forster's tern
Concentration, Units in1: Toxicity: Ability to Accumulate2: Source:
Log Log
Sediment Water Tissue (Sample Type) Effects BCF BAF BSAF Reference Comments3
Lake Poygan site: Birds from [27] F; Green Bay,
8.0 pg/g; (egg) Green Bay had Lake Michigan,
(n = 6) increased and Lake Poygan,
incubation Wisconsin
Green Bay site: period, reduced
37.3 pg/g; (egg) hatchability,
(n = 6) lower body
weight,
increased liver
to body weight
ratio, and
occurrence of
edema when
compared to
birds from Lake
Poygan. There
was a
significantly
higher
incidence of
congenital
abnormalities in
dead embryos
and chicks from
Green Bay.
-------
Summary of Biological Effects Tissue Concentrations for 2,3,7,8-TCDD
Species:
Taxa
Ardea herodias,
Great blue heron
chicks
Concentration, Units in1:
Toxicity:
Sediment Water Tissue (Sample Type) Effects
Nicomekl site:
10±0.9 ng/kg;
(egg)
Ability
Log
BCF
to Accumulate2:
Log
BAF BSAF
Source:
Reference
[28]
Comments3
L; eggs were
collected from
three British
Vancouver site:
(n = 12)
Crofton site: 2
11±33.7 ng/kg (egg)
(n = 6)
Depression of
135±49.6 ng/kg (egg) growth
compared to
Nicomekl site.
Presence of
edema.
Depression of
growth
compared to
Nicomekl site.
Presence of
edema.
Columbia colonies
with different
levels of
contamination and
incubated in the
laboratory
-------
Summary of Biological Effects Tissue Concentrations for 2,3,7,8-TCDD
Species:
Taxa
Mustela vison,
Mink
Concentration, Units in1: Toxicity:
Sediment Water Tissue (Sample Type) Effects
Diet: 2 pg/g5 21 pg/g5 (liver) LOAEL;
reduced kit
body weights
followed by
reduced
survival
Diet: 3 pg/g5 34 pg/g5 (liver) Reduced kit
body weights
followed by
reduced
survival
Diet: 7 pg/g5 50 pg/g5 (liver) Significant
decrease in
number of live
kits whelped
per female
Ability to Accumulate2:
Log Log
BCF BAF BSAF
log
BMF=
1.05
log
BMF =
1.06
log
BMF =
1.04
Source:
Reference Comments3
[30] L; BMP =
biomagnification
factor = V[/vd,
V[ = lipid-
normalized
concentration in
tissue;
vd = lipid-
normalized dietary
concentration
1 Concentration units based on wet weight unless otherwise noted.
2 BCF = bioconcentration factor, BAF = bioaccumulation factor, BSAF = biota-sediment accumulation factor.
3 L = laboratory study, spiked sediment, single chemical; F = field study, multiple chemical exposure; other unusual study conditions or observations noted.
4 This entry was excerpted directly from the Environmental Residue-Effects Database (ERED, www.wes.army.mil/el/ered, U.S. Army Corps of Engineers and U.S.
Environmental Protection Agency). The original publication was not reviewed and the reader is strongly urged to consult the publication to confirm the information
presented here.
5 Not clear from reference if concentration is based on wet or dry weight.
-------
BIOACCUMULATION SUMMARY 2,3,7,8-TCDD
References
1. Podoll, R.T., et al., 1986, Environ. Sci. Technol 20:490-492 (cited in: USEPA. 1996.
Hazardous Substances Data Bank (HSDB). National Library of Medicine online (TOXNET).
U.S. Environmental Protection Agency, Office of Health and Environmental Assessment,
Environmental Criteria and Assessment Office, Cinncinati, OH. February).
2. USEPA. 1989. Chemical fate rate constants for SARA section 313 chemicals and Superfund
Health Evaluation Manual chemicals. Prepared by Chemical Hazard Assessment Division,
Syracuse Research Corporation, for U.S. Environmental Protection Agency, Office of Toxic
Substances, Exposure Evaluation Division, Washington, DC, and Environmental Criteria and
Assessment Office, Cincinnati, OH. August 11.
3. Karickhoff, S.W., and J.M. Long. 1995. Internal report on summary of measured, calculated
and recommended log Kow values. Draft. Prepared by U.S. Environmental Protection Agency,
Office of Research and Development, Environmental Research Laboratory-Athens, for E.
Southerland, Office of Water, Office of Science and Technology, Standards and Applied
Science Division, Washington, DC. April 10.
4. USEPA. 1995. Health Effects Assessment Summary Tables: FY-1995 Annual. EPA/540/R-
95/036. U.S. Environmental Protection Agency, Office of Solid Waste and Emergency
Response, Washington, DC.
5. Safe, S. 1990. Polychlorinated biphenyls (PCBs), dibenzo-p-dioxins (PCDDs), dibenzofurans
(PCDFs), and related compounds: Environmental and mechanistic considerations which support
the development of toxicity equivalency factors (TEE). Crit. Rev. Toxicol. 21:51-88.
6. Braune, B.M. and RJ. Norstrom. 1989. Dynamics of organochlorine compounds in herring
gulls: HI. Tissue distribution and bioaccumulation in Lake Ontario gulls. Environ. Toxicol.
Chem. 8:957-968.
7. USEPA. 1993. Interim report on data and methods for assessment of 2,3,7,8-
tetrachlorodibenzo-^-dioxin risks to aquatic life and associated wildlife. EPA/600/R-93/055.
U.S. Environmental Protection Agency, Office of Research and Development, Washington, DC.
8. Pruell, R.J., N.I. Rubinstein, B.K. Taplin, J.A. LiVolsi, and R.D. Bowen. 1993. Accumulation
of polychlorinated organic contaminants from sediment by three benthic marine species. Arch.
Environ. Contam. Toxicol. 24:290-297.
9. Kuehl, D.W., P.M. Cook, A.R. Batterman, D. Lothenbach, and B.C. Butterworth. 1987.
Bioavailability of polychlorinated dibenzo-p-dioxins and dibenzofurans from contaminated
Wisconsin River sediment to carp. Chemosphere 16(4):667-679.
10. Eisler, R. 1986. Dioxin hazards to fish, wildlife, and invertebrates: A synoptic review. U.S.
Fish Wildl. Serv. Biol. Rep. 85 (1.8):37.
311
-------
BIOACCUMULATION SUMMARY 2,3,7,8-TCDD
11. USEPA. 1989. Interim procedures for estimating risks associated with exposure to mixtures of
chlorinated dibenzo-p-dioxins and dibenzofurans (CDDs and CDFs) and 1989 update.
EPA/625/3-89/016. U.S. Environmental Protection Agency, Risk Assessment Forum,
Washington, DC.
12. Cooper, K.R. 1989. Effects of polychlorinated dibenzo-p-dioxins and polychlorinated
dibenzofurans on aquatic organisms. Rev. Aquat. Sci. 1:227-242.
13. Mehrle, P.M., D.R. Buckler, E.E. Little, L.M. Smith, J.D. Petty, P.M. Peterman, D.L. Stalling,
G.M. DeGraeve, JJ. Coyle, and WJ. Adams. 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.
14. Rubinstein, N.I., R.J. Pruell, B.K. Taplin, J.A. LiVolsi, and C.B. Norwood. 1990.
Bioavailability of 2,3,7,8-TCDD, 2,3,7,8-TCDF and PCBs to marine benthos from Passaic River
sediments. Chemosphere 20(7-9):1097-1102.
15. Schell, J.D. Jr., D.M. Campbell, and E. Lowe. 1993. Bioaccumulation of 2,3,7,8-
tetrachlorodibenzo-/?-dioxin in feral fish collected from a bleach-kraft paper mill receiving
stream. Environ. Toxicol. Chem. 12:2077-2082.
16. Cook, P.M., D.W. Kuehl, M.K. Walker, and R.E. Peterson. 1991. Bioaccumulation and toxicity
of TCDD and related compounds in aquatic ecosystems. Abstract, in Dioxin '92.
17. 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 minnow (Pimephales promelas).
Chemosphere 15:1503-1511.
18. Sijm, D.T.H.M., H. Wever, and A. Opperhuizen. 1993. Congener-specific biotransformation
and bioaccumulation of PCDDs and PCDFs from fly ash in fish. Environ. Toxicol. Chem. 12:
1895-1907.
19. Wisk, J.D., and K.R. Cooper. 1990. The stage specificity of 2,3,7,8-tetrachlorodibenzo-j?-dioxin
in embryos of the Japanese medaka (Oryzz'as latipes). Environ. Toxicol. Chem. 9:1159-1169.
20. Schmieder, P., D. Lothenbach, J. Tietge, R. Erickson, and R. Johnson. 1995. [3H]-2,3,7,8-
TCDD uptake and elimination kinetics of medaka (Oryzias latipes). Environ. Toxicol. Chem.
14(10):1735-1743.
21. Walker, M.K., J.M. Spitsbergen, J.R. Olson, and R.E. Peterson. 1991. 2,3,7,8-
Tetrachorodibenzo-p-dioxin (TCDD) toxicity during early life stage development of lake trout
(Salvelinus namaycush). Can. J. Fish. Aquat. Sci. 48:875-883.
22. Frakes, R.A., C.Q. T. Zeeman, and B. Mower. 1993. Bioaccumulation of 2,3,7,8-
tetrachlorodibenzo-/?-dioxin (TCDD) by fish downstream of pulp and paper mills in Maine.
Ecotoxicol. Environ. Saf. 25:244-252.
312
-------
BIOACCUMULATION SUMMARY 2,3,7,8-TCDD
23. Henry, T.R., M.W. Hornung, C.C. Abnet, and R.E. Peterson. 1995. Early life stage toxicity of
2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in zebrafish (Danio rerio). Poster presentation at
the 16th Annual Meeting of the Society of Environmental Toxicology and Chemistry (SETAR),
Second SET AC World Congress, November 5-9, 1995, Vancouver, British Columbia, Canada.
24. Wannamacher, R., A. Rebstock, E. Kulzer, D. Schrenk, and K.W. Bock. 1992. Effects of
2,3,7,8-tetrachlorodibenzo-p-dioxin on reproduction and oogenesis in zebrafish (Brachydanio
rerio). Chemosphere 24:1361-1368.
25. Elliott, J.E., RJ. Norstrom, A. Lorenzen, L.E. Hart, H. Philibert, S.W. Kennedy, JJ. Stegeman,
G.D. Bellward, and K.M. Cheng. 1995. Biological effects of polychlorinated dibenzo-p-dioxins,
dibenzofurans, and biphenyls in bald eagle (Haliaeetus leucocephalus) chicks. Environ. Toxicol.
Chem. 15(5):782-793.
26. Henny, C.J., S.A. Ganusevich, F.P. Ward, and T.R. Schwartz. 1994. Organochlorine pesticides,
chlorinated dioxins and furans, and PCBs in peregrine falcon Falco peregrinus eggs from the
Kola Penninsula, Russia. In Raptor Conservation Today, ed. B.U. Meyburg and R.D.
Chancellor, pp. 739-749. WWGPB/The Pica Press.
27. Kubiak, T.J., HJ. Harris, L.M. Smith, T.R. Schwartz, D.L. Stalling, J.A. Trick, L. Sileo, D.E.
Docherty, and T.C. Erdman. 1989. Microcontaminants and reproductive impairment of the
Forster's tern on Green Bay, Lake Michigan-1983. Arch. Environ. Contain. Toxicol. 18:706-
727.
28. Hart, L.E., K.M. Cheng, P.E. Whitehead, R.M. Shah, RJ. Lewis, S.R. Ruschkowski, R.W. Blair,
D.C. Bennett, S.M. Bandiera, RJ. Norstrom, and G.D. Bellward. 1991. Dioxin contamination
and growth and development in great blue heron embryos. /. Toxicol. Environ. Health 32:331-
344.
29. White, D.H., and J.T. Seginak. 1994. Dioxins and furans linked to reproductive impairment in
wood duck. J.Wildl. Manage. 58(1):100-106.
30. Tillitt, D.E., R.W. Gale, J.C. Meadows, J.L. Zajicek, P.H. Peterman, S.N. Heaton, P.O. Jones,
S J. Bursian, TJ. Kubiak, J.P. Giesy, and RJ. Aulerich. 1996. Dietary exposure of mink to carp
from Saginaw Bay. 3. Characterization of dietary exposure to planar halogenated hydrocarbons,
dioxin equivalents, and biomagnification. Environ. Sci. Technol. 30:283-291.
31. Ashley, C.M., M.G. Simpson, D.M. Holdich, and D.R. BeU. 1996. 2,3,7,8-tetrachloro-dibenzo-/?-
dioxin is a potent toxin and induces cytochrome P450 in the crayfish, Pacifastacus leniusculus.
Aquat. Toxicol. 35:157-169.
32. Branson, D.R., L.T. Takahashi, W.M. Parker, and G.E. Blau. 1985. Bioconcentration kinetics
of 2,3,7,8-tetrachlorodibenzo-/?-dioxin in rainbow trout. Environ. Toxicol. Chem. 4:779-788.
33. Daniel, F.B., S. Cormier, B. Subramanian, D. Williams, J. Torsella, and J. Lech. 1994. Six month
EROD response pattern of dioxin fed brook trout. Abstract, 15th Annual Meeting, Society of
Environmental Toxicology and Chemistry, 30 October-3 November, 1994, Denver, CO.
313
-------
BIOACCUMULATION SUMMARY 2,3,7,8-TCDD
34. Guiney, P., E. Zabel, R. Peterson, P. Cook, J. Casselman, J. Fitzsimons, and H. Simonin. 1993.
Assessment of Lake Ontario lake trout for 2,3,7,8-tetrachlorodibenzo-j?-dioxin equivalents
(TEQS) induced sac fry mortality in 1991. Presentation 519, 14th Annual Meeting, Society of
Environmental Toxicology and Chemistry, Houston, TX.
35. Isensee, A.R., and G.E. Jones. 1975. Distribution of 2,3,7,8-tetrachlorodibenzo-j?-dioxin
(TCDD) in an aquatic model ecosystem. Environ. Set Technol. 9:668-672.
36. Kleeman, J.M., J.R. Olson, and R.E. Peterson. 1988. Species differences in 2,3,7,8-
tetrachlorodibenzo-p-dioxin toxicity and biotransformation in fish. Fund. Appl. Toxicol. 10:206-
213.
37. Kleeman, J.M., J.R. Olson, S.M. Chen, and R.E. Peterson. 1986. 2,3,7,8-tetrachlorodibenzo-p-
dioxin metabolism and disposition in yellow perch. Toxicol. Appl. Pharmacol. 83:402-411.
38. Kleeman, J.M., J.R. Olson, S.M. Chen, and R.E. Peterson. 1986. Metabolism and disposition of
2,3,7,8-tetrachlorodibenzo-/?-dioxin in rainbow trout. Toxicol. Appl. Pharmacol. 83:391-401.
39. Miller, R.A., L.A. Norris, and B.R. Loper. 1979. The response of coho salmon and guppies to
2,3,7,8-tetrachlorodibenzo-/?-dioxin (TCDD) in water. Trans. Amer. Fish. Soc. 108:401-407.
40. Parrott, J.L., P.V. Hodson, M.R. Servos, S.L. Huestis, and G.D. Dixon. 1995. Relative potency
of polychlorinated dibenzo-p-dioxins and dibenzofurans for inducing mixed-function oxygenase
activity in rainbow trout. Environ. Toxicol. Chem. 14(6):1041-1050.
41. Tietge, J.E. 1994. Reproductive and toxicological effects in brook trout following a dietary
exposure to 2,3,7,8-TCDD. Abstract, 15th Annual Meeting, Society of Environmental
Toxicology and Chemistry, Denver, CO, October 30-November 3, 1994.
42. Walker, M.K., L.C. Hufnagle, Jr., M.K. Clayton, and R.E. Peterson. 1992. An egg injection
method for assessing early life stage mortality of polychlorinated dibenzo-p-dioxins,
dibenzofurans, and biphenyls in rainbow trout (Oncorhynchus mykiss). Aquat. Toxicol. 22:15-38.
43. Walker, M.K., E.W. Zabel, and R.E Peterson. 1993. 2,3,7,8-tetrachlorodibenzo-p-dioxin
(TCDD)-induced toxicity during salmonid early life stage development: Cross species and strain
comparisons. Abstract, Society of Environmental Toxicology and Chemistry, 14th Annual
Meeting, Houston, TX, November 14-18, 1993.
44. West, C.W., G.T. Ankley, J.W. Nichols, G.E. Elonen, and D.E. Nessa. 1997. Toxicity and
bioaccumulation of 2,3,7,8-tetrachlorodibenzo-j?-dioxin in long-term tests with the freshwater
benthic invertebrates Chironomus teutons and Lumbriculus variegatus. Environ. Toxicol Chem.
16(6):1287-1294.
45. 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 1: 215-220.
314
-------
BIOACCUMULATION SUMMARY 2,3,7,8-TCDD
46. USEPA. 1995. Great Lakes Water Quality Initiative Technical Support Document for the
procedure to determine bioaccumulation factors. EPA-820-B-95-005. U.S. Environmental
Protection Agency, Office of Water, Washington, DC.
315
-------
316
-------
BIOACCUMULATION SUMMARY p,p -ODD
Chemical Category: PESTICIDE (ORGANOCHLORINE)
Chemical Name (Common Synonyms): CASRN: 72-54-8
1,1' -(2,2-DICHLOROETHYLIDENE)BIS (4-CHLOROBENZENE),
p,p' -DICHLORODIPHEN YLDICHLOROETHANE
4,4' -DICHLORODIPHEN YLDICHLOROETHANE
Chemical Characteristics
Solubility in Water: 0.16 mg/L at 24°C [1] Half-Life: 2.0-15.6 years based on
biodegradation of ODD in aerobic
soils under field conditions [2]
Log Kow: 6.10 [3] Log Koc: 6.0 L/kg organic carbon
Human Health
Oral RfD: Not available [4] Confidence: —
Critical Effect: Lung tumors in male and female mice, liver tumors in male mice, thyroid tumors in
male rats
Oral Slope Factor: 2.4 x 10"1 per (mg/kg)/day [4] Carcinogenic Classification: B2 [4]
Wildlife
Partitioning Factors: Partitioning factors for ODD in wildlife were not calculated in the studies
reviewed. However, based on the data presented in one study reviewed, log BCFs for birds from the
lower Detroit River ranged from 4.97 to 5.22. Concentrations of ODD in birds were 3.5 to 6.1 times
higher than those in sediment.
Food Chain Multipliers: Biomagnification factors of 3.2 and 85 were determined for DDT and DDE,
respectively, from alewife to herring gulls in Lake Ontario [5]. A study of arctic marine food chains
measured biomagnification factors for DDE that ranged from 17.6 to 62.2 for fish to seal, 0.3 to 0.7 for
seal to bear, and 10.7 for fish to bear [6].
Aquatic Organisms
Partitioning Factors: Partitioning factors for ODD in aquatic organisms were not calculated in the
studies reviewed. However, the data from one study reviewed showed BCFs of 17,600 for oligochaetes
and 565,000 for carp. Ratios of ODD in tissue to sediment were 0.65 for oligochaetes and 21 for carp.
BSAFs for clams ranged from 0.120 to 2.745 [22,25]. BSAFs for fish ranged from 0.079 to 2.379
[21,23,24,25].
317
-------
BIOACCUMULATION SUMMARY p,p -DDD
Food Chain Multipliers: Food chain multipliers (FCMs) for trophic level 3 aquatic organisms were
18.5 (all benthic food web), 1.6 (all pelagic food web), and 11.3 (benthic and pelagic food web). FCMs
for trophic level 4 aquatic organisms were 37.4 (all benthic food web), 3.1 (all pelagic food web), and
17.8 (benthic and pelagic food web) [28].
Toxicity/Bioaccumulation Assessment Profile
DDT is very persistent in the environment due to its low vapor pressure, high fat solubility, and
resistance to degradation and photooxidation. DDT is degraded to DDE under aerobic conditions and
to DDD in anoxic systems [7]. These metabolites, DDD and DDE, are similar to DDT in both their
stability and toxicity. Chronic effects of DDT and its metabolites on ecological receptors include
changes in enzyme production, hormonal balance, and calcium metabolism, which may cause changes
in behavior and reproduction. The high octanol-water partition coefficient of DDT indicates that it is
easily accumulated in tissues of aquatic organisms. Laboratory studies have shown that these compounds
are readily bioconcentrated in aquatic organisms, with reported log BCFs for DDT ranging from 3.08
to 7.65 and for DDE ranging from 4.80 to 5.26 [8].
Invertebrate species are generally more susceptible than fish species to effects associated with exposure
to DDT in the water column [8]. In general, the low solubility of DDT and its metabolites in water
suggests that water column exposures are likely to be lower than exposures from ingestion of food or
sediment. Sediments contaminated with pesticides, including DDT, have been shown to affect benthic
communities at low concentrations. Results of laboratory and field investigations suggest that chronic
effects generally occur at total DDT concentrations in sediment exceeding 2 ug/kg [9]. Equilibrium
partitioning methods predict that chronic effects occur at DDT concentrations in sediment of 0.6 to 1.7
Ug/kg [10].
For fish, the primary route of uptake is via prey items, but both DDT and its metabolites can be
accumulated through the skin or gills upon exposure to water. Short-term exposure to DDT
concentrations of less than 1 |ig/L have been reported to elicit toxic responses in both freshwater and
marine fish [8]. DDT may also be transfered to embryos from contaminated adults. DDT concentrations
of 1.1 to 2.4 mg/kg in fish embryos have been associated with fry mortality [11,12].
Eggshell thinning, embryo mortality, and decreased hatchling survival have been linked to chronic
exposure to DDT and its metabolites in the diet of birds. Of the three compounds, evidence strongly
indicates that DDE is responsible for most reproductive toxicity in avian species [13]. Measurements
of residues in eggs of birds are a reliable indicator of adverse effects. There is a large amount of
variability in sensitivity to DDT and its metabolites among bird species, with waterfowl and raptor
species showing the greatest sensitivities. Studies have shown the brown pelican to be most susceptible
to adverse effects, with eggshell thinning and depressed productivity occurring at 3.0 ug/g of DDE in
the egg and total reproductive failure when residues exceed 3.7 |ig/g [13].
318
-------
Summary of Biological Effects Tissue Concentrations for/?,/?'-DDD
Species:
Taxa
Invertebrates
Tubifex sp.,
Oligochaetes
Macomona liliana,
Mollusk
Austrovnus
stutchburyi, Mollusk
Concentration, Units in1:
Sediment Water
water =
0.023 mg/kg 0.85 ng/L
n= 1 n= 1
66.7 |ig/kg
OC
1,096.0
Hg/kg OC
286.4 |ig/kg
OC
20.0 ng/kg
OC
25.0 jig/kg
OC
66.7 |ig/kg
OC
286.4 |ig/kg
OC
20 |ig/kg
OC
25 |ig/kg
OC
Toxicity:
Tissue (Sample Type) Effects
0.015 mg/kg
n= 1
76.3 |ig/kg lipid
765.2 |ig/kg lipid
75.1 |ig/kg lipid
54.9 |ig/kg lipid
22.4 |ig/kg lipid
42.4 |ig/kg lipid
34.4 |ig/kg lipid
27.7 |ig/kg lipid
25.1 |ig/kg lipid
Ability to Accumulate2: Source:
Log Log
BCF BAF BSAF Reference
[14]
1.144 [22]
0.698 [22]
0.262 [22]
2.745 [22]
0.894 [22]
0.635 [22]
0.120 [22]
1.383 [22]
1.002 [22]
Comments3
F; lower Detroit
River
F; %lipid = 2.95;
%sed OC = 0.30
F; %lipid = 2.33;
%sed OC = 0.73
F; %lipid = 2.57;
%sed OC = 0.22
F; %lipid = 2.04;
%sed OC = 0.25
F;%lipid = 3.13;
%sed OC = 0.48
F; %lipid = 5.62;
%sed OC = 0.30
F; %lipid = 4.85;
%sed OC = 0.22
F; %lipid = 3.87;
%sed OC = 0.25
F; %lipid = 4.27;
%sed OC = 0.48
-------
Summary of Biological Effects Tissue Concentrations for/?,/?'-DDD
Species:
Taxa
Corbicula fluminea,
Asian clam
Fish
Anguilla anguilla,
Eel
Corogonus
autumnalis,
Omul (endemic
whitefish )
Oncorhynchus,
Salmo, Salvelinus
Concentration, Units in1: Toxicity:
Sediment Water Tissue (Sample Type) Effects
58.8 ng/kg
OC
159.7 ng/kg
OC
126 |ig/kg
OC
2,667 |ig/kg
OC
82 |ig/kg lipid
82 |ig/kg lipid
10 |ig/kg lipid
particulate: 0.0086-0.15 mg/kg
l.Opg/L lipid
± 1 .0 (whole body)
n=7 n=l
dissolved:
17 pg/L ±7.3
n = 7
754.5 |ig/kg lipid
Ability to Accumulate2: Source:
Log Log
BCF BAF BSAF Reference Comments3
1.394 [25] F;%lipid = 0.61;
%sedOC= 1.19
0.513 [25] F;%lipid = 0.61;
%sedOC=1.19
0.079 [26] F;%lipid=13;
%sed OC = 32
0.283 [24] F;%lipid=ll;
%sed OC = 2.7
sp., Salmonids
Salvelinus
fontinalis,
Brook trout
0.000093
83 ng/kg
4.79 mg/kg
(whole body)4
5.93
Behavior,
NOED
[24] F; %lipid = 11
[18] L; temperature
selection after 24 h
exposure to
chemical
-------
Summary of Biological Effects Tissue Concentrations for/?,/?'-DDD
Species:
Taxa
Salvelinus
namaycush,
Lake trout
Concentration, Units in1:
Sediment Water Tissue (Sample Type)
0.9 mg/kg
(whole body)4
Toxicity:
Effects
Mortality,
LOED
Ability
Log
BCF
to Accumulate2:
Log
BAF BSAF
Source:
Reference
[20]
Comments
L; survival
reduced
3
of fry
Leuciscus cephalus 478 |ig/kg
cabeda, Chub OC
378 |ig/kg lipid
0.790 [21,27] F;%lipid= 1.27;
%sed OC = 2.76
Alburnus alburnus 478 |ig/kg
alborella, Bleak OC
769 |ig/kg lipid
1.608 [21,27]
F;%lipid= 1.95;
%sed OC = 2.76
Cyprinus carpio, water =
Carp 0.023 mg/kg 0.85 ng/L 0.48 ± 0.26 mg/kg
n= 1 n= 1 n = 9
[14]
F; lower Detroit
River; value is
mean ± SD
Pimephales
promelas,
Fathead minnow
0.6 mg/kg
(whole body)4
Reproduction,
LOED
[17] L; significantly
different from
control (p = 0.05)
Gambusia affinis,
Mosquito fish
Catastoma
macrocheilus,
Largescale sucker
530 ng/kg
OC
5.3 mg/kg
(whole body)4
1,261 |ig/kg lipid
Mortality,
NOED
[19]
2.379 [23]
L; no effect on
survivorship after 3
days
F;%lipid= 11.1;
%sedOC= 1.0
-------
Summary of Biological Effects Tissue Concentrations for/?,/?'-DDD
Species:
Taxa
Cottus cognatus,
Slimy sculpin
Comephorus
dybowskii,
Pelagic sculpin
Concentration, Units in1: Toxicity:
Sediment Water Tissue (Sample Type) Effects
2667 |ig/kg 587.5 |ig/kg lipid
OC
0.000093 47 |ig g/kg
Hg/L
paniculate: 0.12-0.16 mg/kg lipid
1 .0 pg/L (whole body)
±1.0 n=l
n = 7
dissolved:
17 pg/L ±7.3
n = 7
Ability to Accumulate2: Source:
Log Log
BCF BAF BSAF Reference Comments3
0.220 [24] F; %lipid = 8;
%sed OC = 2.7
5.70 [24] F; %lipid = 8
[15] F; Lake Baikal,
Siberia
Wildlife
Bucephala clangiila, water =
Goldeneye 0.023 mg/kg 0.85 ng/L
n= 1 n= 1
0.080 ± 0.024 mg/kg
n = 3
[14] F; lower Detroit
River; value is mean
±SD
Aythya affinis,
Lesser scaup
water =
0.023 mg/kg 0.85 ng/L
n= 1 n= 1
0.093 ± 0.027 mg/kg
n = 7
[14] F; lower Detroit
River; value is mean
±SD
Aythya marila,
Greater scaup
water =
0.023 mg/kg 0.85 ng/L
n= 1 n= 1
0.14±0.045 mg/kg
n = 3
[14] F; lower Detroit
River; value is mean
±SD
-------
Summary of Biological Effects Tissue Concentrations for/?,/?'-DDD
Species:
Taxa
Concentration, Units in1:
Toxicity:
Ability to Accumulate2:
Source:
Log Log
Sediment Water Tissue (Sample Type) Effects BCF BAF BSAF Reference Comments3
Falco peregrinus,
Peregrine falcon
(eggs)
9 ng/g (eggs)
n = 6
11. 4% eggshell
thinning
[16] F; Kola Penninsula,
Russia; n = number
of clutches sampled
Phoca siberica,
Baikal seal
particulate: 2.0-2.2 mg/kg5 lipid
l.Opg/L (blubber)
±1.0 n=l
n = 7
dissolved:
17pg/L
±7.3
n = 7
[15]
F; Lake Baikal,
Siberia
1 Concentration units based on wet weight, unless otherwise noted.
2 BCF = bioconcentration factor, BAF = bioaccumulation factor, BSAF = biota-sediment accumulation factor.
3 L = laboratory study, spiked sediment, single chemical; F = field study, multiple chemical exposure; other unusual study conditions or observations noted.
4 This entry was excerpted directly from the Environmental Residue-Effects Database (ERED, www.wes.army.mil/el/ered, U.S. Army Corps of Engineers and U.S.
Environmental Protection Agency). The original publication was not reviewed, and the reader is strongly urged to consult the publication to confirm the information
presented here.
5 Not clear from reference if concentration is based on wet or dry weight.
-------
BIOACCUMULATION SUMMARY p,p -ODD
References
1. Verschueren. Hdbk. Environ. Data Org. Chem., 1983, p. 433. (Cited in: USEPA. 1996.
Hazardous Substances Data Bank (HSDB). National Library of Medicine online (TOXNET).
U.S. Environmental Protection Agency, Office of Health and Environmental Assessment,
Environmental Criteria and Assessment Office, Cincinnati, OH. February.)
2. USEPA. 1989. Chemical fate rate constants for SARA section 313 chemicals and Superfund
Health Evaluation Manual chemicals. Prepared by Chemical Hazard Assessment Division,
Syracuse Research Corporation, for U.S. Environmental Protection Agency, Office of Toxic
Substances, Exposure Evaluation Division, Washington, DC, and Environmental Criteria and
Assessment Office, Cincinnati, OH. August 11.
3. Karickhoff, S.W., and J.M. Long. \995.Internalreportonsummaryofmeasured, calculated and
recommended log Kow values. Draft. Prepared by U.S. Environmental Protection Agency, Office
of Research and Development, Environmental Research Laboratory-Athens, for E. Southerland,
Office of Water, Office of Science and Technology, Standards and Applied Science Division,
Washington, DC. April 10.
4. USEPA. 1995. Integrated Risk Information System (IRIS). National Library of Medicine online
(TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental
Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. September.
5. Braune, B.M., and RJ. Norstrom. 1989. Dynamics of organochlorine compounds in herring
gulls: HI. Tissue distribution and bioaccumulation in Lake Ontario Gulls. Environ. Toxicol.
Chem. 8:957-968.
6. Muir, D.C.G., RJ. Norstrom, and M. Simon. 1988. Organochlorine contaminants in arctic
marine food chains: Accumulation of specific polychlorinated biphenyls and chlordane-related
compounds. Environ. Sci. Technol. 22:1071-1079.
7. Charles, M.J., and R.A. Kites. 1987. Sediments as archives. In Sources and fates of aquatic
pollutants, ed. R.A. Kites and SJ. Eisenreich, Advances In Chemistry Series, Vol. 216, pp. 365-
389. American Chemical Society, Washington, DC.
8. USEPA. 1980. Ambient water quality criteria for DDT. EPA440/5-80-038. U.S. Environmental
Protection Agency, Office of Water Regulations and Standards, Criteria and Standards Division,
Washington, DC.
9. 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. Environ.
Manage. 19(l):81-97.
10. Pavlou, S., R. Kadeg, A. Turner, and M. Marchlik. 1987. Sediment quality criteria methodology
validation: Uncertainty analysis of sediment normalization theory for nonpolar organic
contaminants. Work Assignment 45, Task 3. Battelle, Washington, DC.
324
-------
BIOACCUMULATION SUMMARY p,p -ODD
11. Johnson, H.E., and C. Pecor. 1969. Coho salmon mortality and DDT in Lake Michigan.
Transactions of the 34th North American Wildlife Conference.
12. Smith, R.M., and C.F. Cole. 1973. Effects of egg concentrations of DDT and dieldrin on
reproduction in winter flounder (Pseudopleuronectes americanus). J. Fish. Res. Board Can.
30:1894-1898.
13. Blus, LJ. 1996. DDT, ODD, and DDE in birds. In Environmental contaminants in wildlife, ed.
W. N. Beyer, G.H. Heinz, and A.W. Redmon-Norwood, pp. 49-71. Lewis Publishers, Boca
Raton, FL.
14. Smith., E.V., J.M. Spurr, J.C. Filkins, and JJ. Jones. 1985. Organochlorine contaminants of
wintering ducks foraging on Detroit River sediments. /. Great Lakes Res. 11(3):231-246.
15. Kucklick, J.R., T.F. Bidleman, L.L. McConnell, M.D. Walla, and G.P. Ivanov. 1994.
Organochlorines in the water and biota of Lake Baikal, Siberia. Environ. Sci. Technol. 28:31-37.
16. Henny, C.J., S.A. Ganusevich, F.P. Ward, and T.R. Schwartz. 1994. Organochlorine pesticides,
chlorinated dioxins and furans, and PCBs in peregrine falcon Falco peregrinus eggs from the
Kola Penninsula, Russia. In Raptor conservation today, ed. B.U. Meyburg and R.D. Chancellor,
pp. 739-749. WWGPB/The Pica Press.
17. Jarvinen, A.W., M.J. Hoffman, and T.W. Thorslund. 1977. Long-term toxic effects of DDT food
and water exposure on fathead minnows (Pimephales promelas). J. Fish. Res. Board. Can.
34:2089-2103.
18. Peterson, R.H. 1973. Temperature selection of Atlantic salmon (Salmo salar) and brook trout
(Salvelinus fontinalis) as influenced by various chlorinated hydrocarbons. /. Fish. Res. Bd. Can.
30(8).
19. Metcalf, R.L. 1974. A laboratory model ecosystem to evaluate compounds producing biological
magnification. In Essays in toxicology, ed. W.J. Hayes, Vol. 5, pp. 17-38. Academic Press, New
York, NY.
20. Burdick, G.E., E.J. Harris, H.J. Dean, T.M. Walker J. Skea, and D. Colby. 1964. The
accumulation of DDT in lake trout and the effect on reproduction. Trans. Amer. Fish. Soc.
93:127-136.
21. Galassi, S., G. Gandolfi, and G. Pacchetti. 1981. Chlorinated hydrocarbons in fish from the
River Po (Italy). Sci. Total Environ. 20:231-240.
22. Hickey, C.W., D.S. Roper, P.T. Holland, and T.M. Trower. 1995. Accumulation of organic
contaminants in two sediment-dwelling shellfish with contrasting feeding modes: Deposit-
(Macomona liliana) and filter-feeding (Austovenus stutchburi). Arch. Environ. Contain. Toxicol.
11:21-231.
325
-------
BIOACCUMULATION SUMMARY p,p -ODD
23. Johnson, A., D. Norton, and B. Yake. 1988. Persistence of DDT in the Yakima River drainage,
Washington. Arch. Environ. Contain. Toxi. 17:291-297.
24. Oliver, G.G., and AJ. Niimi. 1988. Chlorinated hydrocarbons in the Lake Ontario ecosystem.
Environ. Set Technol. 22(4):388-397.
25. Pereira, W.E., J.L. Domagalski, F.D. Hostettler, L.R. Brown, and J.B. Rapp. 1996. Occurrence
and accumulation of pesticides and organic contaminants in river sediment, water, and clam
tissues from the San Jaoquin River and tributaries, California. Environ. Toxicol Chem. 15:172-
180.
26. Van der Oost, R. A. Opperhuizen, K. Satumalay, H. Heida, and P.E. Vermulen. 1996.
Biomonitoring aquatic pollution with feral eel (Anguilla anguilla) I. Bioaccumulation: Biota-
sediment ratios of PCBs, OCPs, PCDDs and PCDFs. Aquat. Toxicol. 35:21-46.
27. Galassi, S., and M. Migliavacca. 1986. Organochlorine residues in River Po sediment: testing
the equilibrium condition with fish. Ecotoxicol Environ. Safe. 12:120-126.
28. USEPA. 1998. Ambient water quality criteria derivation methodology human health: Technical
support document. Final draft. EPA-822-B-98-005. U.S. Environmental Protection Agency,
Office of Water, Washington, DC.
326
-------
BIOACCUMULATION SUMMARY p,p -DDE
Chemical Category: PESTICIDE (ORGANOCHLORINE)
Chemical Name (Common Synonyms): CASRN: 72-55-9
1,1 '-(DICHLOROETHYLIDENE)BIS(4-CHLOROBENZENE),
p,p' -DICHLORODIPHEN YLDICHLOROETHYLENE
4,4' -DICHLORODIPHEN YLDICHLOROETHYLENE
Chemical Characteristics
Solubility in Water: 0.065 mg/L at 24°C [1] Half-Life: 2.0 - 15.6 years based on
biodegradation of ODD in aerobic
soils under field conditions [2]
Log Kow: 6.76 [3] Log Koc: 6.65 L/kg organic carbon
Human Health
Oral RfD: No data [4] Confidence: —
Critical Effect: Liver tumors in mice and hamsters, thyroid tumors in female rats
Oral Slope Factor: 3.4 x 10"1 per (mg/kg)/day [4] Carcinogenic Classification: B2 [4]
Wildlife
Partitioning Factors: Based on the data presented in one study, log BCFs for birds collected from the
lower Detroit River ranged from 5.92 to 6.36. Concentrations of DDE in birds were 40 to 108 times
higher than in sediment. BSAFs were calculated for red-winged blackbird eggs and tree swallow eggs
during a study in the Great Lakes area, with values ranging from 13 to 870 as reported in the attached
summary table. BSAFs for tree swallow nestlings were 5 and 49.
Food Chain Multipliers: Biomagnification factors of 3.2 and 85 were determined for DDT and DDE,
respectively, from alewife to herring gulls in Lake Ontario [5]. A study of arctic marine food chains
measured biomagnification factors for DDE that ranged from 17.6 to 62.2 for fish to seal, 0.3 to 0.7 for
seal to bear, and 10.7 for fish to bear [6].
Aquatic Organisms
Partitioning Factors: Partitioning factors for DDE in aquatic organisms were not calculated in the
studies reviewed. However, the data showed ratios of DDT in tissue to sediment of 0.49 for oligochaetes
and 32 for fish from the lower Detroit River. Ratios of DDT in lipid to sediment for three fish species
from Rio de la Plata, Argentina ranged from 87 to 26,000. BSAFs for clams ranged from 1.2313 to
327
-------
BIOACCUMULATION SUMMARY p,p -DDE
107.7 [15,41,36]. BSAFs for dover sole collected in southern California ranged from 1.7 to 3.4. BSAFs
for other species ranged from 1.274 to 140.
Food Chain Multipliers: Food chain multipliers (FCMs) for trophic level 3 aquatic organisms were
23.7 (all benthic food web), 1.7 (all pelagic food web), and 14.4 (benthic and pelagic food web). FCMs
for trophic level 4 aquatic organisms were 57.5 (all benthic food web), 3.7 (all pelagic food web), and
26.7 (benthic and pelagic food web) [46].
Toxicity/Bioaccumulation Assessment Profile
DDT is very persistent in the environment due to its low vapor pressure, high fat solubility, and
resistance to degradation and photooxidation. DDT is degraded to DDE under aerobic conditions and
to DDD in anoxic systems [7]. These metabolites, DDD and DDE, are similar to DDT in both their
stability and toxicity. Chronic effects of DDT and its metabolites on ecological receptors include
changes in enzyme production, hormonal balance, and calcium metabolism, which may cause changes
in behavior and reproduction. The high octanol-water partition coefficient of DDT indicates that it is
easily accumulated in tissues of aquatic organisms. Laboratory studies have shown that these compounds
are readily bioconcentrated in aquatic organisms, with reported log BCFs for DDT ranging from 3.08
to 6.65 and for DDE ranging from 4.80 to 5.26 [8].
Invertebrate species are generally more susceptible than fish species to effects associated with exposure
to DDT in the water column [8]. In general, the low solubility of DDT and its metabolites in water
suggests that water column exposures are likely to be lower than exposures from ingestion of food or
sediment. Sediments contaminated with pesticides, including DDT, have been shown to impact benthic
communities at low concentrations. Results of laboratory and field investigations suggest that chronic
effects generally occur at total DDT concentrations in sediment exceeding 2 |ig/kg [9]. Equilibrium
partitioning methods predict that chronic effects occur at DDT concentrations in sediment of 0.6 to 1.7
Hg/kg [10].
For fish, the primary route of uptake is via prey items, but both DDT and its metabolites can be
accumulated through the skin or gills upon exposure to water. Short-term exposure to DDT
concentrations of less than 1 |ig/L have been reported to elicit toxic responses in both freshwater and
marine fish [8]. DDT may also be transferred to embryos from contaminated adults. DDT
concentrations of 1.1 to 2.4 mg/kg in fish embryos have been associated with fry mortality [11,12].
Eggshell thinning, embryo mortality, and decreased hatchling survival have been linked to chronic
exposure to DDT and its metabolites in the diet of birds. Of the three compounds, evidence strongly
indicates that DDE is responsible for most reproductive toxicity in avian species [13]. Measurements
of residues in eggs of birds are a reliable indicator of adverse effects. There is a large amount of
variability in sensitivity to DDT and its metabolites among bird species, with waterfowl and raptor
species showing the greatest sensitivities. Studies have shown the brown pelican to be most susceptible
to adverse effects, with eggshell thinning and depressed productivity occurring at 3.0 |ig/g of DDE in
the egg and total reproductive failure when residues exceed 3.7 ug/g [13].
328
-------
Summary of Biological Effects Tissue Concentrations forp,p'-DDE
Species:
Taxa
Invertebrates
Tubifex sp.,
Oligochaetes
Viviparus conectus,
Gastropod mollusk
Unio elongatulus,
Bivalve mollusk
Mollusks
(unspecified)
Macomona liliana,
Mollusk
Concentration, Units in1: Toxicity:
Sediment Water Tissue (Sample Type) Effects
Surface
0.012 mg/kg water 0.0059 mg/kg
(n=l) 0.57 ng/L (n=l)
(n=l)
294 |ig/kg 368 |ig/kg lipid
OC
294 |ig/kg 362 |ig/kg lipid
OC
99.67 |ig/kg 229 |ig/kg lipid
OC
36.67 |ig/kg 522.20 |ig/kg lipid
OC
35.62 |ig/kg 573.39 |ig/kg lipid
OC
36.36 |ig/kg 278.21 |ig/kg lipid
OC
20 |ig/kg 328.92 |ig/kg lipid
OC
Ability to Accumulate2: Source:
Log Log
BCF BAF BSAF Reference
[14]
1.2517 [36]
1.2313 [36]
2.298 [37]
14.241 [38]
16.097 [38]
7.652 [38]
16.446 [38]
Comments3
F; lower Detroit
River; value is
mean ± SD
F; %lipid = 7.06;
%sedOC=1.02
F; %lipid = 10.49;
%sedOC= 1.02
F;%lipid= 1.1;
%sed OC = 2.8
F; %lipid = 2.95;
%sed OC = 0.30
F; %lipid = 2.33;
%sed OC = 0.73
F; %lipid = 2.57;
%sed OC = 0.22
F; %lipid = 2.04;
%sed OC = 0.25
-------
Summary of Biological Effects Tissue Concentrations for p,p '-DDE
Species:
Taxa
Austrovenus
stutchburyi, Mollusk
Concentration, Units in1:
Sediment Water
6.25 ng/kg
OC
36.67 |ig/kg
OC
35.62 |ig/kg
OC
36.36 |ig/kg
OC
20 ng/kg
OC
6.25 |ig/kg
OC
Toxicity:
Tissue (Sample Type) Effects
61.34|ig/kglipid
141.64 |ig/kg lipid
148.75 ng/kg lipid
57.94 |ig/kg lipid
59.95 |ig/kg lipid
10.54 |ig/kg lipid
Ability to Accumulate2:
Log Log
BCF BAF BSAF
9.814
3.863
4.176
1.594
2.998
1.686
Source:
Reference
[38]
[38]
[38]
[38]
[38]
[38]
Comments3
F;%lipid = 3.13;
%sed OC = 0.48
F; %lipid = 5.62;
%sed OC = 0.30
F;%lipid=5.21;
%sed OC = 0.73
F; %lipid = 4.85;
%sed OC = 0.22
F; %lipid = 3.87;
%sed OC = 0.25
F; %lipid = 4.27;
%sed OC = 0.48
Corbicula fluminea, 13 |ig/kg
Asian clam OC
Corbicula fluminea, (0-5 cm) Surface
Asian clam 0.3 ng/g dw water
1.8ng/L
1,400 |ig/kg lipid
1.4 |ig/g lipid
(whole tissue)
107.7 [15]
[15]
F; %lipid not
reported; %sed OC
= 2.3
F; Rio de La Plata,
Argentina; lipid
content 2.4-3.8%
0.6 ng/g dw
Corbicula fluminea, 9,664 |ig/kg
Asian clam OC
168 |ig/kg
OC
1.4 |ig/g lipid
(whole tissue)
540,984 |ig/kg lipid
4,098 ng/kg lipid
55.979 [41]
24.393 [41]
F;%lipid = 0.61;
%sedOC = 0.19
F;%lipid = 0.61;
%sedOC = 0.19
-------
Summary of Biological Effects Tissue Concentrations for p,p' -DDE
Species:
Taxa
Astacidae, Crayfish
Chironomus
riparius, Midge
Chironomus
riparius, Midge
Fishes
Anguilla anguilla,
Eel
Concentration, Units in1:
Sediment Water Tissue (Sample Type)
210|ig/kg 2,131 |ig/kg lipid
OC
99.67 |ig/kg 177 |ig/kg lipid
OC
1 .6 mg/kg (whole
body)4
0.27 mg/kg (whole
body)4
0.1 mg/kg (whole
body)4
7.35 mg/kg (whole
body)4
3.75 mg/kg (whole
body)4
5 |ig/kg 156 |ig/kg lipid
OC
Toxicity: Ability to Accumulate2:
Log Log
Effects BCF BAF BSAF
10.148
1.776
Behavior,
NOED
Behavior,
NOED
Behavior,
NOED
Development,
LOED
Development,
NOED
31.200
Source:
Reference
[41]
[37]
[31]
[31]
[31]
[34]
[34]
[43]
Comments3
F;%lipid = 0.61;
%sedOC = 0.19
F;%lipid= 1.3;
%sed OC = 2.8
L; no effect on
swimming behavior
L; no effect on
swimming behavior
L; no effect on
swimming behavior
L; development
time from egg to
4th instar
decreased from 22-
25 days to 19-21
days
L; no effect on
developmental
period of larvae
F; %lipid = 7;
%sed OC = 7
-------
Summary of Biological Effects Tissue Concentrations for p,p' -DDE
Species:
Taxa
Oncorhynchus
mykiss, Rainbow
trout
Concentration, Units in1:
Sediment Water
5 |ig/kg
OC
32 |ig/kg
OC
76 |ig/kg
OC
23 |ig/kg
OC
72 |ig/kg
OC
Toxicity: Ability to Accumulate2:
Log Log
Tissue (Sample Type) Effects BCF BAF BSAF
213 |ig/kg lipid 42.600
2117|ig/kglipid 66.156
849 |ig/kg lipid 11.171
658 |ig/kg lipid 28.609
2,1 76 |ig/kg lipid 30.222
0.15mg/kg (fat)4 Growth, ED40
0.15mg/kg (fat)4 Physiological,
ED30
0.15mg/kg (fat)4 Physiological,
ED30
0.08mg/kg (fat)4 Physiological,
ED35
Source:
Reference
[43]
[43]
[43]
[43]
[43]
[29]
[29]
[29]
[29]
Comments3
F; %lipid = 7;
%sed OC = 14
F; %lipid = 6;
%sedOC= 18
F; %lipid = 10;
%sed OC = 12
F; %lipid = 10;
%sed OC = 12
F;%lipid= 13;
%sed OC = 32
L; 40% decrease in
growth relative to
control
L; 30% decrease in
hemoglobin
content relative to
control
L; 30% increase in
liver size relative to
control
L; 35% increase in
kidney size relative
to control
-------
Summary of Biological Effects Tissue Concentrations forp,p'-DDE
Species: Concentration, Units in1: Toxicity:
Taxa Sediment Water Tissue (Sample Type) Effects
Oncorhynchus, 1,889 jig/kg 7,817 |ig/kg lipid
Salmo, Salveliniis OC
Ability to Accumulate2: Source:
Log Log
BCF BAF BSAF Reference Comments3
4.139 [40] F;%lipid= 11;
%sed OC =2.7
spp., Salmonids
0.000076 860 |ig/kg
7.05
[40]
F; %lipid = 11
Oncorhynchus sp., 99.67 |ig/kg
Salmon OC
925 |ig/kg lipid
9.281 [37]
F;%lipid= 13.1;
%sed OC = 2.8
Prosopium 544.4 |ig/kg
williamsoni, OC
Mountain whitefish
3,500 |ig/kg
OC
2,333 |ig/kg lipid
4,460 |ig/kg lipid
(arithmetic mean of
two samples)
4.285 [39]
1.274 [39]
F; %lipid = 12.0,
%sed OC = 0.9
F; %lipid = 12.25
%sed OC = 0.3
Coregonus
autumnalis, Omul
(endemic whitefish)
particulate:
<14pg/L
n = 7
0.31-0.50 mg/kg lipid
n = 2
dissolved:
17±7.1pg/L
n = 7
-------
Species:
Taxa
Salvelinus
fontinalis,
Brook trout
Salvelinus
namaycush, Lake
trout
Alburnus alburnus
alborella, Bleak fish
Alburnus alburnus
alborella, Bleak fish
Chondrostoma
soetta
Cyprinus carpio,
Common carp
Cyprinus carpio,
Common carp
Concentration, Units in1:
Sediment Water
294 jig/kg
OC
358 ng/kg
OC
294 jig/kg
OC
99.67 |ig/kg
OC
174 |ig/kg
OC
Toxicity:
Tissue (Sample Type) Effects
44.9 mg/kg Behavior,
(whole body)4 LOED
1 .09 mg/kg Mortality,
(whole body)4 LOED
l,092|ig/kglipid
2,113|ig/kglipid
l,179|ig/kglipid
4,209 |ig/kg lipid
l,905|ig/kglipid
Ability to Accumulate2: Source:
Log Log
BCF BAF BSAF Reference
[30]
[33]
3.7143 [36]
5.9022 [35, 45]
4.0102 [36]
42.229 [37]
10.948 [42]
Comments3
L; temperature
selection after 24 h
exposure to
chemical
L; survival of fry
reduced
F;%lipid = 21.43;
%sedOC=1.02
F;%lipid= 1.95;
%sed OC = 2.76
F; %lipid = 9.75;
%sedOC=1.02
F, %lipid= 13.9;
%sed OC = 2.8
F, %lipid = 8.4;
%sedOC = 2.13
-------
Summary of Biological Effects Tissue Concentrations forp,p'-DDE
Species:
Taxa
Concentration, Units in1:
Toxicity:
Ability to Accumulate2:
Log Log
Sediment Water Tissue (Sample Type) Effects BCF BAF BSAF
Source:
Reference Comments
Cyprinus carpio,
Carp
Surface
0.012 mg/kg water 0.57
(n=l) ng/L
(n=l)
0.38 ±0.15 mg/kg
(n = 9)
[14]
F; lower Detroit
River; value is
mean ± SD
Scardinius 294 |ig/kg
erythrophalmus, OC
Rudd
1,473 |ig/kg lipid
6.546 [36] F;%lipid= 11.66;
%sedOC= 1.02
Leuciscus cephalus, 294 |ig/kg
Chub OC
1,473 |ig/kg lipid
5.0102 [36]
F; %lipid = 9.98;
%sedOC= 1.02
Leuciscus cephalus 358 |ig/kg
cabeda, Chub OC
1,953 |ig/kg lipid
5.4553 [35,45] F; %lipid= 1.27;
%sed OC = 2.76
Rutilus pigus
294 |ig/kg
OC
728 |ig/kg lipid
2.4762 [36]
F; %lipid = 12.63;
%sedOC= 1.02
Rutilus rubilio
294 jig/kg
OC
1,167 |ig/kg lipid
3.9694 [36]
F;%lipid= 11.05;
%sedOC=1.02
Catostomus
commersoni,
White sucker
208 ng/kg
OC
1,519 |ig/kg lipid
7.303 [42]
F; %lipid = 7.9;
%sedOC= 1.44
-------
Summary of Biological Effects Tissue Concentrations for p,p' -DDE
Species:
Taxa
mixed Catastoma
sp., Suckers
Catastoma
macrocheilus,
Largescale sucker
Barbus barbus,
Barbel
Siliiris glanis, Wels
fish, juveniles
Siliiris glanis, Wels
fish, adults
Pimelodus albicans,
Mandi
Pimelodus albicans,
Mandi
Gambusia affinis,
Mosquito fish
Concentration, Units in1:
Sediment Water
3,500 |ig/kg
oc
3,010 |ig/kg
OC
294 |ig/kg
OC
294 |ig/kg
OC
294 |ig/kg
OC
0.2 ng/g dw
20 |ig/kg
OC
Toxicity:
Tissue (Sample Type) Effects
3,253 |ig/kg lipid
(arithmetic mean of
two samples)
7,477 |ig/kg lipid
1,333 |ig/kg lipid
73 1 |ig/kg lipid
1,613 |ig/kg lipid
0.6 |ig/g lipid
(n = 2)
(muscle)
600 ng/kg lipid
29.2 mg/kg Mortality,
(whole body)4 NOED
Ability to Accumulate2: Source:
Log Log
BCF BAF BSAF Reference
0.929 [39]
2.484 [39]
4.5340 [36]
2.4864 [36]
5.4864 [36]
[15]
30.0 [15]
[32]
Comments3
F; %lipid = 9.2;
%sed OC = 0.3
F;%lipid= 11.1;
%sedOC=1.0
F;%lipid= 16.43;
%sedOC=1.02
F; %lipid = 3.83;
%sedOC= 1.02
F; %lipid = 5.38;
%sedOC=1.02
F; Rio de La Plata,
Argentina; lipid
content 4%
F; %lipid not
reported; %sed OC
= 1.0
L; no effect on
survivorship after 3
days
-------
Summary of Biological Effects Tissue Concentrations for p,p' -DDE
Species:
Taxa
Ambloplites
rupestris, Rock bass
Sunfish
(unspecified)
Roccus chrysops,
White bass
Micropterus
salmoides,
Smallmouth bass
Dorosoma
cepedianum,
Gizzard shad
Percafluviatilis,
Perch
Stizostedion
vitreum, Walleye
Concentration, Units in1: Toxicity:
Sediment Water Tissue (Sample Type) Effects
99.67 |ig/kg 365 |ig/kg lipid
OC
99.67 ng/kg 254 |ig/kg lipid
OC
99.67 |ig/kg 1, 586 |ig/kg lipid
OC
99.67 ng/kg 1, 352 |ig/kg lipid
OC
99.67 |ig/kg 382 |ig/kg lipid
OC
294 |ig/kg 3,390 |ig/kg lipid
OC
99.67 |ig/kg 2,593 |ig/kg lipid
OC
Ability to Accumulate2: Source:
Log Log
BCF BAF BSAF Reference Comments3
3.662 [37] F; %lipid = 0.7;
%sed OC = 2.8
2.548 [37] F; %lipid = 3.7;
%sed OC = 2.8
15.913 [37] F;%lipid= 1.8;
%sed OC = 2.8
13.565 [37] F; %lipid = 0.6;
%sed OC = 2.8
3.833 [37] F; %lipid = 6.8;
%sed OC = 2.8
11.5306 [36] F; %lipid = 5.84;
%sedOC= 1.02
26.016 [37] F;%lipid= 1.2;
%sed OC = 2.8
-------
Summary of Biological Effects Tissue Concentrations for p,p' -DDE
Species:
Taxa
Microstomus
pacificus, Dover
sole
Concentration, Units in1:
Sediment Water
27 |ig/g dw
(n = 5)
0.09 |ig/g
dw (n = 10)
Toxicity:
Tissue (Sample Type) Effects
16.0ng/g (n = 5)
(muscle)
210ng/g (n = 3)
(liver)
0.24 |ig/g (n = 10)
(muscle)
Ability to Accumulate2:
Log Log
BCF BAF BSAF
log
MBAF
-0.26 1.7
0.79 2.0
log
MBAF
0.43 1.8
Source:
Reference Comments3
[16] F; Southern
California Bight;
modified
bioaccumulation
factor (MBAF) =
Corg ww/ Csed dw;
water content of
tissue was not
measured
0.80 |ig/g (n = 6)
(liver)
1.79
3.4
Oligosarciisjenynsi, 5.7 ng/g dw
Common name not
available
0.5 |ig/g lipid (n = 7)
(muscle)
[15] F; Rio de La Plata,
Argentina; lipid
content 0.32%
Prochilodus 20 |ig/kg
platensis, Curimata OC
Prochilodus 0.2 ng/g dw
platensis, Curimata
2,800 |ig/kg lipid
Three composite
samples: 1.2 (n = 4),
5.2 (n = 4) and 2
(n = 5) |ig/g lipid
(muscle)
140 [15] F, %lipidnot
reported; %sed OC
= 1.0
[15] F; Rio de La Plata,
Argentina; lipid
content 1-12.7%
-------
Summary of Biological Effects Tissue Concentrations forp,p'-DDE
Species:
Taxa
Gar pike
(unspecified)
Comephoms
bybowskii,
Pelagic sculpin,
Concentration, Units in1: Toxicity: Ability to Accumulate2: Source:
Log Log
Sediment Water Tissue (Sample Type) Effects BCF BAF BSAF Reference Comments3
99.67 |ig/kg 1 1,986 ng/kg lipid 120.257 [37] F; %lipid = 0.8;
OC %sed OC = 2.8
paniculate: [17] F; Lake Baikal,
<14pg/L 0.74-0.76 mg/kg lipid Siberia
n = 7 n= 1
dissolved:
17 pg/L ±
7.1
n = 7
Cottus cognatus,
Slimy sculpin
1,889 |ig/kg
OC
0.000076
Hg/L
2,375 |ig/kg lipid
190 |ig/kg
6.40
1.257 [40]
[40]
F; %lipid = 8;
%sed OC = 2.7
F; %lipid =8;
%sed OC = 2.7
Wildlife
Bucephala clangula,
Goldeneye
Surface
water
0.012 mg/kg 0.57 ng/L
(n=l) (n=l)
seston =
0.10 mg/kg
[14]
0.48 ±0.18 mg/kg
(whole body)
(n = 3)
F; lower Detroit
River; value is
mean ± SD
-------
Summary of Biological Effects Tissue Concentrations forp,p'-DDE
Species:
Taxa
Concentration, Units in1:
Toxicity:
Ability to Accumulate2:
Log Log
Sediment Water Tissue (Sample Type) Effects BCF BAF BSAF
Source:
Reference Comments
Aythya affinis,
Lesser scaup
Surface
water
0.012 mg/kg 0.57 ng/L
(n=l) (n=l)
[14]
0.80 ± 0.33 mg/kg
(whole body)
(n = 7)
F; lower Detroit
River; value is
mean ± SD
Aythya marila,
Greater scaup
Surface
water
0.012 mg/kg 0.57 ng/L
(n=l) (n=l)
1.3 ±0.25 mg/kg
(whole body)
(n = 3)
[14]
F; lower Detroit
River; value is
mean ± SD
Falco peregrinus,
Peregrine falcon
|ig/g (egg):
15-30
>30
Young
produced per
active nest:
1.8
2.0
1.0
[26] F; Alaska; young
produced not
adjusted for sample
egg collected
-------
Summary of Biological Effects Tissue Concentrations forp,p'-DDE
Species: Concentration, Units in1:
Taxa Sediment Water
Aquila chrysaetos,
Golden eagle
Haliaeetus
leucocephalus, Bald
eagle
Ardea herodias,
Great blue heron
Tissue (Sample Type)
|ig/g (egg):
0.1
0.1
0.2
0.3
0.3
10|ig/g (egg)
|ig/g (egg):
<2.2
2.2-3.5
3.6-6.2
6.3-11.9
>12
4|ig/g (egg)
5|ig/g (egg)
Toxicity: Ability to Accumulate2: Source:
Log Log
Effects BCF BAF BSAF Reference Comments3
Mean % [24] F; Great Britain;
eggshell percentage of
thinning = thinning based on
7% thickness index
1% [24]
3%
4%
5%
Mean percent [22] F; Oregon and
eggshell Washington
thinning= 10%
Young [23] F
produced per
active nest:
1.0
1.0
0.5
0.3
0.2
Mean percent [18] F; Washington
eggshell
thinning =
10%
13%
-------
Summary of Biological Effects Tissue Concentrations for p,p' -DDE
Species:
Taxa
Plegadis chihi,
White-faced ibis
Egretta thiila,
Snowy egret
Concentration, Units in1:
Sediment Water Tissue (Sample Type)
2|ig/g (egg)
1 |ig/g (egg)
|ig/g (egg):
1-4
4-8
8-16
>16
1 |ig/g (egg)
2|ig/g (egg)
|ig/g (egg):
1-5
5-10
10-20
Toxicity: Ability to Accumulate2:
Log Log
Effects BCF BAF BSAF
Mean percent
eggshell
thinning=
12%
8%
Young
produced per
active nest:
1.8
1.8
1.3
0.8
0.6
Mean percent
eggshell
thinning=
3%
12%
Young
produced per
active nest:
2.2
2.4
1.0
1.0
Source:
Reference Comments3
[20] F; Nevada
[21] F; Nevada; young
produced not
adjusted for sample
egg collected
[20] F; Nevada; young
produced not
adjusted for sample
egg collected
-------
Summary of Biological Effects Tissue Concentrations for p,p' -DDE
Species:
Taxa
Sula bassanus,
Northern gannet
Lams californicus,
California gull
Pelecaniis
occidentalis,
Brown pelican
Concentration, Units in1:
Sediment Water Tissue (Sample Type)
|ig/g (egg)
19
430 mg/kg (brain)4
175 mg/kg (breast)4
3,100 mg/kg (liver)4
220 mg/kg (brain)4
490 mg/kg (breast)4
800 mg/kg (liver)4
750 mg/kg (liver)4
4.4 mg/kg (brain)4
59.5 mg/kg (breast)4
7.15 mg/kg (liver)4
Toxicity: Ability to Accumulate2:
Log Log
Effects BCF BAF BSAF
Mean %
eggshell
thinning =
17%
Mortality, not
available (NA)
Mortality, NA
Mortality, NA
NA, NA
NA, NA
NA
NA
Mortality, NA
Mortality, NA
Mortality, NA
Source:
Reference
[19]
[28]
[28]
[28]
[28]
[28]
[28]
[28]
[28]
[28]
[28]
Comments3
F; Quebec
L
L
L
L
L
L
L
L
L
L
-------
Summary of Biological Effects Tissue Concentrations for p,p' -DDE
Species:
Taxa
Agelaius
phoeniceus, Red-
winged blackbird
(eggs)
Concentration, Units in1:
Sediment Water
40.5 ng/g
TOC = 2.5%
7.9 ng/g
TOC —
-L V^/\_, —
21.0%
373.1 ng/g
TOC = 7.5%
1,1 60.7 ng/g
TOC = 12%
10.4 ng/g
TOC-18.5%
65.4 ng/g
TOC =
11.5%
1.6 ng/g
TOC =
10.5%
0.8 ng/g
TOC =
13.8%
1.3 ng/g
TOC =
11.1%
3.0 ng/g
TOC =
23.9%
Toxicity:
Tissue (Sample Type) Effects
3,088.1 ng/g
777.7 ng/g
648.7 ng/g
1,299.6 ng/g
305.7 ng/g
826.2 ng/g
416.1 ng/g
145.1 ng/g
183.5 ng/g
117.6 ng/g
Ability to Accumulate2:
Log Log
BCF BAF BSAF
41.4
372.7
12.9
13.2
113.3
30.3
582.4
57?
JZ,Zj
326.4
203.7
Source:
Reference Comments3
[25] F; Great Lakes/St.
Lawrence River
basin; 12 wetlands
sites; sediment
concentration
reported as wet
weight
concentration
which may be a
typographical error
-------
Summary of Biological Effects Tissue Concentrations forp,p'-DDE
Species:
Taxa
Tachycineta bicolor,
Tree swallow
Nestlings
Eggs
Concentration, Units in1:
Sediment Water
65.4 ng/g
TOC =
11.5%
0.8 ng/g
TOC =
13.8%
65.4 ng/g
TOC =
11.5%
0.8 ng/g
TOC =
13.8%
Toxicity:
Tissue (Sample Type) Effects
(whole body minus
feet, beak, wings, and
feathers)
288.2 ng/g
22.4 ng/g
794.7 ng/g
458.2 ng/g
Ability to Accumulate2: Source:
Log Log
BCF BAF BSAF Reference Comments3
[25] F; Great Lakes/St.
Lawrence River
basin; 12 wetlands
548.9 sites; sediment
concentration
reported as wet
weight
concentration
which may be a
typographical error
16.2
868.6
3.5 |ig/g (egg)
(n = 6)
11.4% eggshell
thinning
[27] F; Kola Penninsula,
Russia; n = number
of clutches sampled
-------
Summary of Biological Effects Tissue Concentrations for p,p' -DDE
Species:
Concentration, Units in1:
Toxicity:
Ability to Accumulate2:
Source:
Taxa
Phoca siberica,
Baikal seal
Sediment Water
particulate:
<14 pg/L
n = 7
Tissue (Sample Type) Effects
43-44 mg/kg lipid
n= 1
Log
BCF
Log
BAF
BSAF Reference
[17]
Comments3
F; Lake Baikal,
Siberia
dissolved:
17 pg/L ±
7.1
n = 7
1 Concentration units based on wet weight unless otherwise noted.
2 BCF = bioconcentration factor, BAF = bioaccumulation factor, BSAF = biota-sediment accumulation factor.
3 L = laboratory study, spiked sediment, single chemical; F = field study, multiple chemical exposure; other unusual study conditions or observations noted.
4 This entry was excerpted directly from The Environmental Residue-Effects Database (ERED, www.wes.army.mil/el/ered, U.S. Army Corps of Engineers and U.S.
Environmental Protection Agency). The original publication was not reviewed, and the reader is strongly urged to consult the publication to confirm the information
presented here.
-------
BIOACCUMULATION SUMMARY p,p -DDE
References
1. Verschueren. Hdbk. Environ. Data Org. Chem., 1983, p. 433. (Cited in: USEPA. 1996.
Hazardous Substances Data Bank (HSDB). National Library of Medicine online (TOXNET).
U.S. Environmental Protection Agency, Office of Health and Environmental Assessment,
Environmental Criteria and Assessment Office, Cincinnati, OH. February.)
2. USEPA. 1989. Chemical fate rate constants for SARA section 313 chemicals and Superfund
Health Evaluation Manual chemicals. Prepared by Chemical Hazard Assessment Division,
Syracuse Research Corporation, for U.S. Environmental Protection Agency, Office of Toxic
Substances, Exposure Evaluation Division, Washington, DC, and Environmental Criteria and
Assessment Office, Cincinnati, OH. August 11.
3. Karickhoff, S.W., and J.M. Long. 1995. Internal report on summary of measured, calculated
and recommended log Kovf values. Draft. Prepared by U.S. Environmental Protection Agency,
Office of Research and Development, Environmental Research Laboratory-Athens, for E.
Southerland, Office of Water, Office of Science and Technology, Standards and Applied
Science Division, Washington, DC. April 10.
4. USEPA. 1995. Integrated Risk Information System (IRIS). National Library of Medicine online
(TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental
Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. September.
5. Braune, B.M., and RJ. Norstrom. 1989. Dynamics of organochlorine compounds in herring
gulls: III. Tissue distribution and bioaccumulation in Lake Ontario gulls. Environ. Toxicol.
Chem. 8:957-968.
6. Muir, D.C.G., RJ. Norstrom, and M. Simon. 1988. Organochlorine contaminants in arctic
marine food chains: Accumulation of specific polychlorinated biphenyls and chlordane-related
compounds. Environ. Sci. Technol. 22:1071-1079.
7. Charles, M.J., and R. A. Kites. 1987. Sediments as archives. In Sources and fates of aquatic
pollutants, eds. R.A. Kites and S.J. Eisenreich, Advances In Chemistry Series, Vol. 216, pp. 365-
389. American Chemical Society, Washington, DC.
8. USEPA. 1980. Ambient water quality criteria for DDT. EPA440/5-80-038. U.S.
Environmental Protection Agency, Office of Water Regulations and Standards, Criteria and
Standards Division, Washington, DC.
9. 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.
Environ. Manage. 19(l):81-97.
10. Pavlou, S., R. Kadeg, A. Turner, and M. Marchlik. 1987. Sediment quality criteria methodology
validation: Uncertainty analysis of sediment normalization theory for nonpolar organic
contaminants. Work Assignment 56, Task 3. Battelle, Washington, DC.
347
-------
BIOACCUMULATION SUMMARY p,p -DDE
11. Johnson, H.E., and C. Pecor. 1969. Coho salmon mortality and DDT in Lake Michigan.
Transactions of the 34th North American Wildlife Conference.
12. Smith, R.M., and C.F. Cole. 1973. Effects of egg concentrations of DDT and dieldrin on
reproduction in winter flounder (Pseudopleuronectes americanus). J. Fish. Res. Board Can.
30:1894-1898.
13. Blus, LJ. 1996. DDT, ODD, and DDE in birds. In Environmental contaminants in wildlife,
ed. W. N. Beyer, G.H. Heinz, and A.W. Redmon-Norwood, pp. 49-71. Lewis Publishers, Boca
Raton, FL.
14. Smith., E.V. , J.M. Spurr, J.C. Filkins, and JJ. Jones. 1985. Organochlorine contaminants of
wintering ducks foraging on Detroit River sediments. /. Great Lakes Res. 11(3):231-246.
15. Columbo, J.C., M.F. Khalil, M. Arnac, and A.C. Horth. 1990. Distribution of chlorinated
pesticides and individually polychlorinated biphenyls in biotic and abiotic compartments of the
Rio de la Plata, Argentina. Environ. Sci. Technol 24:498-505.
16. Young, D.R., A.J. Mearns, and R.W. Gossett. 1991. Bioaccumulation ofp,p'-DDE and PCB
1254 by a flatfish bioindicator from highly contaminated marine sediments of Southern
California. In Organic substances and sediments in water, ed. R.A. Baker, Vol. 3, pp. 159-169.
Lewis Publishers, Boca Raton, FL.
17. Kucklick, J.R., T.F. Bidleman, L.L. McConnell, M.D. Walla, and G.P. Ivanov. 1994.
Organochlorines in the water and biota of Lake Baikal, Siberia. Environ. Sci. Technol. 28:31 -37.
18. Fitzner, R.E., LJ. Blus, C.J. Henny, and D.W. Carlile. 1988. Organochlorine residues in great
blue herons from the northwestern United States. Colon. Waterbirds 11:293-300.
19. Elliott, J.E., R.J. Norstrom, and J.A. Keith. 1988. Organochlorines and eggshell thinnning in
northern gannets (Sula bassanus) from eastern Canada, 1968-1984. Environ. Pollut. 52:81-102.
20. Henny, C.J., LJ. Blus, and C.S. Hulse. 1985. Trends and effects of Organochlorine residues on
Oregon and Nevada wading birds, 1979-1983. Colon. Waterbirds. 8:117-128.
21. Henny, C.J., and G.B. Herron. 1989. DDE, selenium, mercury, and white-faced ibis
reproduction at Carson Lake, Nevada. /. Wildl. Manage. 53:1032-1045.
22. Anthony, R.G., M.G. Garrett, and C.A. Schuler. 1993. Environmental contaminants in bald
eagles in the Columbia River estuary. /. Wildl. Manage. 57:10-19.
23. Wiemeyer, S.N., C.M Bunck, and C.J. Stafford. 1993. Environmental contaminants in bald
eagle eggs—1980-84—and further interpretations of relationships to productivity and shell
thickness. Arch. Environ. Contain. Toxicol. 24:213-227.
24. Ratcliffe, D.A. 1967. Decrease in eggshell weight in certain birds of prey. Nature. 215:208-
210.
348
-------
BIOACCUMULATION SUMMARY p,p -DDE
25. Bishop, C.A., M.D. Koster, A.A. Chek, DJ.T. Hussell, and K. Jock. 1995. Chlorinated
hydrocarbons and mercury in sediments, red-winged blackbirds (Agelaius phoeniceus) and tree
swallows (Tachycineta bicolor) from wetlands in the Great Lakes-St. Lawrence river basin,
Environ. Toxicol. Chem. 14:491-501.
26. Ambrose, R.E., C.J., Henny, R.E. Hunter, and J.A. Crawford. 1988. Organochlorines in
Alaskan peregrine falcon eggs and their current impact on productivity. In Peregrine falcon
populations: Their management and recovery, ed. T. J. Cade, J.H. Enderson, C.G. Thelander,
and C.M. White, pp. 385-393. Peregrine Fund, Boise, ID.
27. Henny, C.J., S.A. Ganusevich, F.P. Ward, and T.R. Schwartz. 1994. Organochlorine pesticides,
chlorinated dioxins and furans, and PCBs in peregrine falcon Falco peregrinus eggs from the
Kola Penninsula, Russia. In Raptor conservation today, ed. B.U. Meyburg and R.D. Chancellor,
pp. 739-749. WWGPB/The Pica Press.
28. Young, D.R., and T.C. Heeson. 1977. Marine bird deaths at the Los Angeles zoo. Coastal
Water Research Program Annual Report. Southern California Coastal.
29. Poels, C.L.M., M.A. van Der Gaag, and J.FJ. van de Kerkhoff. 1980. An investigation into the
long-term effect of Rhine water on rainbow trout. Water Res. 14:1029-1033.
30. Peterson, R.H. 1973. Temperature selection of Atlantic salmon (Salmo salar) and brook trout
(Salvelinus fontinalis) as influenced by various chlorinated hydrocarbons. /. Fish. Res. B. Can.
30(8).
31. Lydy, M.J., K.A. Bruner, D.M. Fry, and S.W. Fisher. 1990. Effects of sediment and the route
of exposure on the toxicity and accumulation of neutral lipophilic and moderately water soluble
metabolizable compounds in the midge, Chironomus riparius. ASTM STP-1096. Aquatic
toxicology and risk assessment, ed. W.G. Landis, et.al. pp. 140-164, American Society for
Testing and Materials, Philadelphia, PA.
32. Metcalf, R.L. 1974. A laboratory model ecosystem to evaluate compounds producing biological
magnification. In Essays in toxicology, ed. W.J. Hayes, Vol. 5, pp. 17-38, Academic Press, New
York, NY.
33. Burdick, G.E., EJ. Harris, HJ. Dean, T.M. Walker, J. Skea, and D. Colby. 1964. The
accumulation of DDT in lake trout and the effect on reproduction. Trans. Amer. Fish. Soc.
93:127-136.
34. Derr, S.K., and MJ. Zabik. 1972. Biologically active compounds in the aquatic environment:
The uptake and distribution of [l,l-dichloro-2,2-bis(p-chlorophenyl)ethylene], DDE by
Chironomus tentans Fabricius (Diptera: Chironomidae). Trans. Amer. Fish. Soc. 101:323-329.
35. Galassi, S., G. Gandolfi, and G. Pacchetti. 1981. Chlorinated hydrocarbons in fish from the
River Po (Italy). Sci. Total Environ. 20:231-240.
349
-------
BIOACCUMULATION SUMMARY p,p -DDE
36. Galassi, S., L. Guzzella, M. Battegazzore, and A. Carrieri. 1994. Biomagnification of PCBs,
p,p -DDE, and HCB in the River Po ecosystem (northern Italy). Ecotoxicol Environ. Safe.
29:174-186.
37. Haffner, G.D., M. Tomczak, and R. Lazar. 1994. Organic contaminant exposure in the Lake
St. Clair food web. Hydrobiologia 281:19-27.
38. Hickey, C.W., D.S. Roper, P.T. Holland, and T.M. Trower. 1995. Accumulation of organic
contaminants in two sediment-dwelling shellfish with contrasting feeding modes: Deposit-
(Macomona liliana) and filter-feeding (Austovenus stutchburi). Arch. Environ. Contam. Toxicol
11:21-231.
39. Johnson, A., D. Norton, and B. Yake. 1988. Persistence of DDT in the Yakima River drainage,
Washington. Arch. Environ. Contam. Toxicol. 17:291-297.
40. Oliver, G.G., and AJ. Niimi. 1988. Chlorinated hydrocarbons in the Lake Ontario ecosystem.
Environ. Sci. Technol 22(4):388-397.
41. Pereira, W.E., J.L. Domagalski, F.D. Hostettler, L.R. Brown, and J.B. Rapp. 1996. Occurrence
and accumulation of pesticides and organic contaminants in river sediment, water, and clam
tissues from the San Jaoquin River and tributaries, California. Environ. Toxicol. Chem. 15:172-
180.
42. Tate, C.M., and J.S. Heiny. 1996. Organochlorine compounds in bed sediment and fish tissue
in the South Platte River basin, USA, 1992-1993. Arch. Environ. Contam. Toxicol. 11:221-231.
43. Van der Oost, R. A. Opperhuizen, K. Satumalay, H. Heida, and P.E. Vermulen. 1996.
Biomonitoring aquatic pollution with feral eel (Anguilla anguilla) I. Bioaccumulation: Biota-
sediment ratios of PCBs, OCPs, PCDDs and PCDFs. Aqua. Toxicol. 35:21-46.
44. USEPA. 1995. Great Lakes Water Quality Initiative Technical Support Document for the
procedure to determine bio accumulation factors. EPA-820-B-95-005. U.S. Environmental
Protection Agency, Office of Water, Washington, DC.
45. Galassi, S., and M. Migliavacca. 1986. Organochlorine residues in River Po sediment: Testing
the equilibrium condition with fish. Ecotoxicol. Environ. Safe. 12:120-126.
46. USEPA. 1998. Ambient water quality criteria derivation methodology human health: Technical
support document. Final draft. EPA-822-B-98-005. U.S. Environmental Protection Agency,
Office of Water, Washington, DC.
350
-------
BIOACCUMULATION SUMMARY p,p -DDT
Chemical Category: PESTICIDE (ORGANOCHLORINE)
Chemical Name (Common Synonyms): CASRN: 50-29-3
l,l'-(2,2,2-TRICHLOROETHYLIDENE)BIS(4-CHLOROBENZENE),
p,p' -DICHLORODIPHEN YLTRICHLOROETHANE,
4,4' -DICHLORODIPHEN YLTRICHLOROETHANE
Chemical Characteristics
Solubility in Water: 0.0031 - 0.0034 mg/L Half-Life: 2.0 - 15.6 years based on
at 25 °C [1] biodegradation of ODD in
aerobic soils under field
conditions [2]
Log Kow: 6.83 [3] Log Koc: 6.71 L/kg organic carbon
Human Health
Oral RfD: 5 x 10"4 mg/kg/day [4] Confidence: Medium, uncertainty factor
= 100
Critical Effect: Liver lesions in rats, liver tumors in mice and rats
Oral Slope Factor: 3.4 x 10"1 per (mg/kg)/day [4] Carcinogenic Classification: B2 [4]
Wildlife
Partitioning Factors: Partitioning factors for DDT in wildlife were not calculated in the studies
reviewed. However, based on the data in one study, log BCFs for birds from the lower Detroit River
ranged from 4.81 to 5.01. Concentrations of DDT in birds were 2.1 to 3.3 times higher than in sediment.
Food Chain Multipliers: Biomagnification factors of 3.2 and 85 were determined for DDT and DDE,
respectively, from alewife to herring gulls in Lake Ontario [5]. A study of arctic marine food chains
measured biomagnification factors for DDE that ranged from 17.6 to 62.2 for fish to seal, 0.3 to 0.7 for
seal to bear, and 10.7 for fish to bear [6].
Aquatic Organisms
Partitioning Factors: Based on the results from one study reviewed, the log BCF for carp collected
from the lower Detroit River was 4.77. Ratios of DDT in lipids to sediment were 450 in clams and 1,250
to 11,000 in fish from the Rio de la Plata, Argentina. BSAFs for clams ranged from 0.060 to 302.326
[14,33,36]. BSAFs for fish ranged from 0.120 to 88.07.
351
-------
BIOACCUMULATION SUMMARY p,p -DDT
Food Chain Multipliers: Food chain multipliers (FCMs) for trophic level 3 aquatic organisms were
22.5 (all benthic food web), 1.7 (all pelagic food web), and 13.7 (benthic and pelagic food web). FCMs
for trophic level 4 aquatic organisms were 52.5 (all benthic food web), 3.6 (all pelagic food web), and
24.6 (benthic and pelagic food web) [39].
Toxicity/Bioaccumulation Assessment Profile
DDT is very persistent in the environment due to its low vapor pressure, high fat solubility, and
resistance to degradation and photooxidation. DDT is degraded to DDE under aerobic conditions and
to DDD in anoxic systems [7]. These metabolites, DDD and DDE, are similar to DDT in both their
stability and toxicity. Chronic effects of DDT and its metabolites on ecological receptors include
changes in enzyme production, hormonal balance, and calcium metabolism, which may cause changes
in behavior and reproduction. The high octanol-water partition coefficient of DDT indicates that it is
easily accumulated in tissues of aquatic organisms. Laboratory studies have shown that these compounds
are readily bioconcentrated in aquatic organisms, with reported log BCFs for DDT ranging from 3.08
to 6.65 and for DDE ranging from 4.80to 5.26 [8].
Invertebrate species are generally more susceptible than fish species to effects associated with exposure
to DDT in the water column [8]. In general, the low solubility of DDT and its metabolites in water
suggests that water column exposures are likely to be lower than exposures from ingestion of food or
sediment. Sediments contaminated with pesticides, including DDT, have been shown to affect benthic
communities at low concentrations. Results of laboratory and field investigations suggest that chronic
effects generally occur at total DDT concentrations in sediment exceeding 2 |ig/kg [9]. Equilibrium
partitioning methods predict that chronic effects occur at DDT concentrations in sediment of 0.6 to 1.7
Hg/kg [10].
For fish, the primary route of uptake is via prey items, but both DDT and its metabolites can be
accumulated through the skin or gills upon exposure to water. Short-term exposure to DDT
concentrations of less than 1 |ig/L have been reported to elicit toxic responses in both freshwater and
marine fish [8]. DDT may also be transfered to embryos from contaminated adults. DDT concentrations
of 1.1 to 2.4 mg/kg in fish embryos have been associated with fry mortality [11,12].
Eggshell thinning, embryo mortality, and decreased hatchling survival have been linked to chronic
exposure to DDT and its metabolites in the diet of birds. Of the three compounds, evidence strongly
indicates that DDE is responsible for most reproductive toxicity in avian species [13]. Measurements
of residues in eggs of birds are a reliable indicator of adverse effects. There is a large amount of
variability in sensitivity to DDT and its metabolites among bird species, with waterfowl and raptor
species showing the greatest sensitivities. Studies have shown the brown pelican to be most susceptible
to adverse effects, with eggshell thinning and depressed productivity occurring at 3.0 |ig/g of DDE in
the egg and total reproductive failure when residues exceed 3.7 |ig/g [13].
352
-------
Summary of Biological Effects Tissue Concentrations for p,p'-DDT
Species:
Taxa
Invertebrates
Macomona liliana,
Mollusk
Austrovenus
stutchburyi,
Mollusk
Corbiciila fluminea,
Asian clam
Corbiciila fluminea,
Asian clam
Concentration, Units in1:
Sediment Water
63.33 ng/kg
OC
76.71 |ig/kg
OC
127.27
M-g/kg
OC
20.83 |ig/kg
OC
63.33 |ig/kg
OC
76.71 |ig/kg
OC
127.71
M-g/kg
OC
4.3 |ig/kg
OC
3277 ng/kg
OC
Toxicity:
Tissue (Sample Type) Effects
13.22|ig/kglipid
33.91 |ig/kg lipid
24.1 2 |ig/kg lipid
7.35 |ig/kg lipid
8.01 |ig/kg lipid
7.29 |ig/kg lipid
7.63 |ig/kg lipid
1, 300 ng/kg lipid
108,197 |ig/kg lipid
Ability to Accumulate2: Source:
Log Log
BCF BAF BSAF Reference
0.209 [33]
0.442 [33]
0.190 [33]
0.353 [33]
0.126 [33]
0.095 [33]
0.060 [33]
302.326 [14]
33.017 [36]
Comments3
F; %lipid = 2.95;
%sed OC = 0.30
F; %lipid = 2.33;
%sed OC = 0.73
F; %lipid = 2.57;
%sed OC = 0.22
F;%lipid=3.13;
%sed OC = 0.48
F; %lipid = 5.62;
%sed OC = 0.30
F;%lipid=5.21;
%sed OC = 0.73
F; %lipid = 4.85;
%sed OC = 0.22
F; %lipid = not
reported; %sed OC =
2.3
F;%lipid = 0.61;
%sedOC=1.19
-------
Summary of Biological Effects Tissue Concentrations for p,p'-DDT
Species:
Taxa
Corbicula fluminea,
Asian clam
Mercenaria
mercenaria,
Quahog clam
Mya arenaria,
Soft shell clam
Daphnia magna,
Cladoceran
Diporeia spp.,
Amphipod
Concentration, Units in1: Toxicity:
Sediment Water Tissue (Sample Type) Effects
67 |ig/kg 508 |ig/kg lipid
OC
92|ig/kg 1 64 |ig/kg lipid
OC
(0-5 cm) 1.3 |ig/g lipid
2.9 ng/g dw (whole tissue)
0.126mg/kg Behavior,
(whole body)4 NOED
NOED
1.83mg/kg (whole Mortality,
body)4 NOED
19.7 mg/kg (whole Mortality,
body)4 NOED
Ability to Accumulate2: Source:
Log Log
BCF BAF BSAF Reference
7.563 [36]
1.774 [36]
[14]
[29]
[29]
[23]
[22]
Comments3
F;%lipid = 0.61;
%sedOC=1.19
F;%lipid = 0.61;
%sedOC= 1.19
F; Rio de La Plata,
Argentina; lipid
content 2.4-3.8%
L; No effect on
feeding activity
L; no effect on
feeding activity
L; no effect on
survivorship in 3 days
L; no increase in
mortality in 96 hours
-------
Summary of Biological Effects Tissue Concentrations for p,p'-DDT
Species:
Taxa
Gammams
fasciatus,
Amphipod
Palaemonetes
kadiakensis,
Grass shrimp
Orconectes nais,
Crayfish
Ephemera danica,
Mayfly
Hexagenia
bilineata, Mayfly
Siphlonurus sp.,
Mayfly
Concentration, Units in1:
Sediment Water Tissue (Sample Type)
0.336 mg/kg (whole
body)4
0.1 mg/kg
(whole body)4
0.0466 mg/kg
(whole body)4
6 mg/kg
(whole body)4
6 mg/kg
(whole body)4
0.336 mg/kg
(whole body)4
0.2 16 mg/kg
(whole body)4
Toxicity: Ability to Accumulate2:
Log Log
Effects BCF BAF BSAF
Mortality,
NOED
Mortality,
NOED
Mortality,
NOED
Growth, NOED
Mortality,
NOED
Mortality,
NOED
Mortality,
NOED
Source:
Reference Comments3
[23] L; no effect on
survivorship in 3 days
[23] L; no effect on
survivorship in 3 days
[23] L; no effect on
survivorship in 3 days
[20] L
L
[23] L; no effect on
survivorship after 3
days
[23] L; no effect on
survivorship after 3
days
-------
Summary of Biological Effects Tissue Concentrations for p,p'-DDT
Species:
Taxa
Libellula sp.,
Dragonfly
Ischniira verticalis,
Damselfly
Chironomiis sp.,
Midge
Chironomiis
riparius, Midge
Fishes
Sqiialiis acanthias,
Spiny dogfish
Concentration, Units in1:
Sediment Water Tissue (Sample Type)
0.0144mg/kg
(whole body)4
0.075 mg/kg
(whole body)4
0.44 mg/kg
(whole body)4
0.83 mg/kg
(whole body)4
0.18 mg/kg
(whole body)4
0.08 mg/kg
(whole body)4
0.1 mg/kg
(whole body)4
Toxicity:
Effects
Mortality,
NOED
Mortality,
NOED
Mortality,
NOED
Behavior,
LOED
Behavior,
NOED
Behavior,
NOED
Mortality,
NOED
Ability to Accumulate2: Source:
Log Log
BCF BAF BSAF Reference
[23]
[23]
[23]
[24]
[24]
[24]
[32]
Comments3
L; no effect on
survivorship after 2
days
L; no effect on
survivorship after 2
days
L; no effect on
survivorship in 3 days
L; reduced swimming
ability
L; no effect on
swimming behavior
L; no effect on
swimming behavior
L; no effect on
mortality in 24 hours
-------
Summary of Biological Effects Tissue Concentrations for p,p'-DDT
Species:
Taxa
Anguilla anguilla,
Eel
Oncorhynchus,
Salmo, Salvelinus
sp., Salmonids
Salmonids
Oncorhynchus
kisutch,
Coho salmon
Concentration, Units in1:
Sediment Water
23 |ig/kg
OC
8 |ig/kg
OC
14 |ig/kg
OC
25 ng/kg
OC
34 |ig/kg
OC
144 |ig/kg
OC
667 |ig/kg
OC
0.000019
Toxicity:
Tissue (Sample Type) Effects
1 58 |ig/kg lipid
135 |ig/kg lipid
1233 |ig/kg lipid
221 |ig/kg lipid
287 |ig/kg lipid
1064 |ig/kg lipid
727 |ig/kg lipid
80 ng/kg lipid
95 mg/kg Mortality,
(whole body)4 ED50
Ability to Accumulate2: Source:
Log Log
BCF BAF BSAF Reference
6.87 [37]
16.88 [37]
88.07 [37]
8.84 [37]
8.44 [37]
7.39 [37]
1.091 [35]
6.62 [35]
1.67 [38]
[27]
Comments3
F; %lipid = 7; %sed
OC = 7
F; %lipid = 7; %sed
OC= 14
F; %lipid = 6; %sed
OC=18
F; %lipid = 10; %sed
OC=12
F; %lipid = 10; %sed
OC=12
F;%lipid= 13; %sed
OC = 32
F;%lipid= ll;%sed
OC = 2.7
F; %lipid = 1 1
F
L; 50% mortality in
31 days
-------
Summary of Biological Effects Tissue Concentrations for p,p'-DDT
Species:
Taxa
Prosopium
williamsoni,
Mountain whitefish
Corogoniis
autumnalis,
Omul (endemic
whitefish)
Salmo salar,
Atlantic salmon
Salvelinus
namaycush,
Lake trout
Concentration, Units in1: Toxicity:
Sediment Water Tissue (Sample Type) Effects
244 ng/kg 417 |ig/kg lipid
OC
6,433 |ig/kg 772 |ig/kg lipid
OC
particulate: 0.16-0.27 mg/kg5 lipid
5. Ipg/L ± (whole body)
2.3 n = 2
n = 7
dissolved:
50 pg/L ± 23
n = 7
3 mg/kg Morphology,
(whole body)4 NOED
3.9 mg/kg Behavior,
(whole body)4 LOED
Ability to Accumulate2: Source:
Log Log
BCF BAF BSAF Reference Comments3
1.706 [34] F; %lipid = 12.0;
%sed OC = 0.9
0.120 [34] F; %lipid = 12.25;
%sed OC = 0.30
[16] F; Lake Baikal,
Siberia
[26] L; no effect on
metabolic rate or
growth,
resd_conc_wet value
range 3.0-5.0
[21] L; temperature
selection after 24-
hour exposure to
chemical
-------
Summary of Biological Effects Tissue Concentrations for p,p'-DDT
Species:
Taxa
Salvelinus
namaycush,
Lake trout
Carassiiis aiiratiis,
Goldfish
Pimephales
promelas,
Fathead minnow
Concentration, Units in1:
Sediment Water Tissue (Sample Type)
27.8 mg/kg
(whole body)4
3.66 mg/kg
(whole body)4
2 mg/kg
(whole body)4
5.1 mg/kg
(whole body)4
3.8 mg/kg
(whole body)4
24 mg/kg
(whole body)4
Toxicity: Ability to Accumulate2:
Log Log
Effects BCF BAF BSAF
Behavior,
LOED
Mortality,
LOED
Mortality,
LOED
Behavior,
LOED
Reproduction,
LOED
Reproduction,
LOED
Source:
Reference Comments3
[21] L; temperature
selection after 24-
hour exposure to
chemical
[28] L; survival of fry
reduced
[28] L; survival of fry
reduced
[31] L; behavioral
changes, loss of
equilibrium,
convulsions
[19] L; significantly
different from control
(p = 0.05)
[19] L; significantly
different from control
(p = 0.05)
Cyprinus carpio,
Carp
Surface
0.012 mg/kg water
(n=l) 0.39 ng/L
(n=l)
0.023 ±0.012 mg/kg
(n = 9)
[15] F; lower Detroit
River; value is mean
±SD
-------
Summary of Biological Effects Tissue Concentrations for p,p'-DDT
Species: Concentration, Units in1:
Taxa Sediment Water
Mixed Catastoma 6433 |ig/kg
sp., Suckers OC
Catastoma 340 |ig/kg
macrocheilus, OC
Largescale sucker
Pimelodus albicans, 0.4 ng/g dw
(Marine catfish)
Pimelodus albicans, 40.0 |ig/kg
Mandi OC
Gambusia affinis,
Mosquito fish
Leuciscus idus,
Golden ide
Toxicity:
Tissue (Sample Type) Effects
869 |ig/kg lipid
811 ng/kg lipid
0.5 |ig/g lipid (n = 7)
(muscle)
500 ng/kg lipid
18.6 mg/kg Mortality,
(whole body)4 NOED
95 mg/kg Mortality,
(whole body)4 NOED
Ability to Accumulate2: Source:
Log Log
BCF BAF BSAF Reference Comments3
0.135 [34] F; %lipid = 9.2; %sed
OC = 0.30
2.385 [34] F;%lipid= 11.1;
%sedOC=1.0
[14] F; Rio de La Plata,
Argentina; lipid
content 4%
[14] F;%lipid = not
reported; %sed OC =
1.0
[25] L; no effect on
survivorship after 3
days
[30] L; no effect on
survivorship in 3 days
-------
Summary of Biological Effects Tissue Concentrations for p,p'-DDT
Species:
Taxa
Lepomis
macrochirus,
Bluegill
Comephoms
dybowskii,
Pelagic sculpin
Cottus cognatus,
Slimy sculpin
Concentration, Units in1:
Sediment Water
particulate:
5.1pg/L±
2.3
n = 7
dissolved:
50 pg/L ± 23
n = 7
667 |ig/kg
OC
0.000019
Hg/L
Toxicity:
Tissue (Sample Type) Effects
4.2 mg/kg Behavior,
(whole body)4 LOED
0.52-0.64 mg/kg lipid
(whole body)
n= 1
362 |ig/kg lipid
29 |ig/kg lipid
Ability to Accumulate2: Source:
Log Log
BCF BAF BSAF Reference Comments3
[31] L; behavioral
changes, loss of
equilibrium,
convulsions
[16] F; Lake Baikal,
Siberia
0.544 [35] F; %lipid = 8; %sed
OC = 2.7
6.18 [35] F;%lipid =8
Prochilodus
platensis,
common name not
available
0.4 ng/g dw
Three composite
samples (|ig/g lipid):
2.4 (n = 4) (muscle)
9.3 (n = 4) (muscle)
4.3 (n = 5) (muscle)
[14] F; Rio de La Plata,
Argentina; lipid
content 1-12.7%
Prochilodus
platensis,
Curimata
40.0 |ig/kg
OC
5,333.33 |ig/kg lipid
[14] F; %lipid = not
reported; %sed OC:
1.0
-------
Summary of Biological Effects Tissue Concentrations for p,p'-DDT
Species: Concentration, Units in1:
Taxa Sediment Water
Wildlife
Bucephala clangula, 0.012 mg/kg
Goldeneye (n = 1)
Aythya affinis, 0.012 mg/kg
Lesser scaup (n = 1)
Aythya marila, 0.012 mg/kg
Greater scaup (n = 1)
Falco peregrinus,
Peregrine falcon
(eggs)
water =
0.39 ng/L
(n=D
surface
water
0.39 ng/L
(n=l)
surface
water
0.39 ng/L
(n=l)
Toxicity: Ability to Accumulate2: Source:
Log Log
Tissue (Sample Type) Effects BCF BAF BSAF Reference Comments3
0.040 mg/kg
(whole body)
(n = 3)
0.025 mg/kg
(whole body)
(n = 7)
0.040 ± 0.0094 mg/kg
(whole body)
(n = 3)
22ng/g(eggs) 11.4% eggshell
(n = 6) thinning
[15] F; lower Detroit
River; value is mean
±SD
[15] F; lower Detroit
River; value is mean
±SD
[15] F; lower Detroit
River; value is mean
±SD
[17] F; Kola Penninsula,
Russia; n = number
of clutches sampled
Lams californicus,
California gull
440 mg/kg (brain)4 Mortality, NA
183 mg/kg (breast)4 Mortality, NA
3200 mg/kg (liver)4 Mortality, NA
[18]
[18]
[18]
L
L
L
-------
Summary of Biological Effects Tissue Concentrations for p,p'-DDT
Species:
Taxa
Pelecaniis
occidentalis,
Brown pelican
Phalacrocorax
penicillatus,
Brandts cormorant
Phoca siberica,
Baikal seal
Concentration, Units in1:
Sediment Water Tissue (Sample Type)
4.55 mg/kg (brain)4
66 mg/kg (breast)4
7.8 mg/kg (liver)4
230 mg/kg (brain)4
500 mg/kg (breast)4
840 mg/kg (liver)4
8 10 mg/kg (Liver)4
particulate: 17-21 mg/kg5 lipid
5.1pg/L± (blubber)
2.3 n=l
n= 1
dissolved:
50 pg/L ± 23
n= 1
Toxicity: Ability to Accumulate2:
Log Log
Effects BCF BAF BSAF
Mortality, NA
Mortality, NA
Mortality, NA
Mortality, NA
Mortality, NA
Mortality, NA
Mortality, NA
Source:
Reference
[18]
[18]
[18]
[18]
[18]
[18]
[18]
[16]
Comments3
L
L
L
L
L
L
L
F; Lake Baikal,
Siberia
1 Concentration units based on wet weight unless otherwise noted.
2 BCF = bioconcentration factor, BAF = bioaccumulation factor, BSAF = biota-sediment accumulation factor.
3 L = laboratory study, spiked sediment, single chemical; F = field study, multiple chemical exposure; other unusual study conditions or observations noted.
4 This entry was excerpted directly from the Environmental Residue-Effects Database (ERED, www.wes.army.mil/el/ered, U.S. Army Corps of Engineers and U.S.
Environmental Protection Agency). The original publication was not reviewed, and the reader is strongly urged to consult the publication to confirm the
information presented here.
5 Not clear from reference if concentration is based on wet or dry weight.
-------
BIOACCUMULATION SUMMARY p,p -DDT
References
1. Verschueren. Hdbk. Environ. Data Org. Chem.,1983, p. 437 (cited in: USEPA. 1996.
Hazardous Substances Data Bank (HSDB). National Library of Medicine online (TOXNET).
U.S. Environmental Protection Agency, Office of Health and Environmental Assessment,
Environmental Criteria and Assessment Office, Cincinnati, OH. February).
2. USEPA. 1989. Chemical fate rate constants for SARA section 313 chemicals and Superfund
Health Evaluation Manual chemicals. Prepared by Chemical Hazard Assessment Division,
Syracuse Research Corporation, for U.S. Environmental Protection Agency, Office of Toxic
Substances, Exposure Evaluation Division, Washington, DC, and Environmental Criteria and
Assessment Office, Cincinnati, OH. August 11.
3. Karickhoff, S.W., and J.M. Long. 1995. Internal report on summary of measured, calculated
and recommended log Kovf values. Draft. Prepared by U.S. Environmental Protection Agency,
Office of Research and Development, Environmental Research Laboratory-Athens, for E.
Southerland, Office of Water, Office of Science and Technology, Standards and Applied
Science Division, Washington, DC. April 10.
4. USEPA. 1995. Integrated Risk Information System (IRIS). National Library of Medicine online
(TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental
Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. September.
5. Braune, B.M. and RJ. Norstrom. 1989. Dynamics of organochlorine compounds in herring
gulls: III. Tissue distribution and bioaccumulation in Lake Ontario gulls. Environ. Toxicol.
Chem. 8:957-968.
6. Muir, D.C.G., RJ. Norstrom, and M. Simon. 1988. Organochlorine contaminants in arctic
marine food chains: Accumulation of specific polychlorinated biphenyls and chlordane-related
compounds. Environ. Sci. Technol. 22:1071-1079.
7. Charles, M.J., and R. A. Kites. 1987. Sediments as archives. In Sources and fates of aquatic
pollutants, ed. R.A. Kites and S.J. Eisenreich, Advances In Chemistry Series, Vol. 216, pp. 365-
389. American Chemical Society, Washington, DC.
8. USEPA. 1980. Ambient water quality criteria for DDT. EPA440/5-80-038. U.S.
Environmental Protection Agency, Office of Water Regulations and Standards, Criteria and
Standards Division, Washington, DC.
9. 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.
Environ. Manage. 19(l):81-97.
10. Pavlou, S., R. Kadeg, A. Turner, and M. Marchlik. 1987. Sediment quality criteria methodology
validation: Uncertainty analysis of sediment normalization theory for nonpolar organic
contaminants. Work Assignment 56, Task 3. Battelle, Washington, DC.
364
-------
BIOACCUMULATION SUMMARY p,p -DDT
11. Johnson, H.E., and C. Pecor. 1969. Coho salmon mortality and DDT in Lake Michigan.
Transactions of the 34th North American Wildlife Conference.
12. Smith, R.M., and C.F. Cole. 1973. Effects of egg concentrations of DDT and dieldrin on
reproduction in winter flounder (Pseudopleuronectes americanus). J. Fish. Res. Board Can.
30:1894-1898.
13. Blus, LJ. 1996. DDT, ODD, and DDE in birds. In Environmental contaminants in wildlife,
ed. W. N. Beyer, G.H. Heinz, and A.W. Redmon-Norwood, pp. 49-71. Lewis Publishers, Boca
Raton, FL.
14. Columbo, J.C., M.F. Khalil, M. Arnac, and A.C. Horth. 1990. Distribution of chlorinated
pesticides and individually polychlorinated biphenyls in biotic and abiotic compartments of the
Rio de la Plata, Argentina. Environ. Sci. Technol 24:498-505.
15. Smith., E.V., J.M. Spurr, J.C. Filkins, and J.J. Jones. 1985. Organochlorine contaminants of
wintering ducks foraging on Detroit River sediments. /. Great Lakes Res. 11(3):231-246.
16. Kucklick, J.R., T.F. Bidleman, L.L. McConnell, M.D. Walla, and G.P. Ivanov. 1994.
Organochlorines in the water and biota of Lake Baikal, Siberia. Environ. Sci. Technol. 28:31-37.
17. Henny, C.J., S.A. Ganusevich, P.P. Ward, and T.R. Schwartz. 1994. Organochlorine pesticides,
chlorinated dioxins and furans, and PCBs in peregrine falcon Falco peregrinus eggs from the
Kola Penninsula, Russia. In Raptor conservation today, ed. B.U. Meyburg and R.D. Chancellor,
pp. 739-749. WWGPB/The Pica Press.
18. Young, D.R., and T.C. Heeson. 1977. Marine bird deaths at the Los Angeles zoo. Coastal
Water Research Program Annual Report. Southern California Coastal.
19. Jarvinen, A.W., M.J. Hoffman, and T.W. Thorslund. 1977. Long-term toxic effects of DDT
food and water exposure on fathead minnows (Pimephalespromelas). J. Fish. Res. Board. Can.
34:2089-2103.
20. Sodergren, A., and B. Svensson. 1973. Uptake and accumulation of DDT and PCB by
Ephemera danica (Ephemeroptera) in continuous-flow systems. Bull. Environ. Contam. Toxicol.
9(6).
21. Peterson, R.H. 1973. Temperature selection of Atlantic salmon (Salmo salar) and brook trout
(Salvelinus fontinalis) as influenced by various chlorinated hydrocarbons. /. Fish. Res. B. Can.
30(8).
22. Harkey, G.A., P.F. Landrum, and S.J. Klaine. 1994. Comparison of whole-sediment, elutriate
and pore-water exposures for use in assessing sediment-associated organic contaminants in
bioassays. Environ. Toxicol Chem. 13:1315-1329.
23. Johnson, B.T., C.R. Saunders, H.O. Sanders, and R.S. Campbell. 1971. Biological
magnification and degradation of DDT and aldrin by freshwater invertebrates. /. Fish. Res. Bd.
Can. 28:705-709.
365
-------
BIOACCUMULATION SUMMARY p,p -DDT
24. Lydy, M.J., K.A. Bruner, D.M. Fry, and S.W. Fisher. 1990. Effects of sediment and the route
of exposure on the toxicity and accumulation of neutral lipophilic and moderately water soluble
metabolizable compounds in the midge, Chironomus riparius. ASTM STP-1096. Aquatic
toxicology and risk assessment, ed. W.G. Landis, et.al. pp. 140-164. American Society for
Testing and Materials, Philadelphia, PA.
25. Metcalf, R.L. 1974. A laboratory model ecosystem to evaluate compounds producing biological
magnification. In Essays in toxicology, ed. WJ. Hayes, Vol. 5, pp. 17-38. Academic Press, New
York, NY.
26. Addison, R.F., M.E. Zinck, and J.R. Leahy. 1976. Metabolism of single and combined doses
of 14C-aldrin and 3H-/?,/?'DDT by Atlantic salmon (Salmo salar) fry. /. Fish. Res. B. Can.
33:2073-2076.
27. Buhler, D.R., and W.E. Shanks. 1970. Influence of body weight on chronic oral DDT toxicity
in coho salmon. /. Fish. Res. B. Can. 27:347-358.
28. Burdick, G.E., EJ. Harris, HJ. Dean, T.M. Walker, J. Skea, and D. Colby. 1964. The
accumulation of DDT in lake trout and the effect on reproduction. Trans. Amer. Fish. Soc.
93:127-136.
29. Butler, P. A. 1971. Influence of pesticides on marine ecosystems. Proc. Royal Soc. London,
Ser. B 177:321-329.
30. Freitag, D., L. Ballhorn, H. Geyer, and F. Korte. 1985. Environmental hazard profile of organic
chemicals: An experimental method for the assessment of the behaviour of organic chemicals
in the ecosphere by means of laboratory tests with 14C labelled chemicals. Chemosphere
14:1589-1616.
31. Gakstatter, J.H., and C.M. Weiss. 1967. The elimination of DDT-C14, dieldrin-C14, and
lindane-C14 from fish following a single sublethal exposure in aquaria. Trans. Amer. Fish. Soc.
96:301-307.
32. Guarino, A.M., and S.T. Arnold. 1979. Xenobiotic transport mechanisms and pharmacokinetics
in the dogfish shark. In Pesticide andxenobiotic metabolism in aquatic organisms, ed. M.A.Q.
Khan et al., pp. 233-258.
33. Hickey, C.W., D.S. Roper, P.T. Holland, and T.M. Trower. 1995. Accumulation of organic
contaminants in two sediment-dwelling shellfish with contrasting feeding modes: Deposit-
(Macomona liliana) and filter-feeding (Austovenus stutchburi). Arch. Environ. Contam. Toxicol.
11:21-231.
34. Johnson, A., D. Norton, and B. Yake. 1988. Persistence of DDT in the Yakima River drainage,
Washington. Arch. Environ. Contam. Toxi. 17:291-297.
35. Oliver, G.G., and AJ. Niimi. 1988. Chlorinated hydrocarbons in the Lake Ontario ecosystem.
Environ. Sci. Technol 22(4):388-397.
366
-------
BIOACCUMULATION SUMMARY p,p -DDT
36. Pereira, W.E., J.L. Domagalski, F.D. Hostettler, L.R. Brown, and J.B. Rapp. 1996. Occurrence
and accumulation of pesticides and organic contaminants in river sediment, water, and clam
tissues from the San Jaoquin River and tributaries, California. Environ. Toxicol Chem. 15:172-
180.
37. Van der Oost, R. A. Opperhuizen, K. Satumalay, H. Heida, and P.E. Vermulen. 1996.
Biomonitoring aquatic pollution with feral eel (Anguilla anguilla) I. Bioaccumulation: Biota-
sediment ratios of PCBs, OCPs, PCDDs and PCDFs. Aquat. Toxicol. 35:21-46.
38. USEPA. 1995. Great Lakes Water Quality Initiative Technical Support Document for the
procedure to determine bio accumulation factors. EPA-820-B-95-005. U.S. Environmental
Protection Agency, Office of Water, Washington, DC.
39. USEPA. 1998. Ambient water quality criteria derivation methodology• human health: Technical
support document. Final draft. EPA-822-B-98-005. U.S. Environmental Protection Agency,
Office of Water, Washington, DC.
367
-------
368
-------
BIOACCUMULATION SUMMARY DIAZINON
Chemical Category: PESTICIDE (ORGANOPHOSPHATE)
Chemical Name (Common Synonyms): DIAZINON CASRN: 333-41-5
Chemical Characteristics
Solubility in Water: 0.004% at 20°C [1] Half-Life: No data [2]
Log Kow: 3.70 [3] Log Koc: 3.64 L/kg organic carbon
Human Health
Oral RfD: 9 x 10'4 mg/kg/day [4] Confidence: —
Critical Effect: Decreased cholinesterase activity
Oral Slope Factor: No data [4,5] Carcinogenic Classification: No data [4,5]
Wildlife
Partitioning Factors: Partitioning factors for diazinon in wildlife were not found in the literature.
Food Chain Multipliers: Food chain multipliers for diazinon in wildlife were not found in the
literature.
Aquatic Organisms
Partitioning Factors: Partitioning factors for diazinon in aquatic organisms were not found in the
literature. Log BCFs ranged from 0.69 to 1.23 (invertebrates) and from 1.59 to 2.90 (fishes).
Food Chain Multipliers: Food chain multipliers for diazinon in aquatic organisms were not found in
the literature.
Toxicity/Bioaccumulation Assessment Profile
Diazinon is relatively toxic to aquatic organisms. The acute toxicity for aquatic invertebrates ranged
from 0.9 |ig/L (48-h LC50) for Daphniapulex [6] to 200|ig/L (96-h LC50) for Gammarus lacustris [7],
while chronic toxicity ranged from 0.27 |ig/L (30-d LC50) for Gammarus pseudolimneaus to 4.6 |ig/L
(30-d LC50) for Acroneuria lycorias [8]. The maximum acceptable concentration (MATC) for diazinon
based on the exposure with sheepshead minnows, was 0.47 |ig/L [5], and 3.2 |ig/L based on the exposure
with fathead minnows [9].
369
-------
BIOACCUMULATION SUMMARY DIAZINON
The mode of toxic action of organophosphorus compounds is related to the inhibition of
acetylcholinesterase in tissue of animals [10]. A representative of organophosphorus insecticides,
diazinon shows species-selective toxicity in fish [11]. For example, diazinon was about 10 times more
toxic to the guppy than to the zebra fish [12] and 22 times more potent to loach than killifish [10]. Both
the guppy and zebra fish metabolized diazinon to 2-isopropyl-6-methyl-4-pyrimidinol (pyrimidinol). The
species-specific oxidative transformation of diazinon or inhibition of acetylcholinesterase are
responsible for the differences in diazinon toxicity. During the exposure of pretreated fish (guppies and
zebra fish) to diazinon [13], the tissue concentration of pyrimidinol initially increased, then declined to
very low levels. Keizer et al. [13] hypothesized that the toxicity of diazinon to guppy is due to its
metabolism to a highly toxic metabolite, e.g., diazoxon whereas toxicity to zebra fish is related to
bioaccumulation of the parent compound. Fish reached an apparent steady state after 48 hours [12] or
96 hours [14].
Diazinon was most rapidly excreted from the gallbladder followed by liver, muscle, and kidney [11]. The
slow excretion rate from kidney was probably because diazinon was transported from all parts of the fish
to the kidney before excretion [15]. The log BCFs for eels exposed to 56 ug/L of diazinon were 2.90 in
liver, 3.20 in muscle, and 3.36 in gill tissue [16]. Diazinon elimination from the selected tissues was
rapid; it was not detected in any tissue after 24-hour exposure in clean water [16]. The results of the
study by Kanazawa [17] showed that the concentration of diazinon in tissue of the freshwater fish
reached a maximum after 4 days and then decreased gradually. The uptake of diazinon by killifish was
not influenced if the fish were exposed to the individual pesticide, or to a pesticide mixture [18].
Diazinon was identified as a major toxicant in municipal effluents [19], indicating persistence of this
pesticide in the environment. According to Lee et al. [20 ], the toxicity of diazinon can be induced by
dissolved organic materials.
370
-------
Summary of Biological Effects Tissue Concentrations for Diazinon
Species:
Taxa
Concentration, Units in1:
Toxicity:
Sediment Water Tissue (Sample Type) Effects
Ability to Accumulate2:
Log Log
BCF BAF BSAF
Source:
Reference Comments3
Invertebrates
Cipangopoludina
malleata,
Pond snail
lOjig/L
0.77
[21]
Procambams
clarkii, Crayfish
lOjig/L
0.69
[21]
Indoplanorbis
exustus, Red snail
lOjig/L
1.23
[21]
Fishes
Pseudorasbora
parva,
Topmouth gudgeon
Anguilla anguilla,
Eel
SOjig/L H.3ng/g
10 ng/L 80 ng/g (liver)
2.32
2.90
[22]
[16]
Anguilla anguilla,
Eel
10 |ig/L 160 ng/g (muscle)
2.90
[16]
Gnathopogon
caerulescens,
Willow shiner
2.39
[23]
-------
Summary of Biological Effects Tissue Concentrations for Diazinon
Species: Concentration, Units in1:
Taxa Sediment Water
Pseudorasbora
parva,
Topmouth gudgeon
Pseudorasbora 0.7 mg/kg
parva,
Motsugo
Brachydanio rerio, Ingestion
Zebra fish
Zacco slatypus,
Pale chub
Plecoglossus
altivelis,
Ayu sweetfish
Toxicity:
Tissue (Sample Type) Effects
211 mg/kg (4-day) Bleeding,
17 mg/kg (30 day) abnormal
swimming
1,550 mg/kg Mortality,
(whole body)4 ED 100
Ability to Accumulate2:
Log Log
BCF BAF BSAF
2.18
1.81
2.18
1.79
Source:
Reference Comments3
[23] F
[17] L
[13] L; Lethal body burden
[23] F
[23] F
Cyprinodon
variegatus,
Sheepshead minnow
1.8 |ig/L
3.5
6.5 |ig/L
0.26 mg/kg in 4d,
0.11 mg/kg in 7d,
0.31 mg/kg in 14d
0.38 mg/kg in 4d,
0.21 mg/kg in 7d,
0.49 mg/kg in 14d
1.3 mg/kg in 4d,
0.5 mg/kg in 7d,
1.4 mg/kg in 14d
2.17
2.17
2.33
[14]
[14]
[14]
Cyprinodon
variegatus,
Sheepshead minnow
0.3 mg/kg
(whole body)4
Morphology,
LOED
[14] L; body darkened,
lateral curvature of
body
-------
Summary of Biological Effects Tissue Concentrations for Diazinon
Species: Concentration, Units in1:
Taxa Sediment Water Tissue (Sample Type)
1 .4 mg/kg
(whole body)4
0.5 mg/kg
(whole body)4
0.05 mg/kg
(whole body)4
1 .4 mg/kg
(whole body)4
0.5 mg/kg
(whole body)4
0.3 mg/kg
(whole body)4
0.05 mg/kg
(whole body)4
0.05 mg/kg
(whole body)4
1 .4 mg/kg
(whole body)4
0.5 mg/kg
(whole body)4
0.3 mg/kg
(whole body)4
1 .4 mg/kg
(whole body)4
Toxicity: Ability to Accumulate2:
Log Log
Effects BCF BAF BSAF
Morphology, not
applicable
Morphology, not
applicable
Mortality,
NOED
Mortality,
NOED
Mortality,
NOED
Mortality,
NOED
Mortality,
NOED
Physiological,
LOED
Physiological,
NA
Physiological,
NA
Physiological,
NA
Reproduction,
ED50
Source:
Reference
[14]
[14]
[14]
[14]
[14]
[14]
[14]
[14]
[14]
[14]
[14]
[14]
Comments3
L; body darkened,
lateral curvature of
body
L; body darkened,
lateral curvature of
body
L; no effect on
morphology or
appearance
L; no effect on
mortality
L; no effect on
mortality
L; no effect on
mortality
L; no effect on
mortality
L; inhibition of
acetylcholinesterase
activity
L; 71% inhibition of
acetylcholinesterase
activity
L; inhibition of
acetylcholinesterase
activity
L; inhibition of
acetylcholinesterase
activity
L; 45-55% reduction
in average number of
eggs produced
-------
Summary of Biological Effects Tissue Concentrations for Diazinon
Species:
Taxa
Poecilia reticulata,
Guppy
Poecilia reticulata,
Guppy
Concentration, Units in1:
Sediment Water Tissue (Sample Type)
0.5 mg/kg
(whole body)4
0.3 mg/kg
(whole body)4
0.05 mg/kg
(whole body)4
0.8 mg/L 25.8 |ig/g in 24h,
90.3 |ig/g in 48h,
167.7|ig/gin96h,
109 mg/kg
(whole body)4
2,430 mg/kg
(whole body)4
2,430 mg/kg
(whole body)4
Toxicity: Ability to Accumulate2:
Log Log
Effects BCF BAF BSAF
Reproduction,
ED50
Reproduction,
ED50
Reproduction,
LOED
Mortality,
ED 100
Mortality,
ED 100
Mortality,
ED 100
Source:
Reference
[14]
[14]
[14]
[13]
[24]
[24]
Comments3
L; 45-55% reduction
in average number of
eggs produced
L; 45-55% reduction
in average number of
eggs produced
L; statistically
significant reduction
in number of eggs
produced
L; lethal body burden
L; lifestage: 2-3
months
L; lifestage: 2-3
months
1 Concentration units based on wet weight unless otherwise noted.
2 BCF = bioconcentration factor, BAF = bioaccumulation factor, BSAF = biota-sediment accumulation factor.
3 L = laboratory study, spiked sediment, single chemical; F = field study, multiple chemical exposure; other unusual study conditions or observations noted.
4 This entry was excerpted directly from the Environmental Residue-Effects Database (ERED, www.wes.army.mil/el/ered, U.S. Army Corps of Engineers and U.S.
Environmental Protection Agency). The original publication was not reviewed, and the reader is strongly urged to consult the publication to confirm the
information presented here.
-------
BIOACCUMULATION SUMMARY DIAZINON
References
1. Budavari, Merck index, llth ed., 1989, p. 472. (Cited in: USEPA. 1995. Hazardous Substances
Data Bank (HSDB). National Library of Medicine online (TOXNET). U.S. Environmental
Protection Agency, Office of Health and Environmental Assessment, Environmental Criteria and
Assessment Office, Cincinnati, OH. September.)
2. USEPA. 1989. Chemical fate rate constants for SARA section 313 chemicals and Superfund Health
Manual chemicals. Prepared by Chemical Hazard Assessment Division, Syracuse Research
Corporation, for U.S. Environmental Protection Agency, Office of Toxic Substances, Exposure
Evaluation Division, Washington, DC, and Environmental Criteria and Assessment Office,
Cincinnati, OH. August 11.
3. Karickhoff, S.W., and J.M. Long. 1995. Internal report on summary of measured, calculated, and
recommended log Kow values. Draft. Prepared by U.S. Environmental Protection Agency, Office
of Research and Development, Environmental Research Laboratory-Athens, for E. Southerland,
Office of Water, Office of Science and Technology, Standards and Applied Science Division,
Washington, DC. April 10.
4. USEPA. 1995. Health effects assessment summary tables: FY-1995 Annual. EPA/540/R-95/036.
U.S. Environmental Protection Agency, Office of Solid Waste and Emergency Response,
Washington, DC.
5. USEPA. 1997. Integrated Risk Information System (IRIS). National Library of Medicine online
(TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental
Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. January.
6. Sanders, H.O., and O.B. Cope. 1966. Toxicities of several pesticides to two species of cladocerans.
Trans. Amer. Fish. Soc. 95:165-169.
7. Sanders, H.O. 1970. Toxicities of some herbicides to six species of freshwater crustaceans. /. Wat.
Pollut. Contr. Fed. 42:1544-1550.
8. Bell, H.L. 1971. Unpublished data. National Water Quality Laboratory, Duluth, Minnesota.
9. Allison, D.T., and R.O. Hermanutz. 1977. Toxicity ofdiazinon to brook trout and fathead minnows.
EPA-600/3-77-060. U.S. Environmental Protection Agency, Office of Research and Development,
Duluth, MN.
10. Oh, H.S., S.K. Lee, Y.H. Kim, and J.K. Roah. 1991. Mechanism of selective toxicity of diazinon
to killifish (Oryzias latipes) and loach (Misgurnus anguillicaudatus). ASTM STP 1124. Aquatic
toxicology and risk assessment, ed. M.A. Mayes and M.G. Barron, pp. 343-353. American Society
for Testing and Materials, Philadelphia, PA.
11. Vittozzi, L., and G. De Angelis. 1991. A critical review of comparative acute toxicity data on
freshwater fish. Aquat. Toxicol. 19:167-204.
375
-------
BIOACCUMULATION SUMMARY DIAZINON
12. Keizer, J., G. D'Agostino, and L. Vittozzi. 1991. The importance of biotransformation in the
toxicity of xenobiotics to fish. I. Toxicity and bioaccumulation of diazinon in guppy (Poecilia
reticulata) and zebra fish (Brachydanio rerio). Aquat. Toxicol. 21:239-254.
13. Keizer, J., G. D'Agostino, R. Nagel, F. Gramenzi, and L.Vittozzi. 1993. Comparative diazinon
toxicity in guppy and zebra fish: Different role of oxidative metabolism. Environ. Tax. Chem.
12:1243-1250.
14. Goodman, L.R., DJ. Hansen, D.L. Coppage, J.C. Moore, and E. Matthews. 1979. Diazinon, chronic
toxicity to, and brain acetylcholinesterase inhibition in, the sheepshead minnow, Cyprinodon
variegatus. Trans. Am. Fish. Soc. 108:479-488.
15. Tsuda, T., S. Aoki, M. Kojima, and H. Harada. 1990. Bioconcentration and excretion of diazinon,
IBP, malathion and fenitrothion by carp. Comp. Biochem. Physiol 1:23-26.
16. Sancho, E., M.D. Ferrando, E. Andreu, and M. Gamon. 1993. Bioconcentration and excretion of
diazinon by eel. Bull. Environ. Contain. Toxicol. 50:578-585.
17. Kanazawa, J. 1975. Uptake and excretion of organophosphorus and carbamate insecticides by
freshwater fish, motsugo, Pseudorasboraparva. Bull. Environ. Contain. Toxicol. 14:346-352.
18. Tsuda, T., S. Aoki, T. Inoue, and M. Kojima. 1995. Accumulation and excretion of diazinon,
fenthion and fenitrothion by killifish: Comparison of individual and mixed pesticides. Wat. Res.
29:455-458.
19. Amato, J.R., D.I. Mount, EJ. Durhan, M.T. Lukasewych, G.T. Ankley, and E.D. Robert. 1992. An
example of the identification of diazinon as a primary toxicant in an effluent. Environ. Toxicol.
Chem. 11:209-216.
20. Lee, S.K., D. Freitag, C. Steinberg, A. Kettrup, and Y.H. Kim. 1993. Effects of dissolved humic
materials on acute toxicity of some organic chemicals to aquatic organisms. Water Res. 27:199-204.
21. Tsuda, T., S. Auki, M. Kojima, and T. Fujita. 1992. Pesticides in water and fish from rivers flowing
into Lake Biwa. Chemosphere 24:1523-1531.
22. Kanazawa, J. 1978. Bioconcentration ratio of diazinon by freshwater fish and snail. Bull. Environ.
Contain. Toxicol. 20:613-617.
23. Kanazawa, J. 1983. A method of predicting the bioconcentration potential of pesticides by using
fish. Japan Agricult. Res. Quart. 17:173-179.
24. Ohayo-mitoko, G.J.A., and J.W. Deneer. 1993. Lethal body burdens of four organophosphorus
pesticides in the guppy (Poecilia reticulata). Sci. Tot. Environ., Supp.:559-565.
376
-------
BIOACCUMULATION SUMMARY
DICOFOL
Chemical Category: PESTICIDE (ORGANOCHLORINE)
Chemical Name (Common Synonyms): DICOFOL
CASRN: 115-32-2
Chemical Characteristics
Solubility in Water: 1.2 mg/L at 20° C
(99% purity) [1]
Log Kow: No data [3]
Half-Life: No data [2]
LogKoc: —
Human Health
Oral RfD: 1 x 10'3 mg/kg/day [4] Confidence: —
Critical Effect: Increase in liver to body weight ratios in rats
Oral Slope Factor: No data [5] Carcinogenic Classification: C [6]
Wildlife
Partitioning Factors: Partitioning factors for dicofol in wildlife were not found in the literature.
Food Chain Multipliers: Food chain multipliers for dicofol in wildlife were not found in the literature.
Aquatic Organisms
Partitioning Factors: Log BCFs ranging from 4.02-4.16 were reported in a study exposing fathead
minnows to dicofol [10].
Food Chain Multipliers: Food chain multipliers for dicofol in aquatic organisms were not found in the
literature.
Toxicity/Bioaccumulation Assessment Profile
Dicofol is an organochlorine compound used as a miticide. The principal commercial dicofol product,
Kelthane, is made from DDT [7]. Clark et al. [7] reported reduction in eggshell weight and thickness of
American kestrels due to dicofol. They also observed that 10 |ig/g of dicofol reduced hatchability of
eggs. They suggested that dicofol concentrations above 3 |ig/g in food may affect bird reproduction. The
48-h and 100-h LCSOs for grass shrimp (Crangon franciscorum) exposed to dicofol (Kelthane) were 590
and 100 |ig/L, respectively [8].
377
-------
BIOACCUMULATION SUMMARY DICOFOL
The major metabolite of dicofol is l,l-bis(4-chlorophenol)2,2dichloroethanol (pp-DCD) [9]. Because
dicofol is more lipophilic than its metabolites, it was abundant in every tissue except for liver and brain.
The dicofol metabolites are less toxic than dicofol and they have less impact on the formation of normal
eggshells by doves [9]. The bioconcentration of dicofol in fathead minnows was reduced by 35 percent
by clay particles (65 mg/L) indicating that more than 30 percent of the dicofol sorbed onto clay and was
biologically unavailable to the fish [10]. Bioconcentration factors at the two dicofol concentrations were
not significantly different and steady-state concentrations occured with 40 to 60 days of exposure at
10,500 to 13,900 times water levels.
378
-------
Summary of Biological Effects Tissue Concentrations for Dicofol
Species:
Taxa
Concentration, Units in1: Toxicity:
Sediment Water Tissue (Sample Type) Effects
Ability to Accumulate2:
BSAF
Log
BCF
Log
BAF
Source:
Reference Comments3
Fishes
Pimephales
promelas,
Fathead minnow
Wildlife
Streptopelia risoria, 32 mg/kg
Ring neck dove (diet)
12.38 |ig/L
4.02-4.16
4.12-4.14
116.5|ig/g in fat
1.07|ig/g in liver
4.55|ig/g in heart
0.37|ig/g in brain
[10] L
[10] L
[9] L
1 Concentration units based on wet weight unless otherwise noted.
2 BCF = bioconcentration factor, BAF = bioaccumulation factor, BSAF = biota-sediment accumulation factor.
3 L = laboratory study, spiked sediment, single chemical; F = field study, multiple chemical exposure; other unusual study conditions or observations noted.
-------
BIOACCUMULATION SUMMARY DICOFOL
References
1. Verschueren. HDBK Environ. Data Org. Chem. 1983, p.786. (Cited in: USEPA. 1995.
Hazardous Substances Data Bank (HSDB). National Library of Medicine online (TOXNET).
U.S. Environmental Protection Agency, Office of Health and Environmental Assessment,
Environmental Criteria and Assessment Office, Cincinnati, OH. September).
2. USEPA. 1989. Chemical fate rate constants for SARA section 313 chemicals and Superfund
Health Manual chemicals. Prepared by Chemical Hazard Assessment Division, Syracuse
Research Corporation, for U.S. Environmental Protection Agency, Office of Toxic Substances,
Exposure Evaluation Division, Washington, DC, and Environmental Criteria and Assessment
Office, Cincinnati, OH. August 11.
3. Karickhoff, S.W., and J.M. Long. 1995. Internal report on summary of measured, calculated,
and recommended log Kow values. Draft. Prepared by U.S. Environmental Protection Agency,
Office of Research and Development, Environmental Research Laboratory-Athens, for E.
Southerland, Office of Water, Office of Science and Technology, Standards and Applied Science
Division, Washington, DC. April 10.
4. USEPA. 1993. Reference dose tracking report. U.S. Environmental Protection Agency, Office
of Pesticide programs, Health Effects Division, Washington, DC.
5. USEPA. 1997. Integrated Risk Information System (IRIS). National Library of Medicine online
(TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental
Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. January.
6. USEPA. 1992. Classification list of chemicals evaluated for carcinogenicity potential. U.S.
Environmental Protection Agency, Office of Pesticide Programs, Washington, DC.
7. Clark, D.R. Jr., J.W. Spann, and C.M. Bunck. 1990. Dicofol (Kelthane)-induced eggshell
thinning in captive American kestrels. Environ. Toxicol. Chem. 9:1063-1069.
8. Khorram, S., and A.W. Knight. 1977. The toxicity of Kelthane to the grass shrimp (Crangon
franciscorum). Bull. Environ. Contam. Toxicol. 15:398-401.
9. Schwarzbach, S .E. 1991. The role of dicof ol metabolites in the eggshell thinning response of ring
neck doves. Arch. Environ. Contam. Toxicol. 20:200-205.
10. Eaton, J.G., V.R. Mattson, L.H. Mueller, and D.K. Tanner. 1983. Effects of suspended clay on
bioconcentration of Kelthane in fathead minnows. Arch. Environ. Contam. Toxicol. 12:439-445.
380
-------
BIOACCUMULATION SUMMARY
DIELDRIN
Chemical Category: PESTICIDE (ORGANOCHLORINE)
Chemical Name (Common Synonyms): DIELDRIN
CASRN: 60-57-1
Chemical Characteristics
Solubility in Water: 186 ng/L at 25°C [1]
Log Kow: 5.37 [3]
Half-Life: 175 days to 3 years, based on
unacclimated aerobic soil grab
sample data and reported half-life
in soil based on field data [2]
Log Koc: 5.28 L/kg organic carbon
Oral RfD: 5 x 10'5 mg/kg/day [4]
Human Health
Confidence: Medium, uncertainty factor =100
Critical Effect: Liver lesions (focal proliferation and focal hyperplasia) in rats, liver carcinomas in
mice
Oral Slope Factor: 1.6 x 10+1 per (mg/kg)/day [4] Carcinogenic Classification: B2 [4]
Wildlife
Partitioning Factors: Log BCFs for tadpole and juvenile frogs have been measured at 2.20 to 3.33,
whereas log BCFs for adult frogs were 1.57 to 2.58. Dieldrin appears to bioconcentrate to a lesser extent
in frogs than in fish. Mallard ducklings exposed to dieldrin-contaminated water for drinking and
swimming had log BCFs ranging from 1.69 to 2.21 in liver, 0.98 to 1.97 in muscle, 2.25 to 2.84 in skin,
and 2.85 to 3.30 in lipid. Mallard ducklings exposed for longer periods had log BCFs up to 9.30. BSAFs
were calculated for red-winged blackbirds and tree swallow eggs during a study in the Great Lakes area,
with values ranging from 7.5 to 448, as reported in the attached summary table. The BSAF for tree
swallow nestings was 341.
Food Chain Multipliers: A biomagnification factor of 16 has been reported for dieldrin for herring gulls
feeding on ale wife in Lake Ontario [5]. A study of arctic marine food chains measured biomagnification
factors for dieldrin that ranged from 2.2 to 2.4 for fish to seal, 4.9 to 5.5 for seal to bear, and 11.4 for fish
to bear [6].
Aquatic Organisms
Partitioning Factors: In older studies, the following log BCFs have been reported for dieldrin: 4.51 in
freshwater alga [7]; from 3.38 to 4.83 in fish [8]; and log 3.20 in a saltwater mussel [9]. A log BCF of
5.36 was found for rainbow trout [34]. BSAFs ranging from 1.120 to 7.134 were reported to bivalves
[33].
381
-------
BIOACCUMULATION SUMMARY DIELDRIN
Food Chain Multipliers: Food chain multipliers (FCMs) for trophic level 3 aquatic organisms were 8.6
(all benthic food web), 1.2 (all pelagic food web), and 5.5 (benthic and pelagic food web). FCMs for
trophic level 4 aquatic organisms were 10.8 (all benthic food web), 1.9 (all pelagic food web), and 5.8
(benthic and pelagic food web) [36].
Toxicity/Bioaccumulation Assessment Profile
Dieldrin is the name of an insecticide that was used in the United States for locust and mosquito control
until production and importation were banned. In addition to man-made production, dieldrin is derived
from the oxidation of aldrin, which is also an insecticide. Aldrin is readily converted to dieldrin under
normal environmental conditions [10]. In addition, aldrin is readily metabolized to dieldrin, so the effects
seen in animals exposed to aldrin may be caused by dieldrin [11]. Dieldrin is one of the most persistent
of the chlorinated hydrocarbons, and is highly resistant to biodegradation and abiotic degradation. In
water, volatilization of dieldrin to the atmosphere is probably an important process, but transformation
processes in soils and sediment are slow. Dieldrin sorbs tightly to soil and sediment, particularly if
substantial amounts of organic carbon are present.
Dieldrin is toxic to aquatic organisms, birds, and mammals and is capable of producing carcinogenic,
teratogenic, and reproductive effects [10]. Teratogenic effects include cleft palate, webbed foot, and
skeletal anomalies. Reproductive effects include decreased fertility, increased fetal death, and effects on
gestation [10].
In aquatic organisms, the acute toxicity of dieldrin ranges from 0.5 to 740 ug/L for freshwater and 0.7
to > 100 ug/L for saltwater organisms [12]. Differences between dieldrin concentrations causing acute
lethality and chronic toxicity in species acutely sensitive to this insecticide are small; acute-chronic ratios
ranged from 2.4 to 12.8 for three species [12]. Dieldrin is generally an order of magnitude more toxic
to fish than is aldrin [11]. LCSOs for freshwater and saltwater aquatic invertebrates exposed to sediment
spiked with dieldrin in the laboratory have been shown to range from 0.0041 to 386 ug/g dw [12].
Bioconcentration factors for dieldrin in various aquatic organisms range from 400 to 68,000 [8],
indicating that dieldrin will show moderate to significant bioaccumulation in various aquatic species.
Mammals appear to be more sensitive to dieldrin poisoning than birds. Brain concentrations associated
with lethality in mammals are 5 mg/kg and in birds are 10 mg/kg [11]. Concentrations as low as 1 mg/kg
in the brain might trigger irreversible starvation in sensitive individuals of birds [13]. Major effects on
reproduction in wildlife are not expected to occur at dieldrin concentrations of less than one half those
causing mortality [11]. Dieldrin is commonly found in the brain, tissues, and eggs of fish-eating birds
that also have residues of organochlorines such as DDE and PCBs. Based on a number of literature
studies, the State of New York proposed a dietary fish flesh criterion of 0.12 mg/kg to protect piscivorous
wildlife [14]. There are limited studies relating aldrin concentrations to toxicity because of the rapid
conversion of aldrin into dieldrin.
382
-------
Summary of Biological Effects Tissue Concentrations for Dieldrin
Species:
Taxa
Invertebrates
Crassostrea
virginica,
Eastern oyster
Crassostrea
virginica,
Eastern oyster
Crassostrea
virginica,
Eastern oyster
Concentration, Units in1:
Sediment Water Tissue (Sample Type)
107 mg/kg
(whole body)4
1 1 mg/kg
(whole body)4
1.03 mg/kg
(whole body)4
1 .44 mg/kg
(whole body)4
18.6 mg/kg
(whole body)4
1 .44 mg/kg
(whole body)4
18.6 mg/kg
(whole body)4
13.9 mg/kg
(whole body)4
Toxicity: Ability to Accumulate2:
Log Log
Effects BCF BAF BSAF
Cellular, NOED
Cellular, NOED
Cellular, NOED
Behavior, LOED
Behavior, NA
Mortality,
NOED
Mortality,
NOED
Growth, NOED
Source:
Reference
[23]
[23]
[23]
[29]
[29]
[29]
[29]
[31]
Comments3
L; no histological
effects on structure of
gill, gut or mantle
L; erratic shell
movements, extended
shell closure indicated
irritation
L; no effect on
mortality within 168
hours
L; estimated NOED -
no statistical summary
in text
-------
00
-f^
Summary of Biological Effects Tissue Concentrations for Dieldrin
Species:
Taxa
Macomona liliana,
Mollusk
Austrovenus
stutchburyi, Mollusk
Mercenaria
mercenaria,
Quahog clam
Concentration, Units in1:
Sediment Water
73.3 ng/kg
OC
52.1 ng/kg
OC
72.7 ng/kg
OC
60.0 ng/kg
OC
20.8 |ig/kg
OC
73.3 ng/kg
OC
52.1 |ig/kg
OC
72.7 ng/kg
OC
60.0 |ig/kg
OC
20.8 |ig/kg
OC
Toxicity:
Tissue (Sample Type) Effects
201.7|ig/kglipid
371.7 |ig/kg lipid
172.0 |ig/kg lipid
76.0 |ig/kg lipid
80.2 |ig/kg lipid
102.7 ng/kg lipid
127.6 |ig/kg lipid
105.2 |ig/kg lipid
67.2 |ig/kg lipid
58.6 |ig/kg lipid
0.38 mg/kg Behavior,
(whole body)4 NOED
Ability to Accumulate2:
Log Log
BCF BAF BSAF
2.752
7.134
2.366
1.267
3.856
1.401
2.449
1.447
1.120
2.817
Source:
Reference
[33]
[33]
[33]
[33]
[33]
[33]
[33]
[33]
[33]
[33]
[22]
Comments3
F, %lipid = 2.95;
%sedOC= 0.30
F, %lipid = 2.33;
%sed OC = 0.73
F, %lipid = 2.57;
%sed OC = 0.22
F, %lipid = 2.04;
%sed OC = 0.25
F, %lipid=3.13;
%sed OC = 0.48
F, %lipid = 5.62;
%sed OC = 0.30
F, %lipid = 5.21;
%sed OC = 0.73
F, %lipid = 4.85;
%sed OC = 0.22
F, %lipid = 3.87;
%sed OC = 0.25
F, %lipid = 4.27;
%sed OC = 0.48
L; no effect on feeding
activity
-------
Summary of Biological Effects Tissue Concentrations for Dieldrin
Species: Concentration, Units in1:
Taxa Sediment Water
My a arenaria,
Soft shell clam
Chlamydotheca
arcuata, Ostracod
Palaemonetes pugio,
Grass shrimp
Penaeiis duorarum,
Pink shrimp
Chironomus riparius,
Midge
Tissue (Sample Type)
0.87 mg/kg
(whole body)4
1 mg/kg
(whole body)4
2.1 mg/kg
(whole body)4
0.09 mg/kg
(whole body)4
0.23 mg/kg
(whole body)4
0.08 mg/kg
(whole body)4
0.01 mg/kg
(whole body)4
1.9 mg/kg
(whole body)4
Toxicity: Ability to Accumulate2:
Log Log
Effects BCF BAF BSAF
Behavior,
NOED
Mortality,
LOED
Mortality,
LOED
Mortality,
NOED
Mortality, ED50
Mortality,
LOED
Mortality,
NOED
Mortality, ED 10
Source:
Reference
[22]
[28]
[31]
[31]
[31]
[31]
[31]
[24]
Comments3
L; no effect on feeding
activity
L; immobility,
mortality,
resd_conc_wet value
L; estimated loed - no
statistical summary in
text
L; estimated noed - no
statistical summary in
text
L; ED50 via Spearman
Karber 1.5 (msl)
L; estimated LOED -
no statistical summary
in text
L; estimated NOED -
no statistical summary
in text
L; all larvae moribund
in 2 hours
-------
00
ON
Summary of Biological Effects Tissue Concentrations for Dieldrin
Species:
Taxa
Fishes
Squalus acanthias,
Spiny dogfish
Oncorhynchus
mykiss,
Rainbow trout
Concentration, Units in1:
Sediment Water Tissue (Sample Type)
1.1 mg/kg
(whole body)4
1.1 mg/kg
(whole body)4
1.1 mg/kg
(whole body)4
1.1 mg/kg
(whole body)4
1 mg/kg
(whole body)4
0.14 mg/kg (fat)4
0.14 mg/kg (fat)4
0.05 mg/kg (fat)4
0.14 mg/kg (fat)4
Toxicity: Ability to Accumulate2:
Log Log
Effects BCF BAF BSAF
Behavior, ED50
Mortality, ED50
Behavior, ED50
Mortality, ED50
Mortality,
NOED
Physiological,
ED30
Physiological,
ED30
Physiological,
ED35
Growth, ED40
Source:
Reference
[24]
[24]
[24]
[24]
[27]
[32]
[32]
[32]
[32]
Comments3
L; 50 - 75% mortality,
lethargy within 2
hours
L; 50 - 75% mortality,
lethargy within 2
hours
L; no effect on
mortality in 24 hours
L; 30% decrease in
hemoglobin content
relative to control
L; 30% increase in
liver size relative to
control
L; 35% increase in
kidney size relative to
control
L; 40% decrease in
growth relative to
control
-------
Summary of Biological Effects Tissue Concentrations for Dieldrin
Species: Concentration, Units in1:
Taxa Sediment Water
Oncorhynchiis
mykiss, Rainbow
trout (juveniles)
Salmonids
Carassiiis auratus,
Goldfish
Leuciscus idus,
Golden ide
Cyprinodon
variegatus,
Sheepshead minnow
Gambiisia affinis,
Mosquito fish
Tissue (Sample Type)
3.8 mg/kg
(whole body)4
151 mg/kg
(whole body)4
52.9 mg/kg
(whole body)4
34 mg/kg
(whole body)4
12.8 mg/kg
(whole body)4
28 mg/kg
(whole body)4
Toxicity: Ability to Accumulate2:
Log Log
Effects BCF BAF BSAF
5.36
6.65
Behavior, LOED
Mortality,
NOED
Mortality,
ED50
Mortality,
LOED
Mortality,
NOED
Mortality,
NOED
Source:
Reference
[34]
[35]
[26]
[25]
[31]
[31]
[31]
[30]
Comments3
L
F
L; hyperexcit-ability
L; no effect on
survivorship in 3 days
L; ED50 via Spearman
Karber 1 .5 (msl)
L; estimated NOED -
no statistical summary
in text
L; no effect on
survivorship after 3
days
oo
-J
-------
00
oo
Summary of Biological Effects Tissue Concentrations for Dieldrin
Species: Concentration, Units in1:
Taxa Sediment Water
Poecilia reticulata,
Guppy
Lepomis
macrochirus,
Bluegill
Wildlife
Xenopus laevis,
African clawed frog
(tadpole stage)
water
exposure
2.3±0.2 |ig/L
water
exposure
1.1±0.1 |ig/L
(water expo-
sure) |ig/L
2.0±0.0
4.2±0.1
9.3±0.2
20.5±0.4
jj.g/L (water
exposure):
0.9±0.1
1.8±0.2
3.8±0.3
9.7±0.4
Toxicity: Ability to Accumulate2: Source:
Log Log
Tissue (Sample Type) Effects BCF BAF BSAF Reference Comments3
10.7 mg/kg Growth, NA
(whole body)4
3.7 mg/kg Behavior, LOED
(whole body)4
0.7 mg/kg5 2.48
(whole body)
1.8±1.2 mg/kg5 3.21±3.04
(whole body)
mg/kg5
(whole body):
0.8 2.60
20.0±0 2.68±0
3.0±0.6 2.51±0.07
7.0 2.53
mg/kg5
(whole body)
0.4±0 2.67±0
0.8±0.2 NOAEL 2.62±1.92
1.5±0.5 LOAEL 2.59±2.11
3.0±1.0 2.49±2.01
[21] L; decreased biomass
of guppy population in
laboratory ecosystem
[26] L; behavioral changes,
loss of equilibrium,
convulsions
[15] L; 28-day exposure;
insufficient tissue for
replicates; values are
mean ± SE
[15] L; 28-day exposure
[15] L; 28-day exposure;
insufficient tissue for
replicates for all
exposures; values are
mean ± SE
[15] L; 24-day exposure;
values are mean ± SE;
effects based on
mortality
-------
Summary of Biological Effects Tissue Concentrations for Dieldrin
Species: Concentration, Units in1:
Taxa Sediment
Xenopus laevis,
African clawed frog
(tadpole stage)
Xenopus laevis,
African clawed frog
(juvenile stage)
Water
water
exposure
5.5 |ig/L
water
exposure
2.1±0.2|ig/L
Toxicity:
Tissue (Sample Type) Effects
1.8mg/kg5 LC50
(whole body)
4.5±0.3 mg/kg5
(whole body)
Ability to Accumulate2: Source:
Log Log
BCF BAF BSAF Reference Comments3
[15] L; 24-day exposure;
LC50 tissue dieldrin
estimated by graphical
extrapolation
[15] L; 28-day exposure;
3.33±2.38 values are mean ± SE
Rana pipiens,
Leopard frog
(tadpole stage)
water
exposure 0.6±0.2 mg/kg5
0.8±0.1 |ig/L (whole body)
water
exposure 0.8±0.1 mg/kg5
2.1±0.1 |ig/L (whole body)
water expo- whole body5
sure (|ig/L) (mg/kg)
0.8±0.1 0.4±0.1
1.9±0.2 0.4±0
4.1±0.3 0.6±0.1
10.0±0.3 2.0±0.1
NOAEL
LOAEL
>.84±2.28
>.59±1.60
2.64±1.18
2.32±0
2.20±1.08
2.30±0
[15] L; 28-day exposure;
values are mean ± SE
[15] L; 28-day exposure;
values are mean ± SE
[15] L; 28-day exposure;
values are mean ± SE;
effects based on
mortality
Rana pipiens,
Leopard frog
(tadpole stage)
water 1.7 mg/kg5
exposure 8.3 (whole body)
LC50
[15] L; 24-day exposure;
LC50 tissue dieldrin
estimated by graphical
extrapolation
-------
Summary of Biological Effects Tissue Concentrations for Dieldrin
Species: Concentration, Units in1:
Taxa Sediment Water
Rana pipiens,
Leopard frog
(adult stage)
Anas platyrhynchos,
Mallard
(ducklings)
water
exposure
10.7±1.3
Hg/L
water
exposure
56.2±4.1
|ig/L
water
exposure
53.4 |ig/L
0.014±1
mg/L
0.052±4
mg/L
Tissue (Sample Type)
0.4±0.4 mg/kg5 (skin)
0.9±0.1 mg/kg5
(muscle)
1.5±0.5 mg/kg5 (liver)
7.3±2.8 mg/kg5 (skin)
17.8±7.8 mg/kg5
(muscle)
21.5±3.3 mg/kg5
(liver)
5.5 mg/kg5 (skin)
10.0 mg/kg5 (muscle)
13.0 mg/kg5 (liver)
24.5 mg/kg (lipid)
2.3 mg/kg (liver)
1.3 mg/kg (muscle)
68.9 mg/kg (lipid)
3.4 mg/kg (liver)
1.15 mg/kg (muscle)
Toxicity: Ability to Accumulate2: Source:
Log Log
Effects BCF BAF BSAF Reference Comments3
1.57±1.57
1.92±0.95
2.15±1.67
2.11±1.69
2.51±2.15
2.58±1.64
LC50
LC50
LC50
No mortality 3.24
or effects on
behavior or
survival
observed
No mortality 3.12
or effects on
behavior or
survival
observed
[15] L; 28-day exposure;
values are mean ± SE
[15] L; 28-day exposure;
values are mean ± SE
[15] L; 28-day exposure;
LC50 tissue dieldrin
estimated by graphical
extrapolation
[18] L; 34-day exposure;
1 -day-old birds had
access to dieldrin-
contaminated water
for drinking and
swimming
-------
Summary of Biological Effects Tissue Concentrations for Dieldrin
Species:
Taxa
Anas platyrhynchos,
Mallard
(ducklings)
Concentration, Units in1:
Sediment Water
0.118±11
mg/L
0.019±2
mg/L
0.075±1
mg/L
0.193±8
mg/L
0.177±11
mg/L
Tissue (Sample Type)
128 mg/kg (lipid)
7.4 mg/kg (liver)
1 . 1 mg/kg (muscle)
37.9 mg/kg (lipid)
13 mg/kg (skin)
1.9 mg/kg (liver)
107 mg/kg (lipid)
39.5 mg/kg (skin)
4.8 mg/kg (liver)
2 17 mg/kg (lipid)
75 mg/kg (skin)
11.3 mg/kg (liver)
125 mg/kg (lipid)
31.5 mg/kg (skin)
Toxicity: Ability to Accumulate2: Source:
Log Log
Effects BCF BAF BSAF Reference Comments3
No mortality 3.04
or effects on
behavior or
survival
observed
No mortality 3.30 [18] L; 24-day exposure;
or effects on 1-day old birds had
behavior or access to dieldrin-
survival contaminated water
observed for drinking and
XT t i-t o ir swimming
No mortality 3.15 &
or effects on
behavior or
survival
observed
No mortality 3.05
or effects on
behavior or
survival
observed
2.84 [18] L; 8-day exposure;
2.25 14-day old birds had
8.6 mg/kg (liver)
2.3 mg/kg (brain)
0.97 mg/kg muscle)
0.97 mg/kg (blood)
1.69
1.11
0.74
0.51
access to dieldrin-
contaminated water
for drinking and
swimming
-------
Summary of Biological Effects Tissue Concentrations for Dieldrin
Species:
Taxa
Falco peregrinus,
Peregrine falcon
Concentration, Units in1:
Sediment Water Tissue (Sample Type)
915 mg/kg (lipid)
305 mg/kg (skin)
52 mg/kg (liver)
395 mg/kg (lipid)
193 mg/kg (skin)
12 mg/kg (liver)
5 mg/kg (brain)
2 mg/kg (muscle)
180 mg/kg (lipid)
102 mg/kg (skin)
7 mg/kg (liver)
2.5 mg/kg (brain)
<1 mg/kg (muscle)
4 mg/kg (lipid)
2 mg/kg (skin)
<1 mg/kg (liver)
<1 mg/kg (brain)
<1 mg/kg (muscle)
59 ng/g (eggs)
(n = 6)
Toxicity:
Effects
96-Hour LC50
24-Day LC50
24-Day LOAEL
24-Day NOAEL
11. 4% eggshell
thinning
Ability to Accumulate2:
Log Log
BCF BAF BSAF
0.74
0.26
-0.52
1.13
0.81
-0.40
-0.70
-1.00
1.05
0.81
-0.40
-0.70
1.12
0.83
Source:
Reference Comments3
[18] L; 24-day exposure;
birds were dosed with
food spiked with
dieldrin at measured
concentrations of 0.3
to 165 mg/kg.
[19] F; Kola Peninsula,
Russia; n = number
of
(eggs)
clutches sampled
Falco tinnunculus,
European kestrel
6-30 mg/kg (liver)
mortality
[16]
-------
Summary of Biological Effects Tissue Concentrations for Dieldrin
Species:
Taxa
Agelaius phoeniceus,
Red-winged
blackbird
(eggs)
Tachycineta bicolor,
Tree swallow
(nestlings)
(eggs)
Concentration, Units in1:
Sediment Water
1.2 ng/g
TOC=21.0%
11.0 ng/g
TOC=7.5%
127.8 ng/g
TOC=12%
0.6 ng/g
TOC=18.5%
0.7 ng/g
TOC=11.5%
0.1 ng/g
TOC=10.5%
0.7 ng/g
TOC=11.5%
0.7 ng/g
TOC=11.5%
Toxicity:
Tissue (Sample Type) Effects
16. 6 ng/g
3 1.0 ng/g
84.6 ng/g
8.9 ng/g
9.1 ng/g
20.0 ng/g
(whole body minus
feet, beak, wings,
and feathers)
2 11. 4 ng/g
19.3 ng/g
Ability to Accumulate2: Source:
Log Log
BCF BAF BSAF Reference Comments3
7.5 [20] F; Great Lakes/St.
Lawrence River basin;
12 wetlands sites;
21 sediment
concentration reported
as wet weight
7.8 concentration which
may be a
typographical error.
57.2 203.7
117.6 ng/g ww
31.1
448
[20] F; Great Lakes/
St. Lawrence River
basin; 12 wetlands
sites; sediment
340.5 concentration reported
as wet weight
concentration
36.9 which may be a
typographical error.
-------
Summary of Biological Effects Tissue Concentrations for Dieldrin
Species:
Taxa
Tyto alba,
Barn owl
Concentration, Units in1:
Sediment Water Tissue (Sample Type)
6-44 mg/kg
(liver)
Toxicity:
Effects
mortality
Ability
Log
BCF
to Accumulate2: Source:
Log
BAF
BSAF Reference Comments3
[17] F
Concentration units based on wet weight unless otherwise noted.
2 BCF = bioconcentration factor, BAF = bioaccumulation factor, BSAF = biota-sediment accumulation factor.
3 L = laboratory study, spiked sediment, single chemical; F = field study, multiple chemical exposure; other unusual study conditions or observations noted.
4 This entry was excerpted directly from the Environmental Residue-Effects Database (ERED, www.wes.army.mil/el/ered, U.S. Army Corps of Engineers and U.S.
Environmental Protection Agency). The original publication was not reviewed, and the reader is strongly urged to consult the publication to confirm the information
presented here.
5 Not clear from reference if concentration is based on wet or dry weight.
-------
BIOACCUMULATION SUMMARY DIELDRIN
References
1. USEPA, Hazard Profile, Dieldrin, 1980, p. 1. (Cited in: USEPA. 1996. Hazardous Substances
Data Bank (HSDB). National Library of Medicine online (TOXNET). U.S. Environmental
Protection Agency, Office of Health and Environmental Assessment, Environmental Criteria and
Assessment Office, Cincinnati, OH. February.)
2. USEPA. 1989. Chemical fate rate constants for SARA section 313 chemicals and Superfund
Health Evaluation Manual chemicals. Prepared by Chemical Hazard Assessment Division,
Syracuse Research Corporation, for U.S. Environmental Protection Agency, Office of Toxic
Substances, Exposure Evaluation Division, Washington, DC, and Environmental Criteria and
Assessment Office, Cincinnati, OH. August 11.
3. Karickhoff, S.W., and J.M. Long. 1995. Internal report on summary of measured, calculated
and recommended log Kow values. Draft. Prepared by U.S. Environmental Protection Agency,
Office of Research and Development, Environmental Research Laboratory-Athens, for E.
Southerland, Office of Water, Office of Science and Technology, Standards and Applied Science
Division, Washington, DC. April 10.
4. USEPA. 1995. Integrated Risk Information System (IRIS). National Library of Medicine online
(TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental
Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. September.
5. Braune, B.M., and RJ. Norstrom. 1989. Dynamics of organochlorine compounds in herring
gulls: III. Tissue distribution and bioaccumulation in Lake Ontario gulls. Environ. Toxicol.
Chem. 8:957-968.
6. Muir, D.C.G., RJ. Norstrom, and M. Simon. 1988. Organochlorine contaminants in arctic
marine food chains: Accumulation of specific polychlorinated biphenyls and chlordane-related
compounds. Environ. Sci. Technol. 22:1071-1079.
7. Neudorf, S., and M.A.Q. Khan. 1975. Pick-up and metabolism of DDT, dieldrin, and
photoaldrin by a freshwater alga (Ankistrodesmus ammalloides) and a microcrustacean (Daphnia
pulex). Bull. Environ. Contain. Toxicol. 13(4):443-450.
8. USEPA. 1980. Ambient water quality criteria for aldrin/dieldrin. EPA 440/5-80-019. U.S.
Environmental Protection Agency, Office of Water Regulations and Standards, Criteria and
Standards Division, Washington, DC.
9. Ernst, W. 1977. Determination of the bioconcentration potential of marine organisms - a steady
state approach. Chemosphere 6(11):731-740.
10. Clement Associates. 1985. Chemical, physical, and biological properties of compounds present
at hazardous waste sites. U.S. Environmental Protection Agency, Washington, DC.
395
-------
BIOACCUMULATION SUMMARY DIELDRIN
11. Peakall, D.B. 1996. Dieldrin and other cyclodiene pesticides in wildlife. In Environmental
contaminants in wildlife, ed., W.N. Beyer, G.H. Heinz, and A.W. Redmon-Norwood, pp. 73-97.
Lewis Publishers, Boca Raton, FL.
12. USEPA. 1993. Sediment quality criteria for the protection of benthic organisms: Dieldrin.
EPA 822/R93-015. U.S. Environmental Protection Agency, Office of Water and Office of
Research and Development, Washington, DC.
13. Heinz, G., and R. Johnson. 1981. Diagnostic brain residues of dieldrin: Some new insights. In
ASTM STP 757, Avian and mammalian wildlife toxicology: Second Conference, ed. D. Lamb
and G. Kenaga, pp. 72-92. American Society of Testing and Materials, Philadelphia, PA.
14. Newell, A.J., D.W. Johnson, and L.K. Allen. 1987. Niagara River biota contamination project:
Fish flesh criteria for piscivorous wildlife. Tech. Rep. 87-3. New York Department of
Environmental Conservation, Bureau of Environmental Protection.
15. Schuytema, G.S., A.V. Nebecker, W.L. Griffis, and K.N. Wilson. 1991. Teratogenesis, toxicity,
and bioconcentration in frogs exposed to dieldrin. Arch. Environ. Contain. Toxicol. 21:332-350.
16. Newton, I., I. Wyllie, and A. Asher. 1992. Mortality from the pesticides aldrin and dieldrin in
British sparrowhawks and kestrels. Ecotoxicology 1:31-44.
17. Newton, I., I. Wyllie, and A. Asher. 1991. Mortality causes in British barn owls, Tyto alba, with
a discussion of aldrin-dieldrin poisoning. Ibis 133:162-169.
18. Nebeker, A.V., W.L. Griffis, T.W. Stutzman, G.S. Schuytema, L.A. Carey, and S.M. Scherer.
1992. Effects of aqueous and dietary exposure of dieldrin on survival, growth and
bioconcentration in mallard ducklings. Environ. Toxicol. Chem. 11:687-699.
19. Henny, C.J., S.A. Ganusevich, F.P. Ward, and T.R. Schwartz. 1994. Organochlorine pesticides,
chlorinated dioxins and furans, and PCBs in peregrine falcon Falco peregrinus eggs from the
Kola Penninsula, Russia. In Raptor conservation today, ed. B.U. Meyburg and R.D. Chancellor,
pp. 739-749. WWGPB/The Pica Press.
20. Bishop, C.A., M.D. Koster, A.A. Chek, D.J.T. Hussell, and K. Jock. 1995. Chlorinated
hydrocarbons and mercury in sediments, red-winged blackbirds (Agelaius phoeniceus) and tree
swallows (Tachycineta bicolor) from wetlands in the Great Lakes-St. Lawrence river basin,
Environ. Toxicol. Chem. 14:491-501.
21. Burnett, K.M., and W.J. Liss. 1990. Multi-steady-state toxicant fate and effect in laboratory
aquatic ecosystems. Environ. Toxicol. Chem. 9:637-647.
22. Butler, P. A. 1971. Influence of pesticides on marine ecosystems. Proc. Royal Soc. London, Series
B 177:321-329.
396
-------
BIOACCUMULATION SUMMARY DIELDRIN
23. Emanuelsen, N., J.L. Lincer, and K. Rifkin. 1978. The residue uptake and histology of American
oysters (Crassostrea virginica Gmelin) exposed to dieldrin. Bull. Environ. Contam. Toxicol.
19:121-129.
24. Estenik, J.F., and WJ. Collins. 1979. In vivo and in vitro studies of mixed-function oxidase in
an aquatic insect, Chironomus riparius. In Pesticide and xenobiotic metabolism in aquatic
organisms, ed. M.A.Q. Khan, JJ. Lech, and JJ. Menn, pp. 349-370. American Chemical Society,
Washington, DC.
25. Freitag, D., L. Ballhorn, H. Geyer, and F. Korte. 1985. Environmental hazard profile of organic
chemicals: An experimental method for the assessment of the behaviour of organic chemicals
in the ecosphere by means of laboratory tests with 14C-labelled chemicals. Chemosphere 14:1589-
1616.
26. Gakstatter, J.H., and C.M. Weiss. 1967. The elimination of DDT-C14, dieldrin-C14, and lindane-
C14 from fish following a single sublethal exposure in aquaria. Trans. Amer. Fish. Soc. 96:301-
307.
27. Guarino, A.M., and S.T. Arnold. 1979. Xenobiotic transport mechanisms and pharmacokinetics
in the dogfish shark. In Pesticide and xenobiotic metabolism in aquatic organisms, ed. M.A.Q.
Khan, JJ. Lech, and JJ. Menn, pp.233-258. American Chemical Society, Washington, DC.
28. Kawatski, J.A., and J.C. Schmulbach. 1971. Accumulation of insecticide in freshwater ostracods
exposed continuously to sublethal concentrations of aldrin or dieldrin. Trans. Amer. Fish. Soc.
100:565-567.
29. Mason, J.W., and D.R. Rowe. 1976. The accumulation and loss of dieldrin and endrin in the
eastern oyster. Arch. Environ. Contam. Toxicol. 4:349-360.
30. Metcalf, R.L. 1974. A laboratory model ecosystem to evaluate compounds producing biological
magnification. In Essays in toxicology, ed. WJ. Hayes, Vol. 5, pp. 17-38. Academic Press. New
York, NY.
31. Parrish, P.P., J.A. Couch, J. Forester, J.M. Patrick, and G.H. Cook. NS. Dieldrin: Effects on
several estuarine organisms. Contribution No. 178, Gulf Breeze Environmental Research
Laboratory, Sabine Island, Gulf Breeze, FL.
32. Poels, C.L.M., M.A. van Der Gaag, and J.F.J. van de Kerkhoff. 1980. An investigation into the
long-term effect of Rhine water on rainbow trout. Water Research (14): 1029-1033.
33. Mickey, C.W., D.S. Roper, P.T. Holland, and T.M. Trower. 1995. Accumulation of organic
contaminants in two sediment-dwelling shellfish with contrasting feeding modes: Deposit-
(Macomona liliana) and filter-feeding (Austovenus stutchburi). Arch. Environ. Contam. Toxicol.
11:221-231.
34. Shubat and Curtis. 1986. Environ. Toxicol. Chem. 5:69-77.
397
-------
BIOACCUMULATION SUMMARY DIELDRIN
35. USEPA. 1995. Great Lakes Water Quality Initiative technical support document for the
procedure to determine bioaccumulation factors. EPA-820-B-95-005. U.S. Environmental
Protection Agency, Office of Water, Washington, DC.
398
-------
BIOACCUMULATION SUMMARY DISULFOTON
Chemical Category: PESTICIDE (ORGANOPHOSPHATE)
Chemical Name (Common Synonyms): DISULFOTON CASRN: 298-04-4
Chemical Characteristics
Solubility in Water: 25 ppm at 23 °C [1] Half-Life: 3 days - 21 days based on aerobic
soil field data [2]
Log Kow: 3.98 [3] Log Koc: 3.91 L/kg organic carbon
Human Health
Oral RfD: 4 X 10"5 mg/kg/day [4] Confidence: Medium, uncertainty factor
= 1000 [4]
Critical Effect: Cholinesterase inhibition and optic nerve degeneration in dogs
Oral Slope Factor: No data [4] Carcinogenic Classification: D [6]
Wildlife
Partitioning Factors: Partitioning factors for disulfoton in wildlife were not found in the literature.
Food Chain Multipliers: Food chain multipliers for disulfoton in wildlife were not found in the
literature.
Aquatic Organisms
Partitioning Factors: Partitioning factors for disulfoton in aquatic organisms were not found in the
literature.
Food Chain Multipliers: Food chain multipliers for disulfoton in aquatic organisms were not found in
the literature.
Toxicity/Bioaccumulation Assessment Profile
The toxicity of insecticidally active organophosphorus compounds like disulfoton to animals is attributed
to their ability to inhibit acetylcholinesterase, which is a class of enzymes that catalyzes the hydrolysis
of the neurotransmitting agent acetylcholine [7].
399
-------
BIOACCUMULATION SUMMARY DISULFOTON
Disulfoton is relatively toxic to aquatic organisms. The acute toxicity for aquatic invertebrates ranged
from 5 |ig/L (96-h LC50) for Pteronarcys californica [8] to 52 |ig/L (96-h LC50) for Gammarus lacustris
[9], while chronic toxicity ranged from 1.4 |ig/L (30-d LC50) for Acroneuria pacifica to 1.9 |ig/L (30-d
LC50) for Pteronarcys californica [10]. Fish are less sensitive to disulfoton. The 96-h LC50 based on the
exposure with fathead minnows was 3700 |ig/L [11]. The toxicity of disulfoton and its most important
degradation products were measured using Daphnia magna [12]. The toxicity of disulfoton (24-h LC50
of 55 |ig/L) was similar to two of its degradation products (disulfoton-sulfoxide and disulfoton). The
remaining degradation products were much less toxic than the parent compound.
400
-------
Summary of Biological Effects Tissue Concentrations for Disulfoton
Species:
Taxa
Concentration, Units in: Toxicity:
Sediment Pore Water Tissue (Sample Type) Effects
Ability to Accumulate:
BCF BAF BSAF
Source:
Reference Comments
Invertebrates
[NO DATA FOUND]
Fishes
[NO DATA FOUND]
Wildlife
[NO DATA FOUND]
-------
BIOACCUMULATION SUMMARY DISULFOTON
References
1. NRC. Drinking Water and Health. 1977. p. 615. (Cited in: USEPA. 1995. Hazardous
Substances Data Bank (HSDB). National Library of Medicine online (TOXNET). U.S.
Environmental Protection Agency, Office of Health and Environmental Assessment,
Environmental Criteria and Assessment Office, Cincinnati, OH. September.)
2. USEPA. 1989. Chemical fate rate constants for SARA section 313 chemicals and Superfund
Health Manual chemicals. Prepared by Chemical Hazard Assessment Division, Syracuse
Research Corporation, for U.S. Environmental Protection Agency, Office of Toxic Substances,
Exposure Evaluation Division, Washington, DC, and Environmental Criteria and Assessment
Office, Cincinnati, OH. August 11.
3. Karickhoff, S.W., and J.M. Long. 1995. Internal report on summary of measured, calculated,
and recommended log Kow values. Draft. Prepared by U.S. Environmental Protection Agency,
Office of Research and Development, Environmental Research Laboratory-Athens, for E.
Southerland, Office of Water, Office of Science and Technology, Standards and Applied Science
Division, Washington, DC. April 10.
4. USEPA. 1992. Reference dose tracking report. U.S. Environmental Protection Agency, Office
of Pesticide Programs, Health Effects Division, Washington, DC.
5. USEPA. 1997. Integrated Risk Information System (IRIS). National Library of Medicine online
(TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental
Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. January.
6. USEPA. 1992. Classification list of chemicals evaluated for carcinogenicity potential. U.S.
Environmental Protection Agency, Office of Pesticide Programs, Washington, DC.
7. Fukuto, T.R. 1990. Mechanism of action of organophosphorus and carbamate insecticides.
Environ. Health Perspect. 87:245-254.
8. Sanders, H.O., and O.B. Cope. 1968. The relative toxicities of several pesticides to naiads of
three species of stoneflies. Limnol. Oceanogr. 13:112-117.
9. Sanders, H.O. 1969. Toxicity of pesticides to the crustacean, Gammarus lacustris. Bureau of
Sport Fisheries and Wildlife Technical Paper 25. U.S. Government Printing Office, Washington,
DC.
10. Jensen, L.D., and A.R. Gaufin. 1964. Long-term effects of organic insecticides on two species
of stonefly naiads. Tran. Amer. Fish. Soc. 93:357-363.
11. Pickering, Q.H., C. Henderson, and A.E. Lemke. 1962. The toxicity of organic phosphorus
insecticides to different species of warmwater fishes. Trans. Amer. Fish. Soc. 91:175-184.
402
-------
BIOACCUMULATION SUMMARY DISULFOTON
12. Galli, R., H.W. Rich, and R. Scholtz. 1994. Toxicity of organophosphate insecticides and their
metabolites to the water flea Daphnia magna, the Microtox test and an acetylcholinesterase
inhibition test. Aquat Toxicol 30:259-269.
403
-------
BIOACCUMULATION SUMMARY DISULFOTON
404
-------
BIOACCUMULATION SUMMARY
1,2,3,4,7,8-HexaCDF
Chemical Category: POLYCHLORINATED DIBENZOFURANS
Chemical Name (Common Synonyms):
1,2,3,4,7,8-HEXACHLORODIBENZOFURAN
CASRN: 70648-26-9
Chemical Characteristics
Solubility in Water: No data [1]
LogKow: No data [3]
Half-Life: No data [2]
LogKoc: —
Human Health
Oral RfD: No data [4]
Critical Effect: —
Oral Slope Factor: No data [4]
Confidence:
Carcinogenic Classification:
Wildlife
Partitioning Factors: Partitioning factors for 1,2,3,4,7,8-hexaCDF in wildlife were not found in the
studies reviewed.
Food Chain Multipliers: Limited information was found reporting on specific biomagnification factors
of PCDDs and PCDFs through terrestrial wildlife. Due to the toxicity, high K,,w values, and highly
persistent nature of the PCDDs and PCDFs, they possess a high potential to bioaccumulate and
biomagnify through the food web. PCDDs and PCDFs have been identified in fish and wildlife
throughout the global aquatic and marine environments [5]. Studies conducted in Lake Ontario indicated
that biomagnification of 2,3,7,8-tetrachlorodibenzo-p-dioxin (2,3,7,8-TCDD) appears to be significant
between fish and fish-eating birds but not between fish and their food. When calculated for older
predaceous fish such as lake-trout-eating young smelt, the biomagnification factor (BMP) can equal 3.
The BMF from alewife to herring guUs in Lake Ontario was 32 for 2,3,7,8-TCDD [6]. Log BMFs of 1.70
to 1.81 were reported for mink from 1,2,3,4,7,8-hexaCDF-contaminated diet exposures.
EPA has developed risk-based concentrations of 2,3,7,8-TCDD in different media that present low and
high risk to fish, mammalian, and avian wildlife. These concentrations were developed based on toxic
effects of 2,3,7,8-TCDD and its propensity to bioaccumulate in fish, mammals, and birds.
405
-------
BIOACCUMULATION SUMMARY
1,2,3,4,7,8-HexaCDF
Environmental Concentrations Associated With 2,3,7,8-TCDD Risk to Aquatic Life and Associated
Wildlife [7]
Organism
Fish Concentration
(Pg/g)
Sediment
Concentration
(pg/g dry wt.)
Water Concentration (pg/L)
POC=0.2
POC=1.0
Low Risk
Fish
Mammalian Wildlife
Avian Wildlife
50
0.7
6
60
2.5
21
0.6
0.008
0.07
3.1
0.04
0.35
High Risk to Sensitive Species
Fish
Mammalian Wildlife
Avian Wildlife
80
7
60
100
25
210
1
0.08
0.7
5
0.4
3.5
Note: POC - Paniculate organic carbon
Fish lipid of 8% and sediment organic carbon of 3% assumed where needed.
For risk to fish, BSAF of 0.3 used; for risk to wildlife, BSAF of 0.1 used.
Low risk concentrations are derived from no-effects thresholds for reproductive effects (mortality in embryos and
young) in sensitive species.
High risk concentrations are derived from TCDD doses expected to cause 50 to 100% mortality in embryos and
young of sensitive species.
Aquatic Organisms
Partitioning Factors: Partitioning factors for 1,2,3,4,7,8-hexaCDF in aquatic organisms were not found
in the studies reviewed.
Food Chain Multipliers: No specific food chain multipliers were identified for 1,2,3,7,8-hexaCDF.
Food chain multiplier information was only available for 2,3,7,8-TCDD. Biomagnification of 2,3,7,8-
TCDD does not appear to be significant between fish and their prey. Limited data for the base of the
Lake Ontario lake trout food chain indicated little or no biomagnification between zooplankton and forage
fish. BMFs based on fish consuming invertebrate species are probably close to 1.0 because of the 2,3,7,8-
TCDD biotansformation by forage fish. BMFs greater than 1.0 might exist between some zooplankton
species and their prey due to the lack of 2,3,7,8-TCDD biotransformation in invertebrates [7]. Log BMFs
of 1.70 to 1.81 were determined for mink [13].
Toxicity/Bioaccumulation Assessment Profile
The polychlorinated dibenzo-p-dioxins (PCDDs) and polychlorinated dibenzofurans (PCDFs) each
consist of 75 isomers that differ in the number and position of attached chlorine atoms. The PCDDs and
PCDFs are polyhalogenated aromatic compounds and exhibit several properties common to this group
of compounds. These compounds tend to be highly lipophilic and the degree of lipophilicity is increased
with increasing ring chlorination [5]. In general, the PCDDs and PCDFs exhibit relative inertness to
acids, bases, oxidation, reduction, and heat, increasing in environmental persistence and chemical stability
406
-------
BIOACCUMULATION SUMMARY
1,2,3,4,7,8-HexaCDF
with increasing chlorination [8,5]. Because of their lipophilic nature, the PCDDs and PCDFs have been
detected in fish, wildlife, and human adipose tissue, milk, and serum [5].
Each isomer has its own unique chemical and lexicological properties. The most toxic of the PCDD and
PCDF isomers is 2,3,7,8-TCDD, one of the 22 possible congeners of tetrachlorodibenzo-j?-dioxin [9].
Toxicity equivalency factors (TEFs) have been developed by EPA relating the toxicities of other PCDD
and PCDF isomers to that of 2,3,7,8-TCDD [9]. The biochemical mechanisms leading to the toxic
response resulting from exposure to PCDDs and PCDFs are not known in detail, but experimental data
suggest that an important role in the development of systemic toxicity resulting from exposure to these
chemicals is played by an intracellular protein, the Ah receptor. This receptor binds halogenated
polycyclic aromatic molecules, including PCDDs and PCDFs. In several mouse strains, the expression
of toxicity of 2,3,7,8-TCDD-related compounds, including cleft palate formation, liver damage, effects
on body weight gain, thymic involution, and chloracnegenic response, has been correlated with their
binding affinity for the Ah receptor, and with their ability to induce several enzyme systems [9].
Toxicity Equivalency Factors (TEF) for PCDD and PCDF Isomers [9]
Isomer
Total TetraCDD
2,3,7,8-TCDD
Other TCDDs
Total PentaCDDs
2,3,7,8-PentaCDDs
Other PentaCDDs
Total HexaCDDs
2,3,7,8-HexaCDDs
Other HexaCDDs
Total HeptaCDDs
2,3,7,8-HeptaCDDs
Other HeptaCDDs
Total TetraCDFs
2,3,7,8-TetraCDF
Other TetraCDFs
Total PentaCDFs
2,3,7,8-PentaCDFs
Other PentaCDFs
Total HexaCDFs
2,3,7,8-HexaCDFs
Other HexaCDFs
Total HeptaCDFs
2,3,7,8-HeptaCDFs
Other HeptaCDFs
TEF
1
1
0.01
0.5
0.5
0.005
0.04
0.04
0.0004
0.001
0.001
0.00001
0.1
0.1
0.001
0.1
0.1
0.001
0.01
0.01
0.0001
0.001
0.001
0.00001
407
-------
BIOACCUMULATION SUMMARY 1,2,3,4,7,8-HexaCDF
In natural systems, PCDDs and PCDFs are typically associated with sediments, biota, and the organic
carbon fraction of ambient waters [7]. Congener-specific analyses have shown that the 2,3,7,8-substituted
PCDDs and PCDFs were the major compounds present in most sample extracts [5]. Results from limited
epidemiology studies are consistent with laboratory-derived threshold levels to 2,3,7,8-TCDD impairment
of reproduction in avian wildlife. Population declines in herring gulls (Larus argentatus) on Lake
Ontario during the early 1970s coincided with egg concentrations of 2,3,7,8-TCDD and related chemicals
expected to cause reproductive failure based on laboratory experiments (2,3,7,8-TCDD concentrations
in excess of 1,000 pg/g). Improvements in herring gull reproduction through the mid-1980s were
correlated with declining 2,3,7,8-TCDD concentrations in eggs and lake sediments [7]. Based on limited
information on isomer-specific analysis from animals at different trophic levels, it appears that at higher
trophic levels, i.e., fish-eating birds and fish, there is a selection of the planar congeners with the 2,3,7,8-
substituted positions [10].
PCDDs and PCDFs are accumulated by aquatic organisms through exposure routes that are determined
by the habitat and physiology of each species. With log K,,w>5, exposure through ingestion of
contaminated food becomes an important route for uptake in comparison to respiration of water [7]. The
relative contributions of water, sediment, and food to uptake of 2,3,7,8-TCDD by lake trout in Lake
Ontario was examined by exposing yearling lake trout to Lake Ontario smelt and sediment from Lake
Ontario along with water at a 2,3,7,8-TCDD concentration simulated to be at equilibrium with the
sediments. Food ingestion was found to contribute approximately 75 percent of total 2,3,7,8-TCDD [7].
There have been a number of bioconcentration studies of 2,3,7,8-TCDD using model ecosystem and
single species exposure. Although there is variation in the actual log BCF values, in general, the algae
and plants have the lowest BCF values, on the order of a few thousand. A value of 4.38 has been reported
for the snail Physa sp. Crustacea and insect larva appear to have the next highest log BCF values,
followed by several species of fish, with the highest log BCF value of 4.79 [10].
Exposure of juvenile rainbow trout to 2,3,7,8-TCDD and 2,3,7,8-TCDF in water for 28 days resulted in
adverse effects on survival, growth, and behavior at extremely low concentrations. A no-observed-effects
concentration (NOEC) for 2,3,7,8-TCDD could not be determined because the exposure to the lowest
dose of 0.038 ng/L resulted in significant mortality [11]. A number of biological effects have been
reported in fish following exposure to 2,3,7,8-TCDD including enzyme induction, immunological effects,
wasting syndrome, dermatological effects, hepatic effects, hematological effects, developmental effects,
and cardiovascular effects [10].
408
-------
Summary of Biological Effects Tissue Concentrations for 1,2,3,4,7,8-HexaCDF
Species:
Taxa
Fishes
Salmonids
Wildlife
Falco peregrinus,
Peregrine falcon
Mustela vison,
Mink
Concentration, Units in1: Toxicity:
Sediment Water Tissue (Sample Type) Effects
3.2ng/g (eggs) 11.4% eggshell
(n = 6) thinning
Diet: 1 pg/g4 33 pg/g4 (liver) LOAEL;
reduced kit body
weights
followed by
reduced survival
2 pg/g4 73 pg/g4 (liver) Reduced kit
body weights
followed by
reduced survival
3 pg/g4 130 pg/g4 (liver) Significant
decrease in
number of live
kits whelped per
female
Ability to Accumulate2:
Log Log
BCF BAF BSAF
0.0045
No BMP
reported
Log
BMF =
1.70
Log
BMF =
1.81
Source:
Reference Comments3
[14] F
[12] F; Kola Peninsula,
Russia
[13] L; BMP = lipid-
normalized
concentration in
the liver divided
by the lipid-
normalized dietary
concentration
1 Concentration units based on wet weight unless otherwise noted.
2 BCF = bioconcentration factor, BAF = bioaccumulation factor, BSAF = biota-sediment accumulation factor.
3 L = laboratory study, spiked sediment, single chemical; F = field study, multiple chemical exposure; other unusual study conditions or observations noted.
4 Not clear from reference if concentration is based on wet or dry weight.
-------
BIOACCUMULATION SUMMARY 1,2,3,4,7,8-HexaCDF
References
1. USEPA. 1996. Hazardous Substances Data Bank (HSDB). National Library of Medicine online
(TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental
Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. February.
2. USEPA. 1989. Chemical fate rate constants for SARA section 313 chemicals and Superfund
Health Evaluation Manual chemicals. Prepared by Chemical Hazard Assessment Division,
Syracuse Research Corporation, for U.S. Environmental Protection Agency, Office of Toxic
Substances, Exposure Evaluation Division, Washington, DC, and Environmental Criteria and
Assessment Office, Cincinnati, OH. August 11.
3. Karickhoff, S.W., and J.M. Long. 1995. Internal report on summary of measured, calculated
and recommended log Kow values. Draft. Prepared by U.S. Environmental Protection Agency,
Office of Research and Development, Environmental Research Laboratory-Athens, for E.
Southerland, Office of Water, Office of Science and Technology, Standards and Applied Science
Division, Washington, DC. April 10.
4. USEPA. 1996. Integrated Risk Information System (IRIS). National Library of Medicine online
(TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental
Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. September.
5. Safe, S. 1990. Polychlorinated biphenyls (PCBs), dibenzo-p-dioxins (PCDDs), dibenzofurans
(PCDFs), and related compounds: Environmental and mechanistic considerations which support
the development of toxicity equivalency factors (TEE). Crit. Rev. Toxicol. 21:51-88.
6. Braune, B.M., and RJ. Norstrom. 1989. Dynamics of organochlorine compounds in herring
gulls: HI. Tissue distribution and bioaccumulation in Lake Ontario gulls. Environ. Toxicol.
Chem. 8:957-968.
7. USEPA. 1993. Interim report on data and methods for assessment of 2,3,7,8-
tetrachlorodibenzo-^-dioxin risks to aquatic life and associated wildlife. EPA/600/R-93/055.
U.S. Environmental Protection Agency, Office of Research and Development, Washington, DC.
8. Eisler, R. 1986. Dioxin hazards to fish, wildlife, and invertebrates: a synoptic review. U.S. Fish
Wildl. Serv. Biol. Rep. 85 (1.8). 37 pp.
9. USEPA. 1989. Interim procedures for estimating risks associated with exposure to mixtures of
chlorinated dibenzo-^-dioxins and dibenzofurans (CDDs and CDFs) and 1989 update.
EPA/625/3-89/016. U.S. Environmental Protection Agency, Risk Assessment Forum,
Washington, DC.
10. Cooper, K.R. 1989. Effects of polychlorinated dibenzo-p-dioxins and polychlorinated
dibenzofurans on aquatic organisms. Rev. Aquat. Sci. 1:227-242.
11. 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.J. Coyle, and WJ. Adams. 1988. Toxicity and bioconcentration of 2,3,7,8-
410
-------
BIOACCUMULATION SUMMARY 1,2,3,4,7,8-HexaCDF
tetrachlorodibenzodioxin and 2,3,7,8-tetrachlorodibenzofuran in rainbow trout. Environ. Toxicol
Chem. 7:47-62.
12. Henny, C.J., S.A. Ganusevich, P.P. Ward, and T.R. Schwartz. 1994. Organochlorine pesticides,
chlorinated dioxins and furans, and PCBs in peregrine falcon Falco peregrinus eggs from the
Kola Penninsula, Russia. In Raptor conservation today, ed. B.U. Meyburg and R.D. Chancellor,
pp. 739-749. WWGPB/The Pica Press.
13. Tillitt, D.E., R.W. Gale, J.C. Meadows, J.L. Zajicek, P.M. Peterman, S.N. Heaton, P.O. Jones, SJ.
Bursian, TJ. Kubiak, J/P. Giesy, and RJ. Aulerich. 1996. Dietary exposure of mink to carp
from Saginaw Bay. 3. Characterization of dietary exposure to planar halogenated hydrocarbons,
dioxin equivalents, and biomagnification. Environ. Sci. Technol. 30:283-291.
14. USEPA. 1995. Great Lakes Water Quality Initiative technical support document for the
procedure to determine bioaccumulation factors. EPA-820-B-95-005. U.S. Environmental
Protection Agency, Office of Water, Washington, DC.
411
-------
412
-------
BIOACCUMULATION SUMMARY
1,2,3,7,8-PentaCDF
Chemical Category: POLYCHLORINATED DIBENZOFURANS
Chemical Name (Common Synonyms):
1,2,3,7,8-PENTACHLORODIBENZOFURAN
CASRN: 57117-41-6
Chemical Characteristics
Solubility in Water: No data [1]
Log Kow: No data [3]
Half-Life: No data [2]
LogKoc: —
Human Health
Oral RfD: No data [4]
Critical Effect: —
Oral Slope Factor: No data [4]
Confidence:
Carcinogenic Classification:
Wildlife
Partitioning Factors: Partitioning factors for 1,2,3,7,8-pentaCDF in wildlife were not found in the
studies reviewed.
Food Chain Multipliers: Limited information was found reporting on specific biomagnification factors
of PCDDs and PCDFs through terrestrial wildlife; no information was available for 1,2,3,7,8-pentaCDF,
specifically. Due to the toxicity, high K^w values, and highly persistent nature of the PCDDs and PCDFs,
they possess a high potential to bioaccumulate and biomagnify through the food web. PCDDs and PCDFs
have been identified in fish and wildlife throughout the global aquatic and marine environments [5].
Studies conducted in Lake Ontario indicated that biomagnification of 2,3,7,8-tetrachlorodibenzo-p-dioxin
(2,3,7,8-TCDD) appears to be significant between fish and fish-eating birds but not between fish and their
food. When calculated for older predaceous fish such as lake-trout-eating young smelt, the log
biomagnification factor (BMP) can equal 0.48. The log BMF from alewife to herring gulls in Lake
Ontario was 1.51 for 2,3,7,8-TCDD [6].
EPA has developed risk-based concentrations of 2,3,7,8-TCDD in different media that present low and
high risk to fish, mammalian, and avian wildlife. These concentrations were developed based on toxic
effects of 2,3,7,8-TCDD and its propensity to bioaccumulate in fish, mammals, and birds.
413
-------
BIOACCUMULATION SUMMARY
1,2,3,7,8-PentaCDF
Environmental Concentrations Associated With 2,3,7,8-TCDD Risk to Aquatic Life and associated
Wildlife [7]
Organism
Fish Concentration
(Pg/g)
Sediment
Concentration
(pg/g dry wt.)
Water Concentration (pg/L)
POC=0.2
POC=1.0
Low Risk
Fish
Mammalian Wildlife
Avian Wildlife
50
0.7
6
60
2.5
21
0.6
0.008
0.07
3.1
0.04
0.35
High Risk to Sensitive Species
Fish
Mammalian Wildlife
Avian Wildlife
80
7
60
100
25
210
1
0.08
0.7
5
0.4
3.5
Note: POC - Paniculate organic carbon
Fish lipid of 8% and sediment organic carbon of 3% assumed where needed.
For risk to fish, BSAF of 0.3 used; for risk to wildlife, BSAF of 0.1 used.
Low risk concentrations are derived from no-effects thresholds for reproductive effects (mortality in embryos and
young) in sensitive species.
High risk concentrations are derived from TCDD doses expected to cause 50 to 100% mortality in embryos and
young of sensitive species.
Aquatic Organisms
Partitioning Factors: Partitioning factors for 1,2,3,7,8-pentaCDF in aquatic organisms were not found
in the studies reviewed.
Food Chain Multipliers: No specific food chain multipliers were identified for 1,2,3,7,8-pentaCDF.
Food chain multiplier information was only available for 2,3,7,8-TCDD. Biomagnification of 2,3,7,8-
TCDD does not appear to be significant between fish and their prey. Limited data for the base of the
Lake Ontario lake trout food chain indicated little or no biomagnification between zooplankton and forage
fish. BMFs based on fish consuming invertebrate species are probably close to 1.0 because of the 2,3,7,8-
TCDD biotransformation by forage fish. BMFs greater than 1.0 might exist between some zooplankton
species and their prey due to the lack of 2,3,7,8-TCDD biotransformation in invertebrates [7].
Toxicity/Bioaccumulation Assessment Profile
The polychlorinated dibenzo-p-dioxins (PCDDs) and polychlorinated dibenzofurans (PCDFs) each
consist of 75 isomers that differ in the number and position of attached chlorine atoms. The PCDDs and
PCDFs are polyhalogenated aromatic compounds and exhibit several properties common to this group
of compounds. These compounds tend to be highly lipophilic and the degree of lipophilicity is increased
with increasing ring chlorination [5]. In general, the PCDDs and PCDFs exhibit relative inertness to
acids, bases, oxidation, reduction, and heat, increasing in environmental persistence and chemical stability
with increasing chlorination [8,5]. Because of their lipophilic nature, the PCDDs and PCDFs have been
detected in fish, wildlife, and human adipose tissue, milk, and serum [5].
414
-------
BIOACCUMULATION SUMMARY
1,2,3,7,8-PentaCDF
Each isomer has its own unique chemical and lexicological properties. The most toxic of the PCDD and
PCDF isomers is 2,3,7,8-TCDD, one of the 22 possible congeners of tetrachlorodibenzo-/?-dioxin [8].
Toxicity equivalency factors (TEFs) have been developed by the U.S. EPA relating the toxicities of other
PCDD and PCDF isomers to that of 2,3,7,8-TCDD [9]. The biochemical mechanisms leading to the toxic
response resulting from exposure to PCDDs and PCDFs are not known in detail, but experimental data
suggest that an important role in the development of systemic toxicity resulting from exposure to these
chemicals is played by an intracellular protein, the Ah receptor. This receptor binds halogenated
polycyclic aromatic molecules, including PCDDs and PCDFs. In several mouse strains, the expression
of toxicity of 2,3,7,8-TCDD-related compounds, including cleft palate formation, liver damage, effects
on body weight gain, thymic involution, and chloracnegenic response has been correlated with their
binding affinity for the Ah receptor, and with their ability to induce several enzyme systems [9].
Toxicity Equivalency Factors (TEF) for PCDD and PCDF Isomers [9]
Isomer
TEF
Total TetraCDD
2,3,7,8-TCDD
Other TCDDs
Total PentaCDDs
2,3,7,8-PentaCDDs
Other PentaCDDs
Total HexaCDDs
2,3,7,8-HexaCDDs
Other HexaCDDs
Total HeptaCDDs
2,3,7,8-HeptaCDDs
Other HeptaCDDs
Total TetraCDFs
2,3,7,8-TetraCDF
Other TetraCDFs
Total PentaCDFs
2,3,7,8-PentaCDFs
Other PentaCDFs
Total HexaCDFs
2,3,7,8-HexaCDFs
Other HexaCDFs
Total HeptaCDFs
2,3,7,8-HeptaCDFs
Other HeptaCDFs
1
1
0.01
0.5
0.5
0.005
0.04
0.04
0.0004
0.001
0.001
0.00001
0.1
0.1
0.001
0.1
0.1
0.001
0.01
0.01
0.0001
0.001
0.001
0.00001
In natural systems, PCDDs and PCDFs are typically associated with sediments, biota, and the organic
carbon fraction of ambient waters [7]. Congener-specific analyses have shown that the 2,3,7,8-substituted
PCDDs and PCDFs were the major compounds present in most sample extracts [5]. Results from limited
415
-------
BIOACCUMULATION SUMMARY 1,2,3,7,8-PentaCDF
epidemiology studies are consistent with laboratory-derived threshold levels to 2,3,7,8-TCDD impairment
of reproduction in avian wildlife. Population declines in herring gulls (Larus argentatus) on Lake
Ontario during the early 1970s coincided with egg concentrations of 2,3,7,8-TCDD and related chemicals
expected to cause reproductive failure based on laboratory experiments (2,3,7,8-TCDD concentrations
in excess of 1,000 pg/g). Improvements in herring gull reproduction through the mid-1980s were
correlated with declining 2,3,7,8-TCDD concentrations in eggs and lake sediments [7]. Based on limited
information on isomer-specific analysis from animals at different trophic levels, it appears that at higher
trophic levels, i.e., fish-eating birds and fish, there is a selection of the planar congeners with the 2,3,7,8-
substituted positions [10].
PCDDs and PCDFs are accumulated by aquatic organisms through exposure routes that are determined
by the habitat and physiology of each species. With log K,,w>5, exposure through ingestion of
contaminated food becomes an important route for uptake in comparison to respiration of water [7]. The
relative contributions of water, sediment, and food to uptake of 2,3,7,8-TCDD by lake trout in Lake
Ontario was examined by exposing yearling lake trout to Lake Ontario smelt and sediment from Lake
Ontario along with water at a 2,3,7,8-TCDD concentration simulated to be at equilibrium with the
sediments. Food ingestion was found to contribute approximately 75 percent of total 2,3,7,8-TCDD [7].
There have been a number of bioconcentration studies of 2,3,7,8-TCDD using model ecosystem and
single species exposure. Although there is variation in the actual log BCF values, in general, the algae
and plants have the lowest BCF values, on the order of a few thousand. A value of 4.38 has been reported
for the snail Physa sp. Crustacea and insect larva appear to have the next highest BCF values, followed
by several species of fish, with the highest log BCF value of 4.78 [10].
Exposure of juvenile rainbow trout to 2,3,7,8-TCDD and -TCDF in water for 28 days resulted in adverse
effects on survival, growth, and behavior at extremely low concentrations. A no-observed-effects
concentration (NOEC) for 2,3,7,8-TCDD could not be determined because the exposure to the lowest
dose of 0.038 ng/1 resulted in significant mortality [11]. A number of biological effects have been
reported in fish following exposure to 2,3,7,8-TCDD including enzyme induction, immunological effects,
wasting syndrome, dermatological effects, hepatic effects, hematological effects, developmental effects,
and cardiovascular effects [10].
416
-------
Summary of Biological Effects Tissue Concentrations for 1,2,3,7,8-PentaCDF
Species:
Taxa
Concentration, Units in1: Toxicity:
Sediment Water Tissue (Sample Type) Effects
Ability to Accumulate2: Source:
Log Log
BCF BAF BSAF
Reference Comments3
Fishes
Salmonids
0.013
[15]
Wildlife
Falco peregrinits,
Peregrine falcon
4.0 ng/g (eggs) (n = 6)
11.4% eggshell thinning
[13]
F; Kola
Peninsula,
Russia
Haliaeetus
leucocephalus,
Bald eagle chicks
Powell River site: -160
ng/kg lipid weight basis
(yolk sac)
Reference site: -30
ng/kg lipid weight basis
(yolk sac)
A hepatic cytochrome
P4501A crossreactive
protein (CYP1A) was
induced nearly six-fold
in chicks from Powell
River site compared to
the reference (p<0.05).
No significant
concentration-related
effects were found for
morphological,
physiological, or
histological parameters.
[12]
F; southern
coast of British
Columbia; eggs
were collected
from nests and
hatched in the
lab; - indicates
value was taken
from a figure.
-------
Summary of Biological Effects Tissue Concentrations for 1,2,3,7,8-PentaCDF
Species:
Taxa
Concentration, Units in1: Toxicity:
Sediment Water Tissue (Sample Type) Effects
Ability to Accumulate2: Source:
Log Log
BCF BAF BSAF
Reference Comments3
Mustela vison,
Mink
Diet:
1 Pg/g4
2 pg/g4
4 pg/g4
1 pg/g4 (liver)
2 pg/g4 (liver)
2 pg/g4 (liver)
[14]
LOAEL; reduced kit
body weights followed
by reduced survival
Reduced kit body
weights followed by
reduced survival
Significant decrease in
number of live kits
whelped per female
1 Concentration units based on wet weight unless otherwise noted.
2 BCF = bioconcentration factor, BAF = bioaccumulation factor, BSAF = biota-sediment accumulation factor.
3 L = laboratory study, spiked sediment, single chemical; F = field study, multiple chemical exposure; other unusual study conditions or observations noted.
4 Not clear from reference if concentration is based on wet or dry weight.
-------
BIOACCUMULATION SUMMARY 1,2,3,7,8-PentaCDF
References
1. USEPA. 1996. Hazardous Substances Data Bank (HSDB). National Library of Medicine online
(TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental
Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. February.
2. USEPA. 1989. Chemical fate rate constants for SARA section 313 chemicals and Superfund
Health Evaluation Manual chemicals. Prepared by Chemical Hazard Assessment Division,
Syracuse Research Corporation, for U.S. Environmental Protection Agency, Office of Toxic
Substances, Exposure Evaluation Division, Washington, DC, and Environmental Criteria and
Assessment Office, Cincinnati, OH. August 11.
3. Karickhoff, S.W., and J.M. Long. 1995. Internal report on summary of measured, calculated
and recommended log Kow values. Draft. Prepared by U.S. Environmental Protection Agency,
Office of Research and Development, Environmental Research Laboratory-Athens, for E.
Southerland, Office of Water, Office of Science and Technology, Standards and Applied Science
Division, Washington, DC. April 10.
4. USEPA. 1996. Integrated Risk Information System (IRIS). National Library of Medicine online
(TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental
Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. September.
5. Safe, S. 1990. Polychlorinated biphenyls (PCBs), dibenzo-/?-dioxins (PCDDs), dibenzofurans
(PCDFs), and related compounds: Environmental and mechanistic considerations which support
the development of toxicity equivalency factors (TEE). Cri. Rev. Toxicol. 21:51-88.
6. Braune, B.M., and RJ. Norstrom. 1989. Dynamics of organochlorine compounds in herring
gulls: HI. Tissue distribution and bioaccumulation in Lake Ontario gulls. Environ. Toxicol.
Chem. 8:957-968.
7. USEPA. 1993. Interim report on data and methods for assessment of 2,3,7,8-
tetrachlorodibenzo-^-dioxin risks to aquatic life and associated wildlife. EPA/600/R-93/055.
U.S. Environmental Protection Agency, Office of Research and Development, Washington, DC.
8. Eisler, R. 1986. Dioxin hazards to fish, wildlife, and invertebrates: A synoptic review. U.S. Fish
Wildl. Serv. Biol. Rep. 85 (1.8). 37 pp.
9. USEPA. 1989. Interim procedures for estimating risks associated with exposure to mixtures of
chlorinated dibenzo-p-dioxins and dibenzofurans (CDDs and CDFs) and 1989 update.
EPA/625/3-89/016. U.S. Environmental Protection Agency, Risk Assessment Forum,
Washington, DC.
10. Cooper, K.R. 1989. Effects of polychlorinated dibenzo-p-dioxins and polychlorinated
dibenzofurans on aquatic organisms. Rev. Aquat. Sci. 1:227-242.
11. 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.J. Coyle, and WJ. Adams. 1988. Toxicity and bioconcentration of 2,3,7,8-
419
-------
BIOACCUMULATION SUMMARY 1,2,3,7,8-PentaCDF
tetrachlorodibenzodioxin and 2,3,7,8-tetrachlorodibenzofuran in rainbow trout. Environ. Toxicol
Chem. 7:47-62.
12. Elliott, J.E., RJ. Norstrom, A. Lorenzen, L.E. Hart, H. Philibert, S.W. Kennedy, JJ. Stegeman,
G.D. Bellward, and K.M. Cheng. 1995. Biological effects of polychlorinated dibenzo-p-dioxins,
dibenzofurans, and biphenyls in bald eagle (Haliaeetus leucocephalus) chicks. Environ. Toxicol.
Chem. 15(5):782-793.
13. Henny, C.J., S.A. Ganusevich, F.P. Ward, and T.R. Schwartz. 1994. Organochlorine pesticides,
chlorinated dioxins and furans, and PCBs in peregrine falcon Falco peregrinus eggs from the
Kola Penninsula, Russia. In Raptor conservation to day, ed. B.U. Meyburg and R.D. Chancellor,
pp. 739-749. WWGPB/The Pica Press.
14. Tillitt, D.E., R.W. Gale, J.C. Meadows, J.L. Zajicek, P.M. Peterman, S.N. Heaton, P.O. Jones, SJ.
Bursian, TJ. Kubiak, J.P. Giesy, and RJ. Aulerich. 1996. Dietary exposure of mink to carp
from Saginaw Bay. 3. Characterization of dietary exposure to planar halogenated hydrocarbons,
dioxin equivalents, and biomagnification. Environ. Sci. Technol. 30:283-291.
15. USEPA. 1995. Great Lakes Water Quality Initiative technical support document for the
procedure to determine bio accumulation factors. EPA-820-B-95-005. U.S. Environmental
Protection Agency, Office of Water, Washington, DC.
420
-------
BIOACCUMULATION SUMMARY 2,3,4,7,8-PentaCDF
Chemical Category: POLYCHLORINATED DIBENZOFURANS
Chemical Name (Common Synonyms): CASRN: 57117-31-4
2,3,4,7,8-PENTACHLORODIBENZOFURAN
Chemical Characteristics
Solubility in Water: 0.24 |ig/L [1] Half-Life: No data [2,3]
Log Kow: No data [4], 6.92 [2] Log Koc: 6.80 L/kg organic carbon
Human Health
Oral RfD: No data [5] Confidence: —
Critical Effect: —
Oral Slope Factor: No data [5] Carcinogenic Classification: —
Wildlife
Partitioning Factors: Partitioning factors for 2,3,4,7,8-pentaCDF in wildlife were not found in the
studies reviewed.
Food Chain Multipliers: Limited information was found reporting on specific biomagnification factors
of PCDDs and PCDFs through terrestrial wildlife; no information was available for 2,3,4,7,8-pentaCDF,
specifically. Due to the toxicity, high K^w values, and highly persistent nature of the PCDDs and PCDFs,
they possess a high potential to bioaccumulate and biomagnify through the food web. PCDDs and PCDFs
have been identified in fish and wildlife throughout the global aquatic and marine environments [6].
Studies conducted in Lake Ontario indicated that biomagnification of 2,3,7,8-tetrachlorodibenzo-p-dioxin
(2,3,7,8-TCDD) appears to be significant between fish and fish-eating birds but not between fish and their
food. When calculated for older predaceous fish such as lake-trout-eating young smelt, the
biomagnification factor (BMF) can equal 3. The BMF from alewife to herring gulls in Lake Ontario was
32 for 2,3,7,8-TCDD [7]. Log BMFs of 1.73 to 1.74 were determined for mink [18].
EPA has developed risk-based concentrations of 2,3,7,8-TCDD in different media that present low and
high risk to fish, mammalian, and avian wildlife. These concentrations were developed based on toxic
effects of 2,3,7,8-TCDD and its propensity to bioaccumulate in fish, mammals, and birds.
421
-------
BIOACCUMULATION SUMMARY
2,3,4,7,8-PentaCDF
Environmental Concentrations Associated With 2,3,7,8-TCDD Risk to Aquatic Life and Associated
Wildlife [8]
Organism
Fish Concentration
(Pg/g)
Sediment
Concentration
Water Concentration (pg/L)
POC=0.2
POC=1.0
Low Risk
Fish
Mammalian Wildlife
Avian Wildlife
50
0.7
6
60
2.5
21
0.6
0.008
0.07
3.1
0.04
0.35
High Risk to Sensitive Species
Fish
Mammalian Wildlife
Avian Wildlife
80
7
60
100
25
210
1
0.08
0.7
5
0.4
3.5
Note: POC - Paniculate organic carbon
Fish lipid of 8% and sediment organic carbon of 3% assumed where needed.
For risk to fish, BSAF of 0.3 used; for risk to wildlife, BSAF of 0.1 used.
Low risk concentrations are derived from no-effects thresholds for reproductive effects (mortality in embryos and
young) in sensitive species.
High risk concentrations are derived from TCDD doses expected to cause 50 to 100% mortality in embryos and
young of sensitive species.
Aquatic Organisms
Partitioning Factors: In one study, the BSAF for carp collected from a reservoir in central Wisconsin
was 0.28. The log BCF for goldfish measured during a laboratory exposure of 120 hours was 4.48
Food Chain Multipliers: No specific food chain multipliers were identified for 2,3,4,7,8-pentaCDF.
Food chain multiplier information was only available for 2,3,7,8-TCDD. Biomagnification of 2,3,7,8-
TCDD does not appear to be significant between fish and their prey. Limited data for the base of the
Lake Ontario lake trout food chain indicated little or no biomagnification between zooplankton and forage
fish. BMFs based on fish consuming invertebrate species are probably close to 1.0 because of the 2,3,7,8-
TCDD biotransformation by forage fish. BMFs greater than 1.0 might exist between some zooplankton
species and their prey due to the lack of 2,3,7,8-TCDD biotransformation in invertebrates [8].
Toxicity/Bioaccumulation Assessment Profile
The polychlorinated dibenzo-p-dioxins (PCDDs) and polychlorinated dibenzofurans (PCDFs) each
consist of 75 isomers that differ in the number and position of attached chlorine atoms. The PCDDs and
PCDFs are polyhalogenated aromatic compounds and exhibit several properties common to this group
of compounds. These compounds tend to be highly lipophilic and the degree of lipophilicity is increased
with increasing ring chlorination [6]. In general, the PCDDs and PCDFs exhibit relative inertness to
acids, bases, oxidation, reduction, and heat, increasing in environmental persistence and chemical stability
with increasing chlorination [6,9]. Because of their lipophilic nature, the PCDDs and PCDFs have been
detected in fish, wildlife, and human adipose tissue, milk, and serum [6].
422
-------
BIOACCUMULATION SUMMARY
2,3,4,7,8-PentaCDF
Each isomer has its own unique chemical and lexicological properties. The most toxic of the PCDD and
PCDF isomers is 2,3,7,8-TCDD, one of the 22 possible congeners of tetrachlorodibenzo-j?-dioxin [8].
Toxicity equivalency factors (TEFs) have been developed by the EPA relating the toxicities of other
PCDD and PCDF isomers to that of 2,3,7,8-TCDD [10]. The biochemical mechanisms leading to the
toxic response resulting from exposure to PCDDs and PCDFs are not known in detail, but experimental
data suggest that an important role in the development of systemic toxicity resulting from exposure to
these chemicals is played by an intracellular protein, the Ah receptor. This receptor binds halogenated
polycyclic aromatic molecules, including PCDDs and PCDFs. In several mouse strains, the expression
of toxicity of 2,3,7,8-TCDD-related compounds, including cleft palate formation, liver damage, effects
on body weight gain, thymic involution, and chloracnegenic response, has been correlated with their
binding affinity for the Ah receptor, and with their ability to induce several enzyme systems [10].
Toxicity Equivalency Factors (TEF) for PCDD and PCDF Isomers [10]
Isomer
Total TetraCDD
2,3,7,8-TCDD
Other TCDDs
Total PentaCDDs
2,3,7,8-PentaCDDs
Other PentaCDDs
Total HexaCDDs
2,3,7,8-HexaCDDs
Other HexaCDDs
Total HeptaCDDs
2,3,7,8-HeptaCDDs
Other HeptaCDDs
Total TetraCDFs
2,3,7,8-TetraCDF
Other TetraCDFs
Total PentaCDFs
2,3,7,8-PentaCDFs
Other PentaCDFs
Total HexaCDFs
2,3,7,8-HexaCDFs
Other HexaCDFs
Total HeptaCDFs
2,3,7,8-HeptaCDFs
Other HeptaCDFs
TEF
1
1
0.01
0.5
0.5
0.005
0.04
0.04
0.0004
0.001
0.001
0.00001
0.1
0.1
0.001
0.1
0.1
0.001
0.01
0.01
0.0001
0.001
0.001
0.00001
In natural systems, PCDDs and PCDFs are typically associated with sediments, biota, and the organic
carbon fraction of ambient waters [7]. Congener-specific analyses have shown that the 2,3,7,8-substituted
PCDDs and PCDFs were the major compounds present in most sample extracts [6]. Results from limited
423
-------
BIOACCUMULATION SUMMARY 2,3,4,7,8-PentaCDF
epidemiology studies are consistent with laboratory-derived threshold levels to 2,3,7,8-TCDD impairment
of reproduction in avian wildlife. Population declines in herring gulls (Larus argentatus) on Lake
Ontario during the early 1970s coincided with egg concentrations of 2,3,7,8-TCDD and related chemicals
expected to cause reproductive failure based on laboratory experiments (2,3,7,8-TCDD concentrations
in excess of 1,000 pg/g). Improvements in herring gull reproduction through the mid-1980s were
correlated with declining 2,3,7,8-TCDD concentrations in eggs and lake sediments [8]. Based on limited
information on isomer-specific analysis from animals at different trophic levels, it appears that at higher
trophic levels, i.e., fish-eating birds and fish, there is a selection of the planar congeners with the 2,3,7,8-
substituted positions [11].
PCDDs and PCDFs are accumulated by aquatic organisms through exposure routes that are determined
by the habitat and physiology of each species. With log K,,w>5, exposure through ingestion of
contaminated food becomes an important route for uptake in comparison to respiration of water [8]. The
relative contributions of water, sediment, and food to uptake of 2,3,7,8-TCDD by lake trout in Lake
Ontario was examined by exposing yearling lake trout to Lake Ontario smelt and sediment from Lake
Ontario along with water at a 2,3,7,8-TCDD concentration simulated to be at equilibrium with the
sediments. Food ingestion was found to contribute approximately 75 percent of total 2,3,7,8-TCDD [8].
There have been a number of bioconcentration studies of 2,3,7,8-TCDD using model ecosystem and
single species exposure. Although there is variation in the actual log BCF values, in general, the algae
and plants have the lowest BCF values, on the order of a few thousand. A value of 4.38 has been reported
for the snail Physa sp. Crustacea and insect larva appear to have the next highest BCF values, followed
by several species of fish, with the highest log BCF value of 4.79 [11].
Exposure of juvenile rainbow trout to 2,3,7,8-TCDD and -TCDF in water for 28 days resulted in adverse
effects on survival, growth, and behavior at extremely low concentrations. A no-observed-effects
concentration (NOEC) for 2,3,7,8-TCDD could not be determined because the exposure to the lowest
dose of 0.038 ng/L resulted in significant mortality [12]. A number of biological effects have been
reported in fish following exposure to 2,3,7,8-TCDD including enzyme induction, immunological effects,
wasting syndrome, dermatological effects, hepatic effects, hematological effects, developmental effects,
and cardiovascular effects [11].
424
-------
Summary of Biological Effects Tissue Concentrations for 2,3,4,7,8-PentaCDF
Species:
Taxa
Concentration, Units in1: Toxicity:
Sediment Water Tissue (Sample Type) Effects
Ability to Accumulate2:
LogBCF LogBAF
Source:
BSAF Reference Comments3
Fishes
Carassius auratus,
Goldfish
2.69/2.5 ng/g4
(whole body)
4.48
[14] L; fish were
exposed for 120 hr;
exposure water
contained fly ash
extract; concen-
trations were
measured in water,
but data were not
presented
Cyprinus carpio, 8 pg/g4
Carp
4.4 pg/g4
0.28 [13] F; Petenwell
Reservoir, central
Wisconsin; BSAF
based on 8% tissue
lipid content and
3.1% sediment
organic carbon
Salmonids
0.095
[19]
Wildlife
Falco peregrinus,
Peregrine falcon
27 ng/g (eggs)
(n = 6)
11.4% eggshell
thinning
[17] F; Kola Peninsula,
Russia
-------
Summary of Biological Effects Tissue Concentrations for 2,3,4,7,8-PentaCDF
Species:
Taxa
Haliaeetus
leiicocephaliis,
Bald eagle chicks
Concentration, Units in1:
Sediment Water Tissue (Sample Type)
Powell River site:
-800 ng/kg lipid
weight basis
(yolk sac)
Reference site:
-100 ng/kg lipid
weight basis
(yolk sac)
Toxicity: Ability to Accumulate2:
LogBCF LogBAF
Effects BSAF
A nearly 6-fold
increase in
hepatic
cytochrome
P4501 A cross-
reactive protein
(CYP1A) was
induced in
chicks from
Powell River
site compared to
the reference
(p<0.05). No
significant
concentration-
related effects
were found for
morphological,
physiological, or
histological
parameters.
Source:
Reference Comments3
[15] F; southern coast of
British Columbia;
eggs were collected
from nests and
hatched in the lab;
- indicates value
was taken from a
figure.
-------
Summary of Biological Effects Tissue Concentrations for 2,3,4,7,8-PentaCDF
Species:
Taxa
Concentration, Units in1: Toxicity:
Sediment Water Tissue (Sample Type) Effects
Ability to Accumulate2:
LogBCF LogBAF
BSAF
Source:
Reference Comments
Ardea herodias,
Great blue heron
chicks
Nicomekl site:
<2ng/kg (egg)
Vancouver site:
33±18.5ng/kg (egg)
(n = 12)
Crofton site:
33±7.6 ng/kg (egg)
(n = 6)
Depression of
growth
compared to
Nicomekl site.
Presence of
edema.
Depression of
growth
compared to
Nicomekl site.
Presence of
edema.
[16] L; eggs were
collected from three
British Columbia
colonies with
different levels of
contamination and
incubated in the
laboratory
-------
Summary of Biological Effects Tissue Concentrations for 2,3,4,7,8-PentaCDF
Species:
Taxa
Mustela vison,
Mink
Concentration, Units in1: Toxicity:
Sediment Water Tissue (Sample Type) Effects
Diet: LOAEL;
4pg/g4 170pg/g4 (liver) reduced kit body
weights
followed by
reduced survival
6pg/g4 320pg/g4 (liver) Reduced kit
body weights
followed by
reduced survival
14 pg/g4 490 pg/g4 (liver) Significant
decrease in
number of live
kits whelped per
female
Ability to Accumulate2:
LogBCF LogBAF
BSAF
No BMP
reported
Log BMP
= 1.74
Log BMP
= 1.73
Source:
Reference Comments3
[18] L; BMP = lipid-
normalized
concentration in the
liver divided by the
lipid-normalized
dietary
concentration
1 Concentration units based on wet weight unless otherwise noted.
2 BCF = bioconcentration factor, BAP = bioaccumulation factor, BSAF = biota-sediment accumulation factor.
3 L = laboratory study, spiked sediment, single chemical; F = field study, multiple chemical exposure; other unusual study conditions or observations noted.
4 Not clear from reference if concentration is based on wet or dry weight.
-------
BIOACCUMULATION SUMMARY 2,3,4,7,8-PentaCDF
References
1. USEPA. 1996. Hazardous Substances Data Bank (HSDB). National Library of Medicine online
(TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental
Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. February.
2. MacKay, D.M., W.Y. Shiw, and K.C. Ma. 1992. Illustrated handbook of physical-chemical
properties and environmental fate for organic chemicals Vol. n, Polynuclear aromatic
hydrocarbons, poly chlorinated dioxins and dibenzofurans. Lewis Publishers, Boca Raton, FL.
3. USEPA. 1989. Chemical fate rate constants for SARA section 313 chemicals and Superfund
Health Evaluation Manual chemicals. Prepared by Chemical Hazard Assessment Division,
Syracuse Research Corporation, for U.S. Environmental Protection Agency, Office of Toxic
Substances, Exposure Evaluation Division, Washington, DC, and Environmental Criteria and
Assessment Office, Cincinnati, OH. August 11.
4. Karickhoff, S.W., and J.M. Long. 1995. Internal report on summary of measured, calculated and
recommended log Kow values. Draft. Prepared by U.S. Environmental Protection Agency, Office
of Research and Development, Environmental Research Laboratory-Athens, for E. Southerland,
Office of Water, Office of Science and Technology, Standards and Applied Science Division,
Washington, DC. April 10.
5. USEPA. 1996. Integrated Risk Information System (IRIS). National Library of Medicine online
(TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental
Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. September.
6. Safe, S. 1990. Polychlorinated biphenyls (PCBs), dibenzo-p-dioxins (PCDDs), dibenzofurans
(PCDFs), and related compounds: Environmental and mechanistic considerations which support
the development of toxicity equivalency factors (TEF). Cri. Rev. Toxicol 21:51-88.
7. Braune, B.M., and RJ. Norstrom. 1989. Dynamics of organochlorine compounds in herring
gulls: m. Tissue distribution and bioaccumulation in Lake Ontario gulls. Environ. Toxicol. Chem.
8:957-968.
8. USEPA. 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. U.S. Environmental
Protection Agency, Office of Research and Development, Washington, DC.
9. Eisler, R. 1986. Dioxin hazards to fish, wildlife, and invertebrates: a synoptic review. U.S. Fish
and Wildl. Serv. Biol. Rep. 85 (1.8). 37 pp.
10. USEPA. 1989. Interim procedures for estimating risks associated with exposure to mixtures of
chlorinated dibenzo-p-dioxins and dibenzofurans (CDDs and CDFs) and 1989 update.
EPA/625/3-89/016. U.S. Environmental Protection Agency, Risk Assessment Forum,
Washington, DC.
429
-------
BIOACCUMULATION SUMMARY 2,3,4,7,8-PentaCDF
11. Cooper, K.R. 1989. Effects of polychlorinated dibenzo-p-dioxins and polychlorinated
dibenzofurans on aquatic organisms. Rev. Aquat. Set 1:227-242.
12. Mehrle, P.M., D.R. Buckler, E.E. Little, L.M. Smith, J.D. Petty, P.M. Peterman, D.L. Stalling,
G.M. DeGraeve, JJ. Coyle, and WJ. Adams. 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.
13. Kuehl, D.W., P.M. Cook, A.R. Batterman, D. Lothenbach, and B.C. Butterworth. 1987.
Bioavailability of polychlorinated dibenzo-j?-dioxins and dibenzofurans from contaminated
Wisconsin River sediment to carp. Chemosphere 16(4):667-679.
14. Sijm, D.T.H.M., H. Wever, and A. Opperhuizen. 1993. Congener-specific biotransformation and
bioaccumulation of PCDDs and PCDFs from fly ash in fish. Environ. Toxicol. Chem. 12:1895-
1907.
15. Elliott, J.E., R.J. Norstrom, A. Lorenzen, L.E. Hart, H. Philibert, S.W. Kennedy, JJ. Stegeman,
G.D. Bellward, and K.M. Cheng. 1995. Biological effects of polychlorinated dibenzo-j?-dioxins,
dibenzofurans, and biphenyls in bald eagle (Haliaeetus leucocephalus) chicks. Environ. Toxicol.
Chem. 15(5):782-793.
16. Hart, L.E., K.M. Cheng, P.E. Whitehead, R.M. Shah, RJ. Lewis, S.R. Ruschkowski, R.W. Blair,
D.C. Bennett, S.M. Bandiera, RJ.Norstrom, and G.D. Bellward. 1991. Dioxin contamination
and growth and development in great blue heron embryos. /. Toxicol. Environ. Health 32:331-
344.
17. Henny, C.J., S.A. Ganusevich, F.P. Ward, and T.R. Schwartz. 1994. Organochlorine pesticides,
chlorinated dioxins and furans, and PCBs in peregrine falcon Falco peregrinus eggs from the
Kola Penninsula, Russia. In Raptor conservation today, ed. B.U. Meyburg and R.D. Chancellor,
pp. 739-749. WWGPB/The Pica Press.
18. Tillitt, D.E., R.W. Gale, J.C. Meadows, J.L. Zajicek, P.H. Peterman, S.N. Heaton, P.O. Jones, S.J.
Bursian, T.J. Kubiak, J/P. Giesy, and R.J. Aulerich. 1996. Dietary exposure of mink to carp
from Saginaw Bay. 3. Characterization of dietary exposure to planar halogenated hydrocarbons,
dioxin equivalents, and biomagnification. Environ. Sci. Technol. 30:283-291.
19. USEPA. 1995. Great Lakes Water Quality Initiative technical support document for the
procedure to determine bioaccumulation factors. EPA-820-B-95-005. U.S. Environmental
Protection Agency, Office of Water, Washington, DC.
430
-------
BIOACCUMULATION SUMMARY
2,3,7,8-TCDF
Chemical Category: POLYCHLORINATED DIBENZOFURANS
Chemical Name (Common Synonyms):
2,3,7,8-TETRACHLORODIBENZOFURAN
CASRN: 51207-31-9
Chemical Characteristics
Solubility in Water: No data [1], 0.42 |ig/L [2] Half-Life: No data [3]
Log Kow: No data [4], 6.53 [2] Log Koc: —
Human Health
Oral RfD: No data [5]
Critical Effect: —
Oral Slope Factor: No data [5]
Confidence:
Carcinogenic Classification:
Wildlife
Partitioning Factors: Partitioning factors for 2,3,7,8-TCDF in wildlife were not found in the studies
reviewed.
Food Chain Multipliers: Limited information was found reporting on specific biomagnification factors
of PCDDs and PCDFs through terrestrial wildlife; no information was available for 2,3,7,8-TCDF,
specifically. Due to the toxicity, high Kow values, and highly persistent nature of the PCDDs and PCDFs,
they possess a high potential to bioaccumulate and biomagnify through the food web. PCDDs and PCDFs
have been identified in fish and wildlife throughout the global aquatic and marine environments [6].
Studies conducted in Lake Ontario indicated that biomagnification of 2,3,7,8-tetrachlorodibenzo-p-dioxin
(2,3,7,8-TCDD) appears to be significant between fish and fish-eating birds but not between fish and their
food. When calculated for older predaceous fish such as lake-trout-eating young smelt, the
biomagnification factor (BMF) can equal 3. The BMP from alewife to herring gulls in Lake Ontario was
32 for 2,3,7,8-TCDD [7]. A log BMF of -0.40 was determined for mink [2].
EPA has developed risk-based concentrations of 2,3,7,8-TCDD in different media that present low and
high risk to fish, mammalian, and avian wildlife. These concentrations were developed based on toxic
effects of 2,3,7,8-TCDD and its propensity to bioaccumulate in fish, mammals, and birds.
431
-------
BIOACCUMULATION SUMMARY
2,3,7,8-TCDF
Environmental Concentrations Associated With 2,3,7,8-TCDD Risk to Aquatic Life and Associated
Wildlife [8]
Organism
Fish Concentration
(Pg/g)
Sediment
Concentration
(pg/g dry wt.)
Water Concentration (pg/L)
POC=0.2
POC=1.0
Low Risk
Fish
Mammalian Wildlife
Avian Wildlife
50
0.7
6
60
2.5
21
0.6
0.008
0.07
3.1
0.04
0.35
High Risk to Sensitive Species
Fish
Mammalian Wildlife
Avian Wildlife
80
7
60
100
25
210
1
0.08
0.7
5
0.4
3.5
Note: POC - Paniculate organic carbon
Fish lipid of 8% and sediment organic carbon of 3% assumed where needed.
For risk to fish, BSAF of 0.3 used; for risk to wildlife, BSAF of 0.1 used.
Low risk concentrations are derived from no-effects thresholds for reproductive effects (mortality in embryos and
young) in sensitive species.
High risk concentrations are derived from TCDD doses expected to cause 50 to 100% mortality in embryos and
young of sensitive species.
Aquatic Organisms
Partitioning Factors: In one study, steady-state BSAFs for invertebrates exposed to 2,3,7,8-TCDF in
the laboratory ranged from about 0.3 to 0.7. The BSAF for carp collected from a reservoir in central
Wisconsin was 0.06.
Food Chain Multipliers: No specific food chain multipliers were identified for 2,3,7,8-TCDF. Food
chain multiplier information was only available for 2,3,7,8-TCDD. Biomagnification of 2,3,7,8-TCDD
does not appear to be significant between fish and their prey. Limited data for the base of the Lake
Ontario lake trout food chain indicated little or no biomagnification between zooplankton and forage fish.
BMFs based on fish consuming invertebrate species are probably close to 1.0 because of the 2,3,7,8-
TCDD biotansformation by forage fish. BMFs greater than 1.0 might exist between some zooplankton
species and their prey due to the lack of 2,3,7,8-TCDD biotransformation in invertebrates [8].
Toxicity/Bioaccumulation Assessment Profile
The polychlorinated dibenzo-p-dioxins (PCDDs) and polychlorinated dibenzofurans (PCDFs) each
consist of 75 isomers that differ in the number and position of attached chlorine atoms. The PCDDs and
PCDFs are polyhalogenated aromatic compounds and exhibit several properties common to this group
of compounds. These compounds tend to be highly lipophilic and the degree of lipophilicity is increased
with increasing ring chlorination [6]. In general, the PCDDs and PCDFs exhibit relative inertness to
acids, bases, oxidation, reduction, and heat, increasing in environmental persistence and chemical stability
432
-------
BIOACCUMULATION SUMMARY
2,3,7,8-TCDF
with increasing chlorination [9,6]. Because of their lipophilic nature, the PCDDs and PCDFs have been
detected in fish, wildlife, and human adipose tissue, milk, and serum [6].
Each isomer has its own unique chemical and lexicological properties. The most toxic of the PCDD and
PCDF isomers is one of the 22 possible congeners of tetrachlorodibenzo-p-dioxin [9]. Toxicity
equivalency factors (TEFs) have been developed by EPA relating the toxicities of other PCDD and PCDF
isomers to that of 2,3,7,8-TCDD [10]. The biochemical mechanisms leading to the toxic response
resulting from exposure to PCDDs and PCDFs are not known in detail, but experimental data suggest
that an important role in the development of systemic toxicity resulting from exposure to these chemicals
is played by an intracellular protein, the Ah receptor. This receptor binds halogenated polycyclic aromatic
molecules, including PCDDs and PCDFs. In several mouse strains, the expression of toxicity of 2,3,7,8-
TCDD-related compounds, including cleft palate formation, liver damage, effects on body weight gain,
thymic involution, and chloracnegenic response, has been correlated with their binding affinity for the
Ah receptor, and with their ability to induce several enzyme systems [10].
Toxicity Equivalency Factors (TEF) for PCDD and PCDF Isomers [10]
Isomer
Total TetraCDD
2,3,7,8-TCDD
Other TCDDs
Total PentaCDDs
2,3,7,8-PentaCDDs
Other PentaCDDs
Total HexaCDDs
2,3,7,8-HexaCDDs
Other HexaCDDs
Total HeptaCDDs
2,3,7,8-HeptaCDDs
Other HeptaCDDs
Total TetraCDFs
2,3,7,8-TetraCDF
Other TetraCDFs
Total PentaCDFs
2,3,7,8-PentaCDFs
Other PentaCDFs
Total HexaCDFs
2,3,7,8-HexaCDFs
Other HexaCDFs
Total HeptaCDFs
2,3,7,8-HeptaCDFs
Other HeptaCDFs
TEF
1
1
0.01
0.5
0.5
0.005
0.04
0.04
0.0004
0.001
0.001
0.00001
0.1
0.1
0.001
0.1
0.1
0.001
0.01
0.01
0.0001
0.001
0.001
0.00001
433
-------
BIOACCUMULATION SUMMARY 2,3,7,8-TCDF
In natural systems, PCDDs and PCDFs are typically associated with sediments, biota, and the organic
carbon fraction of ambient waters [7]. Congener-specific analyses have shown that the 2,3,7,8-substituted
PCDDs and PCDFs were the major compounds present in most sample extracts [6]. Results from limited
epidemiology studies are consistent with laboratory-derived threshold levels to 2,3,7,8-TCDD impairment
of reproduction in avian wildlife. Population declines in herring gulls (Larus argentatus) on Lake
Ontario during the early 1970s coincided with egg concentrations of 2,3,7,8-TCDD and related chemicals
expected to cause reproductive failure based on laboratory experiments (2,3,7,8-TCDD concentrations
in excess of 1,000 pg/g). Improvements in herring gull reproduction through the mid-1980s were
correlated with declining 2,3,7,8-TCDD concentrations in eggs and lake sediments [8]. Based on limited
information on isomer-specific analysis from animals at different trophic levels, it appears that at higher
trophic levels, i.e., fish-eating birds and fish, there is a selection of the planar congeners with the 2,3,7,8-
substituted positions [11].
PCDDs and PCDFs are accumulated by aquatic organisms through exposure routes that are determined
by the habitat and physiology of each species. With log K^S, exposure through ingestion of
contaminated food becomes an important route for uptake in comparison to respiration of water [8]. The
relative contributions of water, sediment, and food to uptake of 2,3,7,8-TCDD by lake trout in Lake
Ontario was examined by exposing yearling lake trout to Lake Ontario smelt and sediment from Lake
Ontario along with water at a 2,3,7,8-TCDD concentration simulated to be at equilibrium with the
sediments. Food ingestion was found to contribute approximately 75 percent of total 2,3,7,8-TCDD [8].
There have been a number of bioconcentration studies of 2,3,7,8-TCDD using model ecosystem and
single species exposure. Although there is variation in the actual log BCF values, in general, the algae
and plants have the lowest BCF values, on the order of a few thousand. A value of 4.38 has been reported
for the snail Physa sp. Crustacea and insect larva appear to have the next highest BCF values, followed
by several species of fish, with the highest log BCF value of 4.79 [11].
Exposure of juvenile rainbow trout to 2,3,7,8-TCDD and -TCDF in water for 28 days resulted in adverse
effects on survival, growth, and behavior at extremely low concentrations. A no-observed-effects
concentration (NOEC) for 2,3,7,8-TCDD could not be determined because the exposure to the lowest
dose of 0.038 ng/L resulted in significant mortality [12]. A number of biological effects have been
reported in fish following exposure to 2,3,7,8-TCDD including enzyme induction, immunological effects,
wasting syndrome, dermatological effects, hepatic effects, hematological effects, developmental effects,
and cardiovascular effects [11].
434
-------
Summary of Biological Effects Tissue Concentrations for 2,3,7,8-TCDF
Species:
Taxa
Concentration, Units in1:
Sediment Water
Toxicity:
Ability to Accumulate2:
Source:
Tissue (Sample Type) Effects Log Log
BCF
BAF
BSAF Reference Comments3
Invertebrates
Nereis virens,
Sandworm
334±6 pg/g
dw
n = 6
112±51pg/gdw
(whole body)
-0.25 [13,14] L; 180-day
exposure; sediment
TOC was 57
mg/kg; ~ indicates
approximate value,
as numbers were
estimated from bar
graphs
Macoma nasuta,
Clam
334±6 pg/g
dw
n = 6
51.4±6.8 pg/g dw
-0.7 [13,14] L; 120-day
exposure; sediment
TOC was 57
mg/kg; ~ indicates
approximate value,
as numbers were
estimated from bar
graphs
Palaemonetespugio, 334±6pg/g
Grass shrimp dw
n = 6
58.8±7.7 pg/g dw
-0.6 [13,14] L; 28-day
exposure; sediment
TOC was 57
mg/kg; ~ indicates
approximate value,
as numbers were
estimated from bar
graphs
-------
Summary of Biological Effects Tissue Concentrations for 2,3,7,8-TCDF
Species:
Taxa
Concentration, Units in1:
Sediment Water
Toxicity:
Tissue (Sample Type) Effects
Ability to Accumulate2:
Source:
Log
BCF
Log
BAF
BSAF Reference Comments3
Fishes
Oncorhynchiis
mykiss
(Salmo gairdneri),
Rainbow trout
Water
exposure
0.41 ng/L
Water
exposure
1.79 ng/L
2.5 |ig/kg4
7.6 |ig/kg4
28-Day NOEC
(growth)
28-Day NOEC
(survival)
[15]
[15]
Oncorhynchiis
mykiss,
Rainbow trout
0.00009 mg/kg (whole Growth, NOED
body)4
[15]
L
Salmonids
0.047 [22]
Cyprinus carpio,
Carp
182pg/g4
28pg/g4
0.06 [16] F; Petenwell
Reservoir, central
Wisconsin; BSAF
based on 8% tissue
lipid content and
3.1% sediment
organic carbon
-------
Summary of Biological Effects Tissue Concentrations for 2,3,7,8-TCDF
Species:
Taxa
Concentration, Units in1:
Sediment Water
Toxicity:
Tissue (Sample Type) Effects Log Log
Ability to Accumulate2:
Log Log
BCF BAF BSAF
Source:
Reference Comments3
Wildlife
Falco peregrinus,
Peregrine falcon
30 ng/g (eggs) (n=6) 11.4% eggshell
thinning
[19] F; Kola Peninsula,
Russia
Haliaeetus
leucocephalus,
Bald eagle chicks
Powell River site:
8,000 ng/kg lipid
weight basis (yolk sac)
Reference site: 500
A hepatic
cytochrome
P4501A cross-
reactive protein
(CYP1A) was
ng/kg lipid weight basis induced nearly
(yolk sac)
6-fold in chicks
from Powell
River site
compared to the
reference
(p<0.05). No
significant
concentration-
related effects
were found for
morphological,
physiological, or
histological
parameters.
[17] F; southern coast
of British
Columbia; eggs
were collected
from nests and
hatched in the
laboratory.
-------
Summary of Biological Effects Tissue Concentrations for 2,3,7,8-TCDF
Species:
Taxa
Ardea herodias,
Great blue heron
chicks
Concentration, Units in1: Toxicity:
Tissue (Sample Type) Effects
Sediment Water
Nicomekl site: <1
ng/kg (egg) n = 1 1
Ability to Accumulate2:
Log Log
BCF BAF BSAF
Source:
Reference
[18]
Comments3
L; eggs were
collected from
three British
Vancouver site: 11±4.3 Depression of
ng/kg (egg) n = 12 growth
compared to
Nicomekl site.
Presence of
edema.
Depression of
growth
compared to
Nicomekl site.
Presence of
edema.
Columbia colonies
with different
levels of
contamination and
incubated in the
laboratory
Crofton site: 8±2.3
ng/kg (egg)n = 6
-------
Summary of Biological Effects Tissue Concentrations for 2,3,7,8-TCDF
Species:
Taxa
Concentration, Units in1:
Sediment Water
Toxicity:
Tissue (Sample Type) Effects Log Log
Ability to Accumulate2:
Log Log
BCF BAF BSAF
Source:
Reference Comments3
Aix sponsa,
Wood duck
pg/g (eggs):
% eggs hatched:
Site 1 geometric mean: 47 (9.7 SE)
26 (2.4-244)
Site 2 geometric mean: 62 (10.1 SE)
11 (1.4-60)
Site 3 geometric mean: 79 (3.8 SE)
5.4 (20-50 ppt TEF
-------
Summary of Biological Effects Tissue Concentrations for 2,3,7,8-TCDF
Species:
Taxa
Mustela vison,
Mink
Concentration, Units in1: Toxicity:
Tissue (Sample Type) Effects
Sediment Water
Diet: 2 pg/g5 (liver) LOAEL;
2 pg/g5 reduced kit body
weights
followed by
reduced survival
Reduced kit
4 pg/g5 2 pg/g5 (liver) body weights
followed by
reduced survival
Significant
decrease in
12 pg/g5 3 pg/g5 (liver) number of live
kits whelped per
female
Ability to Accumulate2:
Log Log
BCF BAF BSAF
No BMP
reported
Log
BMF=
-0.4
Log
BMF=
-0.4
Source:
Reference Comments3
[21] L; BMF= lipid-
normalized
concentration in
the liver divided by
the lipid-
normalized dietary
concentration
1 Concentration units based on wet weight, unless otherwise noted.
2 BCF = bioconcentration factor, BAF = bioaccumulation factor, BSAF = biota-sediment accumulation factor.
3 L = laboratory study, spiked sediment, single chemical; F = field study, multiple chemical exposure; other unusual study conditions or observations, noted.
4 This entry was excerpted directly from the Environmental Residue-Effects Database (ERED, www.wes.army.mil/el/ered, U.S. Army Corps of Engineers and U.S.
Environmental Protection Agency). The original publication was not reviewed, and the reader is strongly urged to consult the publication to confirm the information
presented here.
5 Not clear from reference if concentration is based on wet or dry weight.
440
-------
BIOACCUMULATION SUMMARY 2,3,7,8-TCDF
References
1. USEPA. 1996. Hazardous Substances Data Bank (HSDB). National Library of Medicine online
(TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental
Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. February.
2. MacKay, D.M., W.Y. Shiw, and K.C. Ma. 1992. Illustrated handbook of physical-chemical
properties and environmental fate for organic chemicals. Vol. n, Polynuclear aromatic
hydrocarbons, poly chlorinated dioxins and dibenzofurans. Lewis Publishers, Boca Raton, FL.
3. USEPA. 1989. Chemical fate rate constants for SARA section 313 chemicals and Sup erfund
Health Evaluation Manual chemicals. Prepared by Chemical Hazard Assessment Division,
Syracuse Research Corporation, for U.S. Environmental Protection Agency, Office of Toxic
Substances, Exposure Evaluation Division, Washington, DC, and Environmental Criteria and
Assessment Office, Cincinnati, OH. August 11.
4. Karickhoff, S.W., and J.M. Long. 1995. Internal report on summary of measured, calculated
and recommended log Kow values. Draft. Prepared by U.S. Environmental Protection Agency,
Office of Research and Development, Environmental Research Laboratory-Athens, for E.
Southerland, Office of Water, Office of Science and Technology, Standards and Applied Science
Division, Washington, DC. April 10.
5. USEPA. 1996. Integrated Risk Information System (IRIS). National Library of Medicine online
(TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental
Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. September.
6. Safe, S. 1990. Polychlorinated biphenyls (PCBs), dibenzo-p-dioxins (PCDDs), dibenzofurans
(PCDFs), and related compounds: Environmental and mechanistic considerations which support
the development of toxicity equivalency factors (TEF). Crit. Rev. Toxicol. 21:51-88.
7. Braune, B.M., and RJ. Norstrom. 1989. Dynamics of organochlorine compounds in herring
gulls: HI. Tissue distribution and bioaccumulation in Lake Ontario gulls. Environ. Toxicol.
Chem. 8:957-968.
8. USEPA. 1993. Interim report on data and methods for assessment of 2,3,7,8-
tetrachlorodibenzo-^-dioxin risks to aquatic life and associated wildlife. EPA/600/R-93/055.
U.S. Environmental Protection Agency, Office of Research and Development, Washington, DC.
9. Eisler, R. 1986. Dioxin hazards to fish, wildlife, and invertebrates: A synoptic review. U.S. Fish
Wildl. Serv. Biol. Rep. 85 (1.8). 37 pp.
10. USEPA. 1989. Interim procedures for estimating risks associated with exposure to mixtures of
chlorinated dibenzo-p-dioxins and dibenzofurans (CDDs and CDFs) and 1989 update.
EPA/625/3-89/016. U.S. Environmental Protection Agency, Risk Assessment Forum,
Washington, DC.
11. Cooper, K.R. 1989. Effects of polychlorinated dibenzo-/?-dioxins and polychlorinated
dibenzofurans on aquatic organisms. Rev. Aquat. Sci. 1:227-242.
441
-------
BIOACCUMULATION SUMMARY 2,3,7,8-TCDF
12. Mehrle, P.M., D.R. Buckler, E.E. Little, L.M. Smith, J.D. Petty, P.M. Peterman, D.L. Stalling,
G.M. DeGraeve, JJ. Coyle, and WJ. Adams. 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.
13. Pruell, R.J., N.I. Rubinstein, B.K. Taplin, J.A. LiVolsi, and R.D. Bowen. 1993. Accumulation
of polychlorinated organic contaminants from sediment by three benthic marine species. Arch.
Environ. Contain. Toxicol. 24:290-297.
14. Rubinstein, N.I., RJ. Pruell, B.K. Taplin, J.A. LiVolsi, and C.B.Norwood. 1990. Bioavailability
of 2,3,7,8-TCDD, 2,3,7,8-TCDF and PCBs to marine benthos from Passaic River sediments.
Chemosphere 20(7-9): 1097-1102.
15. Mehrle, P.M., D.R. Buckler, E.E. Little, L.M. Smith, J.D. Petty, P.M. Peterman, D.L. Stalling,
G.M. DeGraeve, JJ. Coyle, and W.J. Adams. 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.
16. Kuehl, D.W., P.M. Cook, A.R. Batterman, D. Lothenbach, and B.C. Butterworth. 1987.
Bioavailability of polychlorinated dibenzo-p-dioxins and dibenzofurans from contaminated
Wisconsin River sediment to carp. Chemosphere 16(4):667-679.
17. Elliott, J.E., R.J. Norstrom, A. Lorenzen, L.E. Hart, H. Philibert, S.W. Kennedy, JJ. Stegeman,
G.D. Bellward, and K.M. Cheng. 1995. Biological effects of polychlorinated dibenzo-p-dioxins,
dibenzofurans, and biphenyls in bald eagle (Haliaeetus leucocephalus) chicks. Environ. Toxicol.
Chem. 15(5):782-793.
18. Hart, L.E., K.M. Cheng, P.E. Whitehead, R.M. Shah, R.J. Lewis, S.R. Ruschkowski, R.W. Blair,
D.C. Bennett, S.M. Bandiera, R.J. Norstrom, and G.D. Bellward. 1991. Dioxin contamination
and growth and development in great blue heron embryos. /. Toxicol. Environ. Health 32:331-
344.
19. Henny, C.J., S.A. Ganusevich, F.P. Ward, and T.R. Schwartz. 1994. Organochlorine pesticides,
chlorinated dioxins and furans, and PCBs in peregrine falcon Falco peregrinus eggs from the
Kola Penninsula, Russia. In Raptor conservation today, ed. B.U. Meyburg and R.D. Chancellor,
pp. 739-749. WWGPB/The Pica Press.
20. White, D.H., and J.T. Seginak. 1994. Dioxins and furans linked to reproductive impairment in
wood duck. J.Wildl. Manage. 58(1):100-106.
21. Tillitt, D.E., R.W. Gale, J.C. Meadows, J.L. Zajicek, P.H. Peterman, S.N. Heaton, P.O. Jones, S J.
Bursian, TJ. Kubiak, J.P. Giesy, and R.J. Aulerich. 1996. Dietary exposure of mink to carp
from Saginaw Bay. 3. Characterization of dietary exposure to planar halogenated hydrocarbons,
dioxin equivalents, and biomagnification. Environ. Sci. Technol. 30:283-291.
22. USEPA. 1995. Great Lakes Water Quality Initiative technical support document for the
procedure to determine bio accumulation factors. EPA-820-B-95-005. U.S. Environmental
Protection Agency, Office of Water, Washington, DC.
442
-------
BIOACCUMULATION SUMMARY FLUORANTHENE
Chemical Category: POLYNUCLEAR AROMATIC HYDROCARBON (high molecular weight)
Chemical Name (Common Synonyms): FLUORANTHENE CASRN: 206-44-0
Chemical Characteristics
Solubility in Water: 0.20-0.26 mg/L [1] Half-Life: 140-440 days, aerobic soil
die-away test [2]
Log Kow: 5.12 [3] Log Koc: 5.03 L/kg organic carbon
Human Health
Oral RfD: 4 x 10"2 mg/kg-day [4] Confidence: Low, uncertainty factor = 3000
Critical Effect: Nephropathy, increased liver weights, hematological alterations, and clinical effects
Oral Slope Factor: No data [4] Carcinogenic Classification: D [4]
Wildlife
Partitioning Factors: Partitioning factors for fluoranthene in wildlife were not found in the literature.
Food Chain Multipliers: Food chain multipliers for fluoranthene in wildlife were not found in the
literature.
Aquatic Organisms
Partitioning Factors: The water quality criterion tissue level (WQCTL) for fluoranthene, which is
calculated by multiplying the water quality chronic value (16 |ig/L) by the BCF (1741.8), is 27,869 |ig/kg
[5]. Salinity and particle size of the sediment had no or very little effect on survival of three amphipod
species during exposure to fluoranthene [6]. Log BCFs ranged from -0.92 for Lumbriculues variegatus
[16] to 0.63 for Hyallela azteca [9]. Log BAFs of 0.36 to 0.56 were calculated for the midges
Chironomus tentans [24].
Food Chain Multipliers: Food chain multipliers for fluoranthene in aquatic organisms were not found
in the literature.
Toxicity/Bioaccumulation Assessment Profile
Polynuclear aromatic hydrocarbons, (PAHs) are readily metabolized and excreted by fish and
invertebrates [7], affecting bioaccumulation kinetics and equilibrium tissue residues. According to
McCarty et al. [8], the toxic body residue of individual PAHs in tissues ranged from 513 to 4,248 mg/kg.
443
-------
BIOACCUMULATION SUMMARY FLUORANTHENE
The concentration of 382 ppb produced biological effects in environmental samples (Puget Sound). The
LC50 values for fluoranthene using freshwater amphipods ranged from 11.7 to 150.3 nrnol/g dry weight
[9].
Fluoranthene is relatively toxic to aquatic species (10-day EC50 = 2.3 to 7.4 |ig/L for H. azteca, 10-day
EC50 = 3.0 to 8.7 |ig/L C. tentans). Its toxicity increased 6- to 17-fold under UV light [10]. H. azteca
accumulated up to 1,131 |ig/g of fluoranthene during 10 days of exposure to the LC50 concentration.
Below the toxic level, the concentration of fluoranthene in amphipod tissue reached 200 to 400 |ig/g
within the first 48 hours and then dropped to 100 |ig/g [9]. During 30-day bioaccumulation exposures,
fed H. azteca accumulated significantly more fluoranthene than unfed organisms [11]. Furthermore, in
exposures in which food was added, organisms gained weight and reproduced, even when sediment was
dosed with concentrations approximately 20 to 90 times the 10-day LC50 value, with sediment containing
levels of organic carbon comparable to the Suedel et al. [12] experiments. These data suggest that
animals in fed exposures preferentially consumed the food, given the relatively high accumulation of
compound in animal tissue. Mortality due to narcosis, the mechanism thought to be responsible for PAH
toxicity, ranged from 2 to 8 |imol/g for acute responses and 0.2 to 0.8 |imol/g for chronic exposures in
fish [13]. In the study by Harkey et al. [11], animals accumulated up to 1.4 |imol/g after 30 days in the
highest (1,004 nmol/g) sediment concentration. Previous water-only exposures [14] predicted that a body
burden of 5.6 umol/g in H. azteca needs to be attained to produce 50 percent mortality. The body burden
of fluoranthene associated with 50 percent mortality of Leptocheirus plumulosus was 0.69 |imol/g wet
wt, which is lower than the predicted critical body residue for nonpolar narcotic compounds [15].
444
-------
Summary of Biological Effects Tissue Concentrations for Fluoranthene
Species:
Taxa
Concentration, Units in1:
Sediment Water
Toxicity:
Tissue (Sample Type) Effects
Ability to Accumulate2:
Source:
Log
BCF
Log
BAF
BSAF Reference Comments3
Invertebrates
Lumbriculus
variegatus,
Oligochaete worm
-0.92
[16]
Nereis succinea,
Polychaete worm
0.218 ng/g
OC
0.436 |ig/g
OC
0.48 |ig/g OC
1.4 |ig/gOC
4.55 ng/g OC
10.2 |ig/g
OC
19.5 |ig/g
OC
30.1 |ig/g
OC
9.20 |ig/g lipid
2.55 |ig/g lipid
35.6 |ig/g lipid
4.80 |ig/g lipid
3.79 |ig/g lipid
14.1 |ig/g lipid
24.0 |ig/g lipid
[17] F
Nereis virens,
Sand worm
-0.096 or
-0.10
-0.02
0.52
[18] F
Modiolus demissus,
Northern horse
mussel
0.36
[19] F
Mytilus edulis,
Blue mussel
-0.44
[19]
-------
Summary of Biological Effects Tissue Concentrations for Fluoranthene
Species:
Taxa
Mytilus edulis,
Mussel
Crassostrea
virginica, Eastern
Concentration, Units in1:
Sediment Water Tissue (Sample Type)
627 mg/kg
(whole body)4
1.9 mg/kg
(whole body)4
0.1 12 mg/kg
(whole body)
1.5 mg/kg
(whole body)4
1.5 mg/kg
(whole body)4
62 mg/kg
(whole body)4
Toxicity: Ability to Accumulate2:
Log Log
Effects BCF BAF BSAF
Physiological,
ED50
Physiological,
ED50
Physiological,
LOED
Physiological,
LOED
Reproduction,
LOED
Morphology,
LOED
Source:
Reference
[27]
[28]
[28]
[28]
[28]
[30]
Comments3
L; 50% reduction in
feeding rate
L; 50% reduction in
feeding, clearance rate
and tolerance to aerial
exposure
L; elevated activity of
superoxide dimutase
(SOD)
L; inhibition of
superoxide dimutase
(SOD) and catalase
activity
L; reduced
gametogenesis,
reproductive success rate
L; thickness of digestive
epithelium
oyster
Crassostrea
virginica, Eastern
oyster
-0.15
-0.28
[19]
-------
Summary of Biological Effects Tissue Concentrations for Fluoranthene
Species:
Taxa
Macoma balthica,
Baltic macoma
Macoma nasuta,
Clam
Mercenaria
mercenaria,
Northern quahog
Mya arenaria,
Softshell
Daphnia magna,
Cladoceran
Concentration, Units in1: Toxicity:
Sediment Water Tissue (Sample Type) Effects
0.218|ig/g 7.62 |ig/g lipid
OC 5.12|ig/glipid
0.436 |ig/g
OC 96.2 |ig/g lipid
0.48 |ig/g OC 7.48 |ig/g lipid
1.4 |ig/gOC 5.73 |ig/g lipid
4.55 |ig/g OC 17.2 |ig/g lipid
10.2 |ig/g
OC
19.5 |ig/g
OC
30.1 |ig/g
OC
9 |ig/L 77 nM/g
Ability to Accumulate2: Source:
Log Log
BCF BAF BSAF Reference Comments3
[17] F
0.58 [18] F
0.39
-0.26
-0.05 [19] F
-0.08 [19] F
0.51 [20] L
-------
Summary of Biological Effects Tissue Concentrations for Fluoranthene
Species:
Taxa
Hyalella azteca,
Amphipod
Hyalella azteca,
Amphipod
Concentration, Units in1: Toxicity:
Sediment Water Tissue (Sample Type) Effects
14.2 |ig/L 25.6 |ig/g
44.0 ng/g
44.8 ng/g
65.7 jj.g/g
78.4 ng/g
56.7 |ig/L 169 |ig/g
320 ng/g
458 |ig/g
751 ng/g
86.2 |ig/L 350 |ig/g
531 ng/g
714 |ig/g
800 ng/g
l,192jig/g
100.8 |ig/L 644 |ig/g
898 |ig/g
1,074 |ig/g
l,199|ig/g
1,248 ng/g
41.5|ig/L 307|ig/g
363 |ig/g
515 |ig/g
517 ng/g
763 |ig/g
815ng/g
852 |ig/g
98.3 |ig/L 566 |ig/g
825 |ig/g
829 ng/g
1,035 ng/g
1471 ng/g
1,213 ng/g
1,310 ng/g
Ability to Accumulate2:
Log Log
BCF BAF BSAF
0.51
0.54
0.54
0.56
0.57
0.59
0.55
0.57
0.54
0.60
0.59
0.58
0.62
0.61
0.61
0.59
0.60
0.56
0.58
0.58
0.59
0.60
0.63
0.63
0.60
0.61
0.61
0.61
0.61
0.63
0.60
0.61
0.58
Source:
Reference Comments3
[9] L
[9] L
[9] L
-------
Summary of Biological Effects Tissue Concentrations for Fluoranthene
Species:
Taxa
Hyalella azteca,
Amphipod
Hyalella azteca,
Amphipod
Concentration, Units in1:
Sediment Water Tissue (Sample Type)
168.0 ng/L 855 |ig/g
884 |ig/g
971 ng/g
988 |ig/g
1,265 ng/g
1,375 ng/g
184.7 |ig/L 746 |ig/g
896 |ig/g
1,208 ng/g
1,302 ng/g
1,382 ng/g
1,445 |ig/g
1,581 ng/g
1 58 nmol/g Day 1 : 1 60 nmol/g
Day 2: 140 nmol/g
Day 3: 60 nmol/g
Day 10: 90 nmol/g
Day 17: 110 nmol/g
Day 30: 120 nmol/g
634 nmol/g Day 1 : 900 nmol/g
Day 2: 1,050 nmol/g
Day 3: 850 nmol/g
Day 10: 700 nmol/g
Day 17: 700 nmol/g
Day 30:800 nmol/g
1267 nmol/g Day 1: 1,000 nmol/g
Day 2: 850 nmol/g
Day 3: 950 nmol/g
Day 10: 700 nmol/g
Day 17: 800 nmol/g
Day 30: 1,100 nmol/g
Toxicity:
Effects
no mortality
no mortality
no mortality
no mortality
no mortality
no mortality
no mortality
no mortality
no mortality
no mortality
40% mortality
40% mortality
no mortality
no mortality
no mortality
no mortality
35% mortality
65% mortality
Ability to Accumulate2: Source:
Log Log
BCF BAF BSAF Reference Comments3
0.61
0.59
0.60
0.58
0.59
0.60
0.57
0.58
0.57
0.59
0.59
0.58
0.57
[11] L
-------
Summary of Biological Effects Tissue Concentrations for Fluoranthene
Species:
Taxa
Leptocheirus
plumulosus,
Amphipod
Pontoporeia hoyi,
Amphipod
Rhepoxynius
abronius,
Amphipod
Concentration, Units in1:
Sediment Water
60 ng/g
270 ng/g
1000 ng/g
2 1.3 nmol/g
41.1 nmol/g
11 9.5 nmol/g
327.0 nmol/g
12.09 mg/kg
14.50 mg/kg
25. 11 mg/kg
38 |ig/L or
187 nmol/L
36 nmol/L
77 nmol/L
143 nmol/L
285 nmol/L
5 ng/mL
4 ng/mL
4 ng/mL
14.3 |ig/L
Toxicity: Ability to Accumulate2: Source:
Log Log
Tissue (Sample Type) Effects BCF BAF BSAF Reference Comments3
0.68 |imol/g
78 nmol/g
226 nmol/g
369 nmol/g
721 nmol/g
2,000 ng/g
2,000 ng/g
1,000 ng/g
7- 12 nmol/g
28-57 nmol/g
68-149 nmol/g
71-614 nmol/g
50% mortality [15] L; critical body residue
100% survival
100% survival
93% survival
46% survival
[21] L
1.04-1.36 [14] L
23% mortality [22] L
52% mortality
92% mortality
Chironomus riparius, 4,040 |ig/kg
Midge
181,000|ig/kg
[23]
L
Chironomus tentans 377 |ig/goc 4 |ig/L
Midge
1,220
1,853 ug/go
9,593 ng/g (larvae)
22 ng/g (adult)
33,455 ng/g (larvae)
257 ng/g (adult)
72,790 ng/g (larvae)
9,810 ng/g (adult)
0.36
0.36
0.41
0.41
0.56
0.56
[24]
L
-------
Summary of Biological Effects Tissue Concentrations for Fluoranthene
Species: Concentration, Units in1: Toxicity:
Taxa Sediment Water Tissue (Sample Type) Effects
Fishes
Oncorhynchus 379 \iglg, liver
tnykiss,
Rainbow trout
Ability to Accumulate2:
Log Log
BCF BAF BSAF
Source:
Reference Comments3
[25] F
Cypriniis carpio,
Common carp
183 mg/kg (liver)
Physiological,
NOED
[29] L; no significant
increase in erod enzyme
and P450 la protein
content
Lepomis
macrochims,
Bluegill
4,040 |ig/kg
600 |ig/kg
[23]
L
Pleuronectes vetulus, 320-25,000
English sole ng/g
<6.6 ng/g liver
<2.6 ng/g muscle
[26]
Concentration units based on wet weight unless otherwise noted.
2 BCF = bioconcentration factor, BAF = bioaccumulation factor, BSAF = biota-sediment accumulation factor.
3 L = laboratory study, spiked sediment, single chemical; F = field study, multiple chemical exposure; other unusual study conditions or observations noted.
4 This entry was excerpted directly from the Environmental Residue-Effects Database (ERED, www.wes.army.mil/el/ered, U.S. Army Corps of Engineers and U.S.
Environmental Protection Agency). The original publication was not reviewed, and the reader is strongly urged to consult the publication to confirm the information
presented here.
-------
BIOACCUMULATION SUMMARY FLUORANTHENE
References
1. IARC monographs, 1972-present, 1983, 32:356. (Cited in: USEPA. 1996. Hazardous Substances
Data Bank (HSDB). National Library of Medicine online (TOXNET). U.S. Environmental
Protection Agency, Office of Health and Environmental Assessment, Environmental Criteria and
Assessment Office, Cincinnati, OH. February.)
2. USEPA. 1989. Chemical fate rate constants for SARA section 313 chemicals and Superfund
Health Evaluation Manual chemicals. Prepared by Chemical Hazard Assessment Division,
Syracuse Research Corporation, for U.S. Environmental Protection Agency, Office of Toxic
Substances, Exposure Evaluation Division, Washington, DC, and Environmental Criteria and
Assessment Office, Cincinnati, OH. August 11.
3. Karickhoff, S.W., and J.M. Long. 1995. Internal report on summary of measured, calculated and
recommended log Kow values. Draft. Prepared by U.S. Environmental Protection Agency, Office
of Research and Development, Environmental Research Laboratory-Athens, for E. Southerland,
Office of Water, Office of Science and Technology, Standards and Applied Science Division,
Washington, DC. April 10.
4. USEPA. 1995. Integrated Risk Information System (IRIS). National Library of Medicine online
(TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental
Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. September.
5. Neff, J.M. 1995. Water quality criterion tissue level approach for establishing tissue residue
criteria for chemicals. Report to U.S. Environmental Protection Agency.
6. DeWitt, T.H., R.C. Swartz, and J.O. Lamberson. 1989. Measuring the acute toxicity of estuarine
sediments. Environ. Toxicol. Chem. 8:1035-1048.
7. Stegeman, J.J., and PJ. Kloepper-Sams. 1987. Cytochrome P-450 isozymes and monooxygenase
activity in aquatic animals. Environ. Health Perspect. 71:87-95.
8. McCarty, L.S., D. MacKay, A.D. Smith, G.W. Ozburn, and D.G. Dixon. 1992. Residue-based
interpretation of toxicity and bioconcentration QSARs from aquatic bioassays: Neutral narcotic
organics. Environ. Toxicol. Chem. 11:917-930.
9. Kane-Driscoll, S., G.A. Harkey, and P.G. Landrum. 1997. Accumulation and toxicokinetics of
flouranthene in sediment bioessays with freshwater amphipods. Environ. Toxicol. Chem. 16:742-
753.
10. Brooke, L. 1994. Memorandum to Walter Berry. Summary of results of acute and chronic
exposures of fluoranthene without and with ultraviolet (UV) light to various freshwater organisms.
December 3.
11. Harkey, G.A., S. Kane-Driscoll, and P. Landrum. 1997. Effect of feeding in 30-day
bioaccumulation assays using Hyalella azteca in fluoranthene-dosed sediment. Environ. Toxicol.
Chem. 16:762-769.
452
-------
BIOACCUMULATION SUMMARY FLUORANTHENE
12. Suedel, B.C., J.H. Rodgers, Jr., and P.A. Clifford. 1993. Bioavailability of fluoranthene in
freshwater sediment toxicity tests. Environ. Toxicol Chem. 12:155-165.
13. McCarty, L.S., and D. MacKay. 1993. Enhancing ecotoxicological modeling and assessment.
Environ. Sci. Technol 27:1719-1728.
14. Landrum, P.P., BJ. Eadie, and W.R. Faust. 1991. Toxicokinetics and toxicity of a mixture of
sediment-associated polycyclic aromatic hydrocarbons to the amphipod Diporeia spp. Environ.
Toxicol. Chem. 10:35-46.
15. Driscoll S.K., L. Schaffnerm, and R. Dickhut. 1996. Bioaccumulation and critical body burden of
fluoranthene in estuarine amphipods. Abstract, 17th Annual Meeting Society of Environmental
Toxicology and Chemistry, Washington DC, November 17-21, 1996.
16. Ankley, G.T., P.M. Cook, A.R. Carlson, DJ. Call, J.A. Swenson, H.F. Corcoran, and R.A. Hoke.
1990. Bioaccumulation of PCBs from sediments by oligochaetes and fishes. Can. J. Fish. Aquatic
Sci. 49:2080-2085.
17. Foster, G.D., and D.A. Wright. 1988. Unsubstituted polynuclear aromatic hydrocarbons in
sediments, clams, and clam worms from Chesapeake Bay. Mar. Pollut. Bull. 19:459-465.
18. Brannon, J.M., C.B. Price, FJ. Reilly, Jr., J.C. Pennington, and V.A. McFarland. 1993. Effects
of sediment organic carbon on distribution of radiolabeled fluoranthene and PCBs among sediment,
interstitial water and biota. Bull. Environ. Contain. Toxicol. 51:873-880.
19. NOAA. 1991. The potential for biological effects of sediment-sorb ed contaminants tested in the
National Status and Trends Program. NOAA Technical Memorandum NOS OMA 52. National
Oceanic and Atmospheric Administration, Office of Oceanography and Marine Assessment,
Rockville, MD.
20. Newsted, J.L., and J.P. Giesy. 1987. Predictive models for photoinduced acute toxicity of
polycyclic aromatic hydrocarbons to Daphnia magna Strauss (Cladocera, Crustacea). Environ.
Toxicol. Chem. 6:445-461.
21. Eadie, B.J., P.F. Landrum, and W. Faust. 1982. Polycyclic aromatic hydrocarbons in sediments,
pore water, and the amphipod Pontoporeia hoyi from Lake Michigan. Chemosphere 11:847-857.
22. De Witt, T.H., R.J. Ozretich, R.C. Swartz, J.O. Lamberson, D.W. Schults, G.R. Ditsworth, J.K.P.
Jones, L. Hoselton, and L.M. Smith. 1992. The influence of organic matter quality on the toxicity
and partitioning of sediment-associated fluoranthene. Environ. Toxicol. Chem. 11:197-208.
23. Clements, W.H., J.T. Oris, and T.E. Wissing. 1994. Accumulation and food chain transfer of
fluoranthene and benzo[a]pyrene in Chironomus riparius and Lepomis macrochirus. Arch.
Environ. Cont. Toxicol. 26:261-266.
24. Bell, H.E. 1995. Bioaccumulation and photoinduced toxicity of fluoranthene at different life-
stages of Chironomus tentans. Master's thesis, University of Wisconsin-Madison.
453
-------
BIOACCUMULATION SUMMARY FLUORANTHENE
25. Gerhart, E.H., and R.M. Carlson. 1978. Hepatic mixed-function oxidase activity in rainbow trout
exposed to several polycyclic aromatic compounds. Environ. Res. 17:284-295.
26. Malins, D.C., M.M. Krahn, M.S. Myers, L.D. Rhodes, D.W. Brown, C.A. Krone, B.N. McCain,
and S.L. Chan. 1985. Toxic chemicals in sediments and biota from a creosote-polluted harbor:
Relationships with hepatic neoplasms and other hepatic lesions in English sole (Parophrys vetulus).
Carcinogenesis 6:1463-1469.
27. Donkin, P., J. Widdows, S.V. Evans, C.M. Worrall, and M. Carr. 1989. Quantitative
structure-activity relationships for the effect of hydrophobic organic chemicals on rate of feeding
by mussels (Mytilus edulis). Aquat. Toxicol 14:277-294.
28. Eertman, R.H.M., C.L. Groenink, B. Sandee, and H. Hummel. 1995. Response of the blue mussel
Mytilus edulis L. Following exposure to PAHs or contaminated sediment. Mar. Environ. Res.
39:169-173.
29. Van Der Weidern, M.E.J., F.H.M Hanegraaf, M.L., Eggens, M., Celander, W. Seinen and M. Ven
Den Berg. 1994. Temporal induction of cytochrome P450 la in the mirror carp (Cyprinus carpio)
after administration of several polycyclic aromatic hydrocarbons. Environ. Toxicol. Chem.
13:797-802
30. Weinstein, J.E. 1997. Fluoranthene-induced histological alterations in oysters, Crassostrea
virginica: Seasonal field and laboratory studies. Mar. Environ. Res. 43(3):201-218.
454
-------
BIOACCUMULATION SUMMARY HEPTACHLOR
Chemical Category: PESTICIDE (ORGANOCHLORINE)
Chemical Name (Common Synonyms): HEPTACHLOR CASRN: 76-44-8
Chemical Characteristics
Solubility in Water: 0.03 mg/L [1] Half-Life: No data [2]
Log Kow: 6.26 [3] Log Koc: 6.15 L/kg organic carbon
Human Health
Oral RfD: 5 x 10~4mg/kg/day [4] Confidence: Low, uncertainty factor = 300
[4]
Critical Effect: Liver weight increases in rats; benign and malignant liver tumors in mice
Oral Slope Factor: 4.5 x 10+0 per (mg/kg)/day [4] Carcinogenic Classification: B2 [4]
Wildlife
Partitioning Factors: Partitioning factors for heptachlor in wildlife were not found in the literature.
Food Chain Multipliers: Food chain multipliers for heptachlor in wildlife were not found in the
literature.
Aquatic Organisms
Partitioning Factors: Log BCFs ranged from 5.30 to 11.70 for invertebrates and log BCFs for fishes
ranged from 3.87 to 19.34.
Food Chain Multipliers: Food chain multipliers (FCMs) for trophic level 3 aquatic organisms were 20.8
(all benthic food web), 1.6 (all pelagic food web), and 12.7 (benthic and pelagic food web). FCMs for
trophic level 4 aquatic organisms were 45.8 (all benthic food web), 3.4 (all pelagic food web), and 21.7
(benthic and pelagic food web) [18].
455
-------
BIOACCUMULATION SUMMARY HEPTACHLOR
Toxicity/Bioaccumulation Assessment Profile
Hepatchlor is the most widely used insecticide in the organochlorine class [5]. Heptachlor is resistent to
degradation and, therefore, persistent in the environment. Heptachlor acute toxic effects in animals are
principally due to hyperexcitation in the nervous system and death is frequently ascribed to respiratory
failure [5].
Heptachlor is relatively toxic to aquatic invertebrates. The acute toxicity of heptachlor ranged from 0.11
|ig/L (96-h LC50) for Penaeus duorarum to 1.5 |ig/L (96-h LC50) for Crassostrea virginica [6]. Fish
are also relatively sensitive to heptachlor. The 96-h LC50 values based on the exposure of sheepshead
minnows, pinfish, and spot were 3.68, 3.77, and 0.85|ig/L, respectively [6].
Laboratory bioaccumulation exposures with spot showed that heptachlor was metabolized to heptachlor
epoxide at all concentrations tested [7]. After 3 days of exposure, heptachlor concentrations averaged 52
percent of total residues. At the end of depuration the relative amount of heptachlor decreased to 10
percent, while heptachlor epoxide increased to 44 percent. Cooking (baking, charbroiling, canning, pan
frying and deep frying) reduced the heptachlor contents by an average 40 percent in chinook salmon
fillets [8].
Heptachlor was among chemicals responsible for the widespread decline of peregrine falcon populations
[9]. Heptachlor concentrations above 4 mg/kg in brain is critical and could be associated with falcon
mortality, while a concentration above 1.5 mg/kg in eggs was associated with lower reproductive success
of falcons [9]. Birds whose life cycle depends on the aquatic environment contained higher residues of
heptachlor in their tissue than the seed eaters [10]. The tissues of red-winged blackbirds and tree swallows
demonstrated geographically distinct levels of chlorinated hydrocarbons including heptachlor [11]. The
spatial variation of heptachlor concentration in eggs correlated significantly with those found in
sediments. Higher concentrations of heptachlor in chick tissue rather than in eggs pointed to a local source
of uptake through their diet [11].
456
-------
Summary of Biological Effects Tissue Concentrations for Heptachlor
Species:
Taxa
Invertebrates
Crassostrea
virginica,
Eastern oyster
Crassostrea
virginica,
Eastern oyster
Mercenaria
mercenaria,
Quahog clam
Mya arenaria, Soft
shell clam
Penaeiis duorarum,
Pink shrimp
Concentration, Units in1:
Sediment Water Tissue (Sample Type)
0.08 ng/L 0.43 |ig/g
0.4 |ig/L 3.1 |ig/g
0.91 |ig/L 7.7 |ig/g
4 |ig/L 18 |ig/g
14 |ig/L 55 |ig/g
0.021 mg/kg
(whole body)4
0.0 16 mg/kg
(whole body)4
0.11 mg/kg
(whole body)4
1.3 mg/kg
(whole body)4
0.04 |ig/L 0.01 |ig/g
0.2 |ig/L 0.033 |ig/g
Toxicity: Ability to Accumulate2:
Log Log
Effects BCF BAF BSAF
30% shell 7.59
reduction
28% shell
reduction
33% shell
reduction
78% shell
reduction
98% shell
reduction
Growth, ED 18
Growth, NOED
Behavior, NOED
Behavior, NOED
5% mortality 5.30
82% mortality
Source:
Reference
[6]
[6]
[6]
[6]
[6]
[6]
[6]
[15]
[15]
[6]
[6]
Comments3
L
L
L
L
L
L; exposure media 65%
heptachlor (technical grade)
L; exposure media 65%
heptachlor (technical grade)
L; no effect
L; no effect
L
L
on feeding activity
on feeding activity
-------
Species:
Taxa
Palaemonetes
vulgaris,
Grass shrimp
Fishes
Oncorhynchus
tshawytscha,
Chinook salmon
Cyprinodon
variegatus,
Sheepshead
minnow
Cyprinodon
variegatus,
Sheepshead
minnow
Cyprinodon
variegatus,
Sheepshead
minnow
Concentration, Units in1:
Sediment Water Tissue (Sample Type)
0.13|ig/L 0.062 ug/g
0.44 |ig/L 0.2 |ig/g
2 |ig/L 0.97 |ig/g
5 |ig/L 3.6 |ig/g
27.9 |ig/kg in eggs
2.7 |ig/L 20 |ig/g
3.3 |ig/L 33 |ig/g
3.6 |ig/L 34 |ig/g
4.0 |ig/L 85 |ig/g
8.8 |ig/L 133 |ig/g
4.5 mg/kg
(whole body)4
4.8 mg/kg
(whole body)4
10.4 mg/kg
(whole body)4
Toxicity: Ability to Accumulate2:
Log Log
Effects BCF BAF BSAF
6% mortality 11.70
13% mortality
70% mortality
95% mortality
Rearing mortality
15% mortality 3.87
50% mortality
50% mortality
60% mortality
85% mortality 4.33
Behavior, LOED
Behavior, LOED
Behavior, NA
Source:
Reference
[6]
[6]
[6]
[6]
[12]
[6]
[6]
[6]
[6]
[6]
[16]
[16]
[16]
Comments3
L
L
L
L
F
L
L
L
L
L
L; decreased swimming
activity
L; hyperkinetic behavior
L; hyperkinetic behavior
-------
Summary of Biological Effects Tissue Concentrations for Heptachlor
Species: Concentration, Units in1:
Taxa Sediment Water Tissue (Sample Type)
10.4 mg/kg
(whole body)4
4.5 mg/kg
(whole body)4
4.8 mg/kg
(whole body)4
10.4 mg/kg
(whole body)4
4.5 mg/kg
(whole body)4
4.8 mg/kg
(whole body)4
16 mg/kg
(whole body)4
26 mg/kg
(whole body)4
211 mg/kg
(whole body)4
0.022 mg/kg
(whole body)4
Leiostomus 0.14 jj.g/L 0.34 |ig/g
mnthurus, Spot 0.26 |ig/L 0.64 |ig/g
0.58 |ig/L 1.73 |ig/g
1.03|ig/L 3.70|ig/g
0.5|ig/L 1.5|ig/g
0.65|ig/L 2.3|ig/g
Toxicity: Ability to Accumulate2:
Log Log
Effects BCF BAF BSAF
Mortality, NA
Cellular, NOED
Cellular, NOED
Cellular, NOED
Mortality, NOED
Mortality, NOED
Mortality, LOED
Reproduction,
LOED
Reproduction,
LOED
Mortality, EDS
19.34
25% mortality
35% mortality
Source:
Reference
[16]
[16]
[16]
[16]
[16]
[16]
[17]
[17]
[17]
[6]
[7]
[7]
[7]
[7]
[7]
[7]
Comments3
L; 39% decline in survivorship
L; no effect on liver, kidney,
pancreas, digestive tract
histopathology
L; no effect on liver, kidney,
pancreas, digestive tract
histopathology
L; no effect on liver, kidney,
pancreas, digestive tract
histopathology
L; no significant effect on
mortality
L; no significant effect on
mortality
L; increase in fry mortality
L; decreased egg production
of adults
L; decreased fertility of eggs
produced by adults
L; exposure media 65%
heptachlor (technical grade)
L
L
L
L
L
L
-------
ON
O
Summary of Biological Effects Tissue Concentrations for Heptachlor
Species:
Concentration, Units in1:
Toxicity:
Ability to Accumulate2:
Source:
Taxa
Sediment
Water
Tissue
(Sample Type)
Effects
Log
BCF
Log
BAF
BSAF
Reference
Comments
3
Leiostomus
xanthurus, Spot
2.6 mg/kg
(whole body)4
0.01 mg/kg
(whole body)4
0.01 mg/kg
(whole body)4
Mortality, ED40
Mortality, NOED
Mortality, NOED
[6] L; exposure media 65%
heptachlor (technical grade)
[6] L; exposure media 65%
heptachlor (technical grade)
[6] L; exposure media 65%
heptachlor (technical grade)
Lagodon
rhomboides,
Pin fish
5.7 mg/kg
(whole body)4
Mortality, NOED
[6] L; exposure media 65%
heptachlor (technical grade)
Wildlife
Falco peregrinus
anatum,
American peregrine
0.018-2.070 mg/kg in
eggs (1965-1986)
[9] F
Falco peregrinus
pealei,
Peale's peregrine
0.015-0.049 mg/kg in
eggs (1965-1986)
[9] F
Falco peregrinus
tundrius,
Arctic peregrine
0.087-2.710 mg/kg in
eggs (1965-1987)
[9] F
-------
Summary of Biological Effects Tissue Concentrations for Heptachlor
Species:
Taxa
Concentration, Units in1: Toxicity:
Sediment Water Tissue (Sample Type) Effects
Ability to Accumulate2:
BSAF
Log
BCF
Log
BAF
Source:
Reference Comments3
Martes americana,
Marten
0.3 - 4.5 ng/kg in
muscle;
9.1 - 12.7 ng/kg in liver
[14]
Martes pennanti,
Fishers
1 - 5.7 |ig/kg in muscle
5.8 -17jj.g/kg in liver
[14]
Quail
Woodcock
Agelaius
phoeniceiis,
Red-winged
blackbird
0.2 ng/g
0.2 ng/g
0.2 ng/g
0.86- 1.15mg/kg
0.86- 1.29mg/kg
4.1 ng/g in eggs 1.05
3.7 ng/g in eggs 2.34
4.3 ng/g in eggs 1.71
[13]
[13]
[11]
[11]
[11]
F
F
F
F
F
1 Concentration units based on wet weight unless otherwise noted.
2 BCF = bioconcentration factor, BAF = bioaccumulation factor, BSAF = biota-sediment accumulation factor.
3 L = laboratory study, spiked sediment, single chemical; F = field study, multiple chemical exposure; other unusual study conditions or observations noted.
4 This entry was excerpted directly from the Environmental Residue-Effects Database (ERED, www.wes.army.mil/el/ered, U.S. Army Corps of Engineers and U.S.
Environmental Protection Agency). The original publication was not reviewed, and the reader is strongly urged to consult the publication to confirm the information
presented here.
-------
BIOACCUMULATION SUMMARY HEPTACHLOR
References
1. Kenag, E.E.; Ecotoxicol and Environ. Safety 4:26-38. 1980. (Cited in: USEPA. 1995. Hazardous
Substances Data Bank (HSDB). National Library of Medicine online (TOXNET). U.S.
Environmental Protection Agency, Office of Health and Environmental Assessment,
Environmental Criteria and Assessment Office, Cincinnati, OH. September.)
2. USEPA. 1989. Chemical fate rate constants for SARA section 313 chemicals and Superfund
Health Manual chemicals. Prepared by Chemical Hazard Assessment Division, Syracuse
Research Corporation, for U.S. Environmental Protection Agency, Office of Toxic Substances,
Exposure Evaluation Division, Washington, DC, and Environmental Criteria and Assessment
Office, Cincinnati, OH. August 11.
3. Karickhoff, S.W., and J.M. Long. 1995. Internal report on summary of measured, calculated, and
recommended log Kow values. Draft. Prepared by U.S. Environmental Protection Agency, Office
of Research and Development, Environmental Research Laboratory-Athens, for E. Southerland,
Office of Water, Office of Science and Technology, Standards and Applied Science Division,
Washington, DC. April 10.
4. USEPA. 1997. Integrated Risk Information System (IRIS). National Library of Medicine online
(TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental
Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. January.
5. Coats, J.R. 1990. Mechanisms of toxic action and structure-activity relationships for
organochlorine and synthetic pyrethroid insecticides. Environ. Health Perspect. 87:255-262.
6. Schimmel, S.C., J.M. Patrick, Jr., and J. Forester. 1976. Heptachlor toxicity and uptake by several
estuarine organisms. /. Toxicol. Environ. Health 1:955-965.
7. Schimmel, S.C., J.M. Patrick, Jr., and J. Forester. 1976. Heptachlor: Uptake, depuration, retention
and metabolism by spot, Leiostomus xanthurus. J. Toxicol. Environ. Health 2:169-178.
8. Zabik, M.E., M.J. Zabik, A.M. Booren, M. Nettles, J.H. Song, R. Welch, and H. Humphrey. 1995.
Pesticides and total polychlorinated biphenyls in chinook salmon and carp harvested from the
Great Lakes: Effects of skin-on and skin-off processing and selected cooking methods. /. Agric.
Food Chem. 43:993-1001.
9. Peakall, D.B., D.G. Noble, and J.E. Elliott. 1990. Environmental contaminants in Canadian
peregrine falcons, Falco peregrinus: A toxicological assessment. Can. Field-Naturalist 104:244-
254.
10. Frank, R., and H.E. Braun. 1990. Organochlorine residues in bird species collected dead in Ontario
1972-1988. Bull. Environ. Contam. Toxicol. 44:932-939.
11. Bishop, C.A., M.D. Koster, A.A. Chek, D.J.T. Hussell, and K. Jock. 1995. Chlorinated
hydrocarbons and mercury in sediments, red-winged blackbirds (Agelaius phoeniceus) and tree
swallows (Tachycineta bicolor) from wetlands in the Great Lakes-St. Lawrence River basin.
Environ. Toxicol. Chem. 14:491-501.
462
-------
BIOACCUMULATION SUMMARY HEPTACHLOR
12. Giesy, J.P., J. Newsted, and D.L. Garling. 1986. Relationships between chlorinated hydrocarbon
concentrations and rearing mortality of chinook salmon (Oncorhynchus tshawytschd) eggs from
Lake Michigan./. Great Lakes Res. 12:82-98.
13. Blevins, R.D. 1979. Organochlorine pesticides in gamebirds of eastern Tennessee. Water Air Soil
Pollut. 11:633-657.
14. Sleeves, T., M. Strickland, R. Frank, J. Rasper, and C.W. Douglas. 1991. Organochlorine
insecticide and polychlorinated biphenyl residues in martens and fishers from the Algonquin
region of South-Central Ontario. Bull Environ. Contam. Toxicol. 46:368-373.
15. Butler, P.A. 1971. Influence of pesticides on marine ecosystems. Proc. Royal Soc. London, Series
B 177:321-329.
16. Goodman, L.R., D.J. Hansen, J.A. Couch, and J. Forester. 1977. Effects of heptachlor and
toxaphene on laboratory-reared embryos and fry of the sheepshead minnow. Proceedings, 30th
Annual Conference, Southeastern Association of Fish and Wildlife Agencies, pp. 192-202.
17. Hansen, D.J., and P.R. Parrish. 1977. Suitability of sheepshead minnows (Cyprinodon variegatus)
for life-cycle toxicity tests. In Aquatic toxicology and hazard evaluation, ed. F.L. Mayer et al.,
pp. 117-126. American Society of Testing and Materials, Philadelphia, PA.
18. USEPA. 1998. Ambient water quality criteria derivation methodology human health: Technical
support document. Final draft. EPA-822-B-98-005. U.S. Environmental Protection Agency,
Office of Water, Washington, DC.
463
-------
464
-------
BIOACCUMULATION SUMMARY LEAD
Chemical Category: METAL
Chemical Name (Common Synonyms): LEAD CASRN: 7439-92-1
Chemical Characteristics
Solubility in Water: Insoluble [1] Half-Life: Not applicable, stable [1]
LogKow: - LogKoc: -
Human Health
Oral RfD: Not available [2] Confidence: -
Critical Effect: Changes in levels of certain blood enzymes, altered neurobehavioral development of
children. (These changes may occur at blood lead levels so low as to be essentially without a
threshold; therefore, the RfD workgroup determined that it was inappropriate to develop an RfD for
inorganic lead.)
Oral Slope Factor: Not available [2] Carcinogenic Classification: B2 [2]
Wildlife
Partitioning Factors: Partitioning factors for lead in wildlife were not found in the literature.
Food Chain Multipliers: Food chain multipliers for lead in wildlife were not found in the literature.
Aquatic Organisms
Partitioning Factors: Lead is most soluble in water and is bioavailable at low pH, low organic content,
and low concentrations of calcium, iron, manganese, zinc, and cadmium. Lead is capable of forming
insoluble metal sulfides and can easily complex with humic acid. The common forms of dissolved lead
are lead sulfate, lead chloride, lead hydroxide, and lead carbonate, but the distribution of salts is highly
dependent on the pH of the water. Most lead entering surface waters is precipitated in the sediment as
carbonates or hydroxides [8]. Log BCFs of 5.15 (cladoceran) [12] and 3.56 (midge) [9] were reported
in the literature.
Food Chain Multipliers: Although methylated lead is rapidly taken out from the water, e.g., by rainbow
trout, there is no evidence of biomagnification in the aquatic environment [6 and 7].
465
-------
BIOACCUMULATION SUMMARY LEAD
Toxicity/Bioaccumulation Assessment Profile
The amount of bioavailable lead in sediment is controlled, in large part, by the concentration of acid
volatile sulfides (AVS) and organic mater [3,4,5]. Lead is accumulated by aquatic organisms equally
from water and through dietary exposure [6]. In the sediments, a portion of lead can be transformed to
trimethyllead and tetraalkyllead compounds through chemical and microbial processes. The organolead
compounds are much more toxic to aquatic organisms than are the inorganic lead compounds [7].
Bioaccumulation of organolead compounds is rapid and high; these compounds concentrate in the fatty
tissues of aquatic organisms. Babukutty and Chacko [8] and others reported a strong correlation between
soft tissue concentration of lead in worms and that in the exchangeable fraction of the sediment.
In vertebrates, lead is known to modify the structure and function of the kidney, bone, central nervous
system, and the hematopoietic system. It produces adverse biochemical, histopathological,
neuropsychological, ferotoxic, teratogenic, and reproductive effects. Inhibition of blood delta
aminolevulnic acid dehydratase (ALAD), an enzyme critical in heme formation, has been observed as a
result of exposure to lead in a variety of fish, invertebrates, and birds. At sufficiently high concentrations,
lead effects are manifested in aquatic organisms as reduced growth, fecundity, and survivorship [9].
466
-------
Summary of Biological Effects Tissue Concentrations for Lead
Species:
Taxa
Eichhornia
crassipes,
Water hyacinth
Concentration, Units in1:
Sediment Water Tissue (Sample Type)
4.4 mg/kg (leaf)
4.6 mg/kg (leaf)
135 mg/kg (root)
259 mg/kg (root)
598 mg/kg (root)
1030 mg/kg (root)
6 mg/kg (stem)
16.6 mg/kg (stem)
48.8 mg/kg (stem)
70.6 mg/kg (stem)
4.4 mg/kg (leaf)
4.6 mg/kg (leaf)
135 mg/kg (root)
259 mg/kg (root)
598 mg/kg (root)
1,030 mg/kg (root)
6 mg/kg (stem)
16.6 mg/kg (stem)
48.8 mg/kg (stem)
70.6 mg/kg (stem)
Toxicity: Ability to Accumulate2:
Log Log
Effects BCF BAF BSAF
Growth, NOED
Growth, NOED
Growth, NOED
Growth, NOED
Growth, NOED
Growth, NOED
Growth, NOED
Growth, NOED
Growth, NOED
Growth, NOED
Morphology,
NOED
Morphology,
NOED
Morphology,
NOED
Morphology,
NOED
Morphology,
NOED
Morphology,
NOED
Morphology,
NOED
Morphology,
NOED
Morphology,
NOED
Morphology,
NOED
Source:
Reference
[20]
[20]
[20]
[20]
[20]
[20]
[20]
[20]
[20]
[20]
[20]
[20]
[20]
[20]
[20]
[20]
[20]
[20]
[20]
[20]
Comments3
L; no effect on growth
L; no effect on growth
L; no effect on growth
L; no effect on growth
L; no effect on growth
L; no effect on growth
L; no effect on growth
L; no effect on growth
L; no effect on growth
L; no effect on growth
L; no effect on plant
appearance
L; no effect on plant
appearance
L; no effect on plant
appearance
L; no effect on plant
appearance
L; no effect on plant
appearance
L; no effect on plant
appearance
L; no effect on plant
appearance
L; no effect on plant
appearance
L; no effect on plant
appearance
L; no effect on plant
appearance
ON
-J
-------
ON
OO
Summary of Biological Effects Tissue Concentrations for Lead
Species:
Taxa
Invertebrates
Invertebrates,
field-collected
Tubificidae,
Oligochaete worms
Nereis diversicolor,
Polychaete worm
Dreissena
polymorpha,
Zebra mussel
Concentration, Units in1: Toxicity: Ability to Accumulate2:
Log Log
Sediment Water Tissue (Sample Tvne) Effects BCF BAF BSAF
Total SEM
ug/g ug/g
679 569
113 62
99 55
86 50
38 19
14 4
365 ug/g
138 ug/g
375 ug/g
297 ug/g
283 ug/g
44 ug/g
154 ug/g
35 ug/g
21 Hg/g
299 ug/g
287 ug/g
359 ug/g
Filt Nonfilt Body
ug/L ug/L
<0.2 276 67 ug/g
1.2 120 11 ug/g
0.2 38 10 ug/g
0.3 35 32 ug/g
<0.2 9 4 ug/g
0.4 24 0.5 ug/g
16.5 mg/g
3.7 mg/g
23.5 mg/g
35.8 mg/g
22.6 mg/g
5.9 ug/g
4.4 ug/g
3.4 ug/g
0.7 ug/g
5.8 ug/g
4.9 ug/g
3.5 ug/g
200 mg/kg Physiological,
(whole body)6 ED 100
200 mg/kg Mortality, LOED
(whole body)6
30 mg/kg Physiological,
(whole body)6 LOED
2 mg/kg Mortality, NOED
(whole body)6
Source:
Reference Comments3
[15] F
[14] F
[10] F
[21] L; mussels stopped filtering
[21] L; increased mortality
[21] L; reduced filtration rate
[21] L; no effect on mortality
-------
Summary of Biological Effects Tissue Concentrations for Lead
Species:
Taxa
Concentration, Units in1:
Sediment Water Tissue (Sample Tvne)
4mg/kg
(whole body)6
6mg/kg
(whole body)6
30 mg/kg
(whole body)6
2 mg/kg
(whole body)6
4 mg/kg
(whole body)6
6 mg/kg
(whole body)6
Toxicity: Ability to Accumulate2:
Log Log
Effects BCF BAF BSAF
Mortality, NOED
Mortality, NOED
Mortality, NOED
Physiological,
NOED
Physiological,
NOED
Physiological,
NOED
Source:
Reference
[21]
[21]
[21]
[21]
[21]
[21]
Comments3
L; no effect on mortality
L; no effect on mortality
L; no effect on mortality
L; no effect on filtration
rate
L; no effect on filtration
rate
L; no effect on filtration
rate
Elliptic O.9-28.8
complanata, ug/g
Freshwater mussel
O.9-97.5
ND4 (foot)
ND (muscle)
5.8 ug/g (visceral)
13.0 ug/g
(hepatopancreas)
18.8 ug/g (gills)
13.9 ug/g (mantle)
5.5 ug/g (foot)
3.8 ug/g (muscle)
6.9 ug/g (visceral)
14.3 ug/g
(hepatopancreas)
36.0 ug/g (gills)
33.3 ug/g (mantle)
[16]
ON
-------
Summary of Biological Effects Tissue Concentrations for Lead
Species:
Taxa
Concentration, Units in1:
Toxicity:
Ability to Accumulate2:
Sediment Water
Tissue (Sample Tvne) Effects
Log
BCF
Log
BAF
BSAF
Source:
Reference Comments3
O.9-100.0
VS/S
ND (foot)
ND (muscle)
6.0 ug/g (visceral)
15.3 ug/g
(hepatopancreas)
35.4 ug/g (gills)
35.6 ug/g (mantle)
Balanus crenatus,
Barnacle
Daphnia magna,
Cladoceran
Hyallela azteca,
Amphipod
Total
lig/g
679
113
99
86
38
90mg/kg
(whole body)6
1,880 mg/kg
(whole body)6
5,040 mg/kg
(whole body)6
3.3 ug/L 5.8 ug/g
2.6 ug/L 7.1 ug/g
11.6 ug/L 15.8 ug/g
8.8 ug/L 19.2 ug/g
12.6 ug/L 30.0 ug/g
24.0 ug/L 20.9 ug/g
SEMFiltNonfilt Body
ug/g ug/L ug/L
569 0.2 276 7 ug/g
62 1.2 120 7 ug/g
55 0.2 38 6 ug/g
50 0.3 35 2 ug/g
19 0.2 9 6 ug/g
14 4 0.4 24 0.4 ug/g
Behavior, NOED
Reproduction,
ED 10
Mortality, ED50
60% survival
65% survival
48% survival
31% survival
11% survival
4% survival
[23]
[12]
[12]
[11]
[15]
L; regulation of metals
endpoint - summer
experiment
L; 10% reduction in
number of offspring
L; lethal body burden after
21-day exposure
L
-------
Summary of Biological Effects Tissue Concentrations for Lead
Species:
Taxa
Hyalella azteca,
Freshwater
amphipod
Pontoporeia
affmiss, Amphipod
Concentration, Units in1:
Sediment Water Tissue (Sample Tvne)
70 mg/kg
(whole body)6
160 mg/kg
(whole body)6
90 mg/kg
(whole body)6
115 mg/kg
(whole body)6
4 mg/kg
(whole body)6
4 mg/kg
(whole body)6
Total SEM FiltNonfilt Body
Toxicity: Ability to Accumulate2:
Log Log
Effects BCF BAF BSAF
Mortality, ED50
Mortality, ED50
Mortality, ED50
Mortality, ED50
Mortality, NOED
Mortality, NOED
Source:
Reference
[22]
[22]
[22]
[22]
[24]
[24]
[15]
Comments3
L; lethal body burden
L; lethal body burden
L; lethal body burden
L; lethal body burden
L; body burden estimated
from graph
L; body burden estimated
from graph
F
ug/g ug/g ug/L ug/L
679 569 0.2 276 7 ug/g
113 62 1.2 120 7 ug/g
99 55 0.2 38 6 ug/g
86 50 0.3 35 2 ug/g
38 19 0.2 9 6 ug/g
14 4 0.4 24 0.4 ug/g
Chironomus
riparius,
Midge
0.728 mg/L 2650 ug/g
3.56
[9]
Chironomus gr.
thummi, Midge
13.99 mg/kg
12.80 mg/kg
16.22 mg/kg
normal larvae
deformed larvae
[13]
-------
Summary of Biological Effects Tissue Concentrations for Lead
Species:
Taxa
Chironomus gr.
thummi,
Midge
Fishes
Salvelinus
fontinalis,
Brook trout
Concentration, Units in1:
Sediment Water Tissue (Sample Tvne)
2.56 mg/kg
(whole body)6
24 mg/kg (gill)
30 mg/kg (kidney)
20 mg/kg (liver)
3.2 mg/kg
(red blood cells)
70 mg/kg (gill)
30 mg/kg (kidney)
25 mg/kg (liver)
4.02 mg/kg
(whole body)6
4.02 mg/kg
(whole body)6
70 mg/kg (gill)
30 mg/kg (kidney)
Toxicity: Ability to Accumulate2:
Log Log
Effects BCF BAF BSAF
Morphology,
NOED
Behavior, LOED
Behavior, LOED
Behavior, LOED
Behavior, LOED
Development,
LOED
Development,
LOED
Development,
LOED
Development,
LOED
Growth, LOED
Morphology,
LOED
Morphology,
LOED
Source:
Reference
[13]
[19]
[19]
[19]
[19]
[19]
[19]
[19]
[19]
[19]
[19]
[19]
Comments3
L, 4th instar larvae
L; hyperactivity, erratic
swimming, loss of
equilibrium
L; hyperactivity, erratic
swimming, loss of
equilibrium
L; hyperactivity, erratic
swimming, loss of
equilibrium
L; hyperactivity, erratic
swimming, loss of
equilibrium
L; spinal deformities
L; spinal deformities
L; spinal deformities
L; reduced embryo
hatchability
L; reduced weight gain
L; darkening of caudal
peduncle
L; darkening of caudal
peduncle
-------
Summary of Biological Effects Tissue Concentrations for Lead
Species: Concentration, Units in1:
Taxa Sediment Water Tissue (Sample Type)
25 mg/kg (liver)
4.02 mg/kg
(whole body)6
2.55 mg/kg
(whole body)6
1 .6 mg/kg
(whole body)6
38 mg/kg (gill)
70 mg/kg (gill)
60 mg/kg (gill)
20 mg/kg (gill)
6 mg/kg (gill)
3.2 mg/kg (gonad)
43 mg/kg (kidney)
30 mg/kg (kidney)
100 mg/kg (kidney)
40 mg/kg (kidney)
Toxicity: Ability to Accumulate2:
Log Log
Effects BCF BAF BSAF
Morphology,
LOED
Morphology,
LOED
Development,
NOED
Development,
NOED
Growth, NOED
Growth, NOED
Growth, NOED
Growth, NOED
Growth, NOED
Growth, NOED
Growth, NOED
Growth, NOED
Growth, NOED
Growth, NOED
Source:
Reference
[19]
[19]
[19]
[19]
[19]
[19]
[19]
[19]
[19]
[19]
[19]
[19]
[19]
[19]
Comments3
L; darkening of caudal
peduncle
L; deformed vertebral
column
L; no effect on embryo
hatchability
L; no effect on embryo
hatchability
L; no effect on length or
weight
L; no effect on growth
L; no effect on length or
weight of first generation
fish
L; no effect on length or
weight of first generation
fish
L; no effect on length or
weight of first generation
fish
L; no effect on length or
weight
L; no effect on length or
weight
L; no effect on growth
L; no effect on length or
weight of first generation
fish
L; no effect on length or
weight of first generation
fish
-------
Summary of Biological Effects Tissue Concentrations for Lead
Species:
Taxa
Concentration, Units in1:
Toxicity:
Sediment Water
Tissue (Sample Type) Effects
Ability to Accumulate2:
Log Log
BCF BAF BSAF
Source:
Reference Comments3
8 mg/kg (kidney)
Growth, NOED
13.6 mg/kg (liver) Growth, NOED
25 mg/kg (liver)
18 mg/kg (liver)
16 mg/kg (liver)
4 mg/kg (liver)
0.6 mg/kg (muscle)
1.5 mg/kg
(red blood cells)
4 mg/kg
(red blood cells)
0.5 mg/kg
(red blood cells)
0.2 mg/kg
(red blood cells)
6 mg/kg (spleen)
2.55 mg/kg
(whole body)6
Growth, NOED
Growth, NOED
Growth, NOED
Growth, NOED
Growth, NOED
Growth, NOED
Growth, NOED
Growth, NOED
Growth, NOED
Growth, NOED
Growth, NOED
[19] L; no effect on length or
weight of first generation
fish
[19] L; no effect on length or
weight
[19] L; no effect on growth
[19] L; no effect on length or
weight of first generation
fish
[19] L; no effect on length or
weight of first generation
fish
[19] L; no effect on length or
weight of first generation
fish
[19] L; no effect on length or
weight
[19] L; no effect on length or
weight
[19] L; no effect on length or
weight of first generation
fish
[19] L; no effect on length or
weight of first generation
fish
[19] L; no effect on length or
weight of first generation
fish
[19] L; no effect on length or
weight
[19] L; no effect on weight gain
-------
Summary of Biological Effects Tissue Concentrations for Lead
Species: Concentration, Units in1:
Taxa Sediment Water Tissue (Sample Type)
1 .6 mg/kg
(whole body)6
2.55 mg/kg
(whole body)6
1 .6 mg/kg
(whole body)6
38 mg/kg (gill)
70 mg/kg (gill)
60 mg/kg (gill)
20 mg/kg (gill)
6 mg/kg (gill)
3.2 mg/kg (gonad)
43 mg/kg (kidney)
30 mg/kg (kidney)
100 mg/kg (kidney)
40 mg/kg (kidney)
8 mg/kg (kidney)
13.6 mg/kg (liver)
25 mg/kg (liver)
18 mg/kg (liver)
16 mg/kg (liver)
4 mg/kg (liver)
Toxicity: Ability to Accumulate2:
Log Log
Effects BCF BAF BSAF
Growth, NOED
Morphology,
NOED
Morphology,
NOED
Mortality, NOED
Mortality, NOED
Mortality, NOED
Mortality, NOED
Mortality, NOED
Mortality, NOED
Mortality, NOED
Mortality, NOED
Mortality, NOED
Mortality, NOED
Mortality, NOED
Mortality, NOED
Mortality, NOED
Mortality, NOED
Mortality, NOED
Mortality, NOED
Source:
Reference
[19]
[19]
[19]
[19]
[19]
[19]
[19]
[19]
[19]
[19]
[19]
[19]
[19]
[19]
[19]
[19]
[19]
[19]
[19]
Comments3
L; no effect on weight gain
L; no effect on skeletal
deformities
L; no effect on skeletal
deformities
L; no effect on mortality
L; no effect on mortality
L; no effect on survival of
first generation fish
L; no effect on survival of
first generation fish
L; no effect on survival of
first generation fish
L; no effect on mortality
L; no effect on mortality
L; no effect on mortality
L; no effect on survival of
first generation fish
L; no effect on survival of
first generation fish
L; no effect on survival of
first generation fish
L; no effect on mortality
L; no effect on mortality
L; no effect on survival of
first generation fish
L; no effect on survival of
first generation fish
L; no effect on survival of
first generation fish
-------
Summary of Biological Effects Tissue Concentrations for Lead
Species: Concentration, Units in1:
Taxa Sediment Water Tissue (Sample Type)
0.6 mg/kg (muscle)
1.5 mg/kg
(red blood cells)
4 mg/kg
(red blood cells)
0.5 mg/kg
(red blood cells)
0.2 mg/kg
(red blood cells)
6 mg/kg (spleen)
4.02 mg/kg
(whole body)6
2.55 mg/kg
(whole body)6
1.6 mg/kg
(whole body)6
38 mg/kg (gill)
70 mg/kg (gill)
60 mg/kg (gill)
20 mg/kg (gill)
6 mg/kg (gill)
3.2 mg/kg (gonad)
43 mg/kg (kidney)
Toxicity: Ability to Accumulate2:
Log Log
Effects BCF BAF BSAF
Mortality, NOED
Mortality, NOED
Mortality, NOED
Mortality, NOED
Mortality, NOED
Mortality, NOED
Mortality, NOED
Mortality, NOED
Mortality, NOED
Reproduction,
NOED
Reproduction,
NOED
Reproduction,
NOED
Reproduction,
NOED
Reproduction,
NOED
Reproduction,
NOED
Reproduction,
NOED
Source:
Reference
[19]
[19]
[19]
[19]
[19]
[19]
[19]
[19]
[19]
[19]
[19]
[19]
[19]
[19]
[19]
[19]
Comments3
L; no effect on mortality
L; no effect on mortality
L; no effect on survival of
first generation fish
L; no effect on survival of
first generation fish
L; no effect on survival of
first generation fish
L; no effect on mortality
L; no effect on mortality
L; no effect on mortality
L; no effect on mortality
L; no effect on number of
viable eggs produced
L; no effect on number of
viable eggs produced by
second generation fish
L; no effect on number of
viable eggs produced
L; no effect on number of
viable eggs produced
L; no effect on number of
viable eggs produced
L; no effect on number of
viable eggs produced
L; no effect on number of
viable eggs produced
-------
Summary of Biological Effects Tissue Concentrations for Lead
Species: Concentration, Units in1:
Taxa Sediment Water Tissue (Sample Type)
30 mg/kg (kidney)
100 mg/kg (kidney)
40 mg/kg (kidney)
8 mg/kg (kidney)
13.6 mg/kg (liver)
25 mg/kg (liver)
18 mg/kg (liver)
16 mg/kg (liver)
4 mg/kg (liver)
0.6 mg/kg (muscle)
1.5 mg/kg
(red blood cells)
4 mg/kg
(red blood cells)
0.5 mg/kg
(red blood cells)
0.2 mg/kg
(red blood cells)
6 mg/kg (spleen)
Toxicity:
Effects
Reproduction,
NOED
Reproduction,
NOED
Reproduction,
NOED
Reproduction,
NOED
Reproduction,
NOED
Reproduction,
NOED
Reproduction,
NOED
Reproduction,
NOED
Reproduction,
NOED
Reproduction,
NOED
Reproduction,
NOED
Reproduction,
NOED
Reproduction,
NOED
Reproduction,
NOED
Reproduction,
NOED
Ability to Accumulate2: Source:
Log Log
BCF BAF BSAF Reference
[19]
[19]
[19]
[19]
[19]
[19]
[19]
[19]
[19]
[19]
[19]
[19]
[19]
[19]
[19]
Comments3
L; no effect on number of
viable eggs produced by
second generation fish
L; no effect on number of
viable eggs produced
L; no effect on number of
viable eggs produced
L; no effect on number of
viable eggs produced
L; no effect on number of
viable eggs produced
L; no effect on number of
viable eggs produced by
second generation fish
L; no effect on number of
viable eggs produced
L; no effect on number of
viable eggs produced
L; no effect on number of
viable eggs produced
L; no effect on number of
viable eggs produced
L; no effect on number of
viable eggs produced
L; no effect on number of
viable eggs produced
L; no effect on number of
viable eggs produced
L; no effect on number of
viable eggs produced
L; no effect on number of
viable eggs produced
-------
-J
oo
Summary of Biological Effects Tissue Concentrations for Lead
Species:
Taxa
Pimephales
promelas,
Fathead minnow
Pimephales
promelas,
Fathead minnow
Pimephales
promelas,
Fathead minnow
Concentration, Units
Sediment Water
107 |ig/g
365 ng/g
138 |ig/g
241 |ig/g
375 ng/g
508 |ig/g
297 ng/g
377 ng/g
283 |ig/g
286 |ig/g
in1: Toxicity: Ability to Accumulate2: Source:
Log Log
Tissue (Sample Type) Effects BCF BAF BSAF Reference Comments3
10.5 mg/g [17] F
5.7 mg/g
0.8 mg/g
0.9 mg/g
20.0 mg/g
13.6 mg/g [17] F
11. 9 mg/g
19.5 mg/g
15.1 mg/g
9.3 mg/g
0.816 mg/kg (brain) Behavior, LOED [25] L; significant reduction in
feeding rate and number of
ineffective feeding
0.451 mg/kg (brain) Behavior, LOED
0.451 mg/kg (brain) Behavior, LOED
44.2 mg/kg
(whole body)6
Behavior, LOED
behaviors with 1-day-old
Daphnia
[25] L; significant reduction in
number of ineffective
feeding behaviors in lowest
test concentration with 2-
day-old Daphnia
[25] L; significant reduction in
feeding rate and number of
ineffective feeding
behaviors in lowest test
concentration with 7-day-
old Daphnia
[25] L; significant reduction in
feeding rate and number of
ineffective feeding
behaviors with 1-day-old
Daphnia
-------
Summary of Biological Effects Tissue Concentrations for Lead
Species:
Taxa
Concentration, Units in1:
Toxicity:
Ability to Accumulate2:
Sediment Water
Tissue (Sample Type) Effects
Log
BCF
Log
BAF
BSAF
Source:
Reference Comments3
26.2 mg/kg
(whole body)6
26.2 mg/kg
(whole body)6
Behavior, LOED
Behavior, LOED
0.816 mg/kg (brain) Physiological,
LOED
44.2 mg/kg
(whole body)6
Physiological,
LOED
0.451 mg/kg (brain) Behavior, NOED
0.816 mg/kg (brain) Behavior, NOED
26.2 mg/kg
(whole body)6
Behavior, NOED
[25] L; significant reduction in
number of ineffective
feeding behaviors in lowest
test concentration with 2-
day-old Daphnia
[25] L; significant reduction in
feeding rate and number of
ineffective feeding
behaviors in lowest test
concentration with 7-day-
old Daphnia
[25] L; significant reduction
norepinephrine and
serotonin levels in brain
[25] L; significant reduction
norepinephrine and
serotonin levels in brain
[25] L; no significant reduction
in feeding rate and number
of ineffective feeding
behaviors with 1-day-old
Daphnia
[25] L; no significant reduction
in number of ineffective
feeding behaviors with 2-
day-old Daphnia
[25] L; no significant reduction
in feeding rate and number
of ineffective feeding
behaviors with 1-day-old
Daphnia
-------
00
o
Summary of Biological Effects Tissue Concentrations for Lead
Species:
Taxa
Concentration, Units in1:
Toxicity:
Ability to Accumulate2:
Sediment Water
Tissue (Sample Type) Effects
Log
BCF
Log
BAF
BSAF
Source:
Reference Comments3
44.2 mg/kg
(whole body)6
0.451 mg/kg (brain)
26.2 mg/kg
(whole body)6
Behavior, NOED
Physiological,
NOED
Physiological,
NOED
[25] L; no significant reduction
in number of ineffective
feeding behaviors with 2-
day-old Daphnia
[25] L; no significant reduction
norepinephrine and
serotonin levels in brain
[25] L; No significant reduction
norepinephrine and
serotonin levels in brain
Wildlife
Sterna hirundo,
Common tern
247-389 ng/g (eggs)
912-1559 ng/g
(feathers)
[18]
Sterna forsteri,
Forster tern
174 ng/g (eggs)
1527 ng/g (feathers)
[18]
Sterna dougallii,
Roseate tern
318 ng/g (eggs)
2213 ng/g (feathers)
[18]
Rynchops niger,
Black skimmer
402-664 ng/g (eggs)
832-4091 ng/g
(feathers)
[18]
Lams argentatus,
Herring gull
1720-6743 ng/g (eggs)
1818-2101 ng/g
(feathers)
[18]
-------
Summary of Biological Effects Tissue Concentrations for Lead
Species:
Taxa
Zenaida macroura,
Mourning dove
Concentration, Units in1:
Sediment Water Tissue (Sample Type)
58.35-214.7 mg/kg
dry wt (liver alive)
267.3 mg/kg
dry wt (liver dead)
346- 1,297.6 mg/kg
dry wt (kidney alive)
1,901 mg/kg
drv wt (kidnev dead)
Toxicity: Ability to Accumulate2: Source:
Log Log
Effects BCF BAF BSAF Reference Comments3
Cellular [26] L; dosage was ingested lead
abnormalities shot pellets
increased with
increasing tissue
concentrations
1 Concentration units based on wet weight unless otherwise noted.
2 BCF = bioconcentration factor, BAF = bioaccumulation factor, BSAF = biota-sediment accumulation factor.
3 L = laboratory study, spiked sediment, single chemical; F = field study, multiple chemical exposure; other unusual study conditions or observations noted.
4 ND = not detected.
5 CBR = critical body residue.
6 This entry was excerpted directly from the Environmental Residue-Effects Database (ERED, www.wes.army.mil/el/ered, U.S. Army Corps of Engineers and U.S.
Environmental Protection Agency). The original publication was not reviewed, and the reader is strongly urged to consult the publication to confirm the information
presented here.
-------
BIOACCUMULATION SUMMARY LEAD
References
1. Weast handbook of chemistry and physics, 68th edition, 1987-1988, B-99. (Cited in: USEPA. 1995.
Hazardous Substances Data Bank (HSDB). National Library of Medicine online (TOXNET). U.S.
Environmental Protection Agency, Office of Health and Environmental Assessment, Environmental
Criteria and Assessment Office, Cincinnati, OH. September.)
2. USEPA. 1995. Integrated Risk Information System (IRIS). National Library of Medicine online
(TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental
Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. September.
3. Di Toro, D.M., J.D. Mahony, DJ. Hansen, K.J. Scott, M.B. Hicks, S.M. Mayr, and M.S. Redmond.
1990. Toxicity of cadmium in sediments: The role of acid volatile sulfide. Environ. Toxicol Chem.
9:1487-1502.
4. Casas, A.M., and E.A. Crecelius. 1994. Relationship between acid volatile sulfide and the toxicity
of zinc, lead and copper in marine sediments. Environ. Toxicol. Chem. 13:529-536.
5. Kerndorff, H., and M. Schnitzer. 1980. Sorption of metals on humic acid. Geochim. Cosmochim.
Acta 44:1701-1708.
6. Woodward, D.F., W.G. Brumbaugh, AJ. DeLonay, E.E. Little, and C.E. Smith. 1994. Effects on
rainbow trout fry of a metals-contaminated diet of benthic invertebrates from the Clark Fork River,
Montana. Trans. Amer. Fish. Soc. 123:51-62.
7. Hodson, P.V., D.M. Whittle, P.T.S. Wong, U. Borgmann, R.L. Thomas, Y.K. Chau, J.O. Nriagu,
and DJ. Hallett. 1984. Lead contamination of the Great Lakes and its potential effects on aquatic
biota. In Toxic contaminants in the Great Lakes, ed. J.O. Nriagu and M.S. Simmons, chapter 16:
Advances in Environmental Sciences and Technology, Wiley and Sons, Toronto, Ontario.
8. Babukutty, Y., and J. Chacko. 1995. Chemical partitioning and bioavailability of lead and nickel
in an estuarine system. Environ. Toxicol. Chem. 14:427-434.
9. Timmermans, K.R., W. Peelers, and M. Tonkes. 1992. Cadmium, zinc, lead, and copper in
Chironomus riparius (Meigen) larvae (Diptera, Chironomidae): Uptake and effects. Hydrobiologia
241:119-134.
10. Bryan, G.W., and L.G. Hummerstone. 1971. Adaptation of the polychaete Nereis diversicolor to
estuarine sediments containing high concentrations of heavy metals. Mar. Biol. Ass. 51:845-863.
11. Borgmann, U., W.O. Norwood, and C. Clarke. 1993. Accumulation, regulation and toxicity of
copper, zinc, lead and mercury in Hyalella azteca. Hydrobiologia 259:79-89.
12. Enserink, E.L., J.L. Mass-Diepeveen, and C.J. Van Leeuwen. 1991. Combined effects of metals:
An ecotoxicological evaluation. Water Res. 25:679-687.
482
-------
BIOACCUMULATION SUMMARY LEAD
13. Janssens De Bisthoven, L.G., K.R. Timmermans, and F. Ollevier. 1992. The concentration of
cadmium, lead, copper, and zinc in Chironomus gr. thummi larvae (Diptera, Chironomidae) with
deformed versus normal antennae. Hydrobiologia 239:141-149.
14. Krantzberg, G. 1994. Spatial and temporal variability in metal bioavailability and toxicity of
sediment from Hamilton Harbour, Lake Ontario. Environ. Toxicol Chem. 13:1685-1698.
15. Ingersoll, C.G., W.G. Brumbaugh, FJ. Dwyer, andN. E. Kemble. 1994. Bioaccumulation of metals
by Hyalella azteca exposed to contaminated sediments from the Upper Clark Fork River, Montana.
Environ. Toxicol. Chem. 13:2013-2020.
16. Tessier, A., P.G.C. Campbell, J.C. Auclair, and M. Bisson. 1984. Relationships between the
partitioning of trace metals in sediments and their accumulation in the tissues of the freshwater
mollusk Elliptio complanata in a mining area. Can. J. Fish. Aquat. Sci. 41:1463-1472.
17. Krantzberg, G. 1994. Spatial and temporal variability in metal bioavailability and toxicity of
sediment from Hamilton Harbour, Lake Ontario. Environ. Toxicol. Chem. 13:1685-1698.
18. Burger, P.M., and CJ. Gochfield. 1993. Lead and cadmium accumulation in eggs and fledgling
seabirds in the New York Bight. Environ. Toxicol. Chem. 12:261-267.
19. 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 (Salvelinus fontinalis). J. Fish. Res. Bd. Can.
33:1731-1741.
20. Kay, S.H., W.T. Haller, and L.A. Garrard. 1984. Effects of heavy metals on water hyacinths
(Eichhornia crassipes (mart.) Solms). Aquat. Toxicol. 5:117-128.
21. Kraak, M.H.S., Y.A. Wink, S.C. Stuijfzand, M.C. Buckert-de Jong, CJ. De Groot, and W.
Admiraal. 1994. Chronic ecotoxicity of Zn and Pb to the zebra mussel Dreissena polymorpha.
Aquat. Toxicol. 30:77-89.
22. Maclean, R.S., U. Borgmann, and D.G. Dixon. 1993. Lead accumulation and toxicity in Hyalella
azteca. 14th Annual Meeting Society of Environmental Toxicology and Chemistry, Houston, TX,
November 14-18, 1993.
23. Powell, M.I., and K.N. White. 1990. Heavy metal accumulation by barnacles and its implications
for their use as biological monitors. Mar. Environ.Res. 30:91-118.
24. Sundelin, B. 1984. Single and combined effects of lead and cadmium on Pontoporeia affinis
(Crustacea, Amphipoda) in laboratory soft-bottom microcosms. In Ecotoxicological testing for the
marine environment, Vol. 2, ed. G. Persoone, E. Jaspers, and C. Claus. State University of Ghent
and Institute of Marine Scientific Research, Bredene, Belgium.
25. Weber, D.N., A. Russo, D.B. Seale, and R.E. Spieler. 1991. Waterborne lead affects feeding
abilities and neurotransmitter levels of juvenile fathead minnows (Pimephales promelas). Aquatic
Toxicol. 21:71-80.
483
-------
BIOACCUMULATION SUMMARY LEAD
26. Kendall, R.J., and P.P. Scanlon. 1983. Histologic and ultrastructural lesions of mourning doves
(Zenaida macroura) poisoned by lead shot. Poult. Sci. 62:952-956.
484
-------
BIOACCUMULATION SUMMARY METHYLMERCURY
Chemical Category: METAL
Chemical Name: METHYLMERCURY CASRN: 22967-92-6
Chemical Characteristics
Solubility in Water: No data [1] Half-Life: No data [2]
LogKow: - LogKoc: -
Human Health
Oral RfD: 1 x 10"4 mg/kg-day [3] Confidence: Medium, uncertainty factor = 10
Critical Effect: Developmental neurologic abnormalities in infants
On May 1, 1995, IRIS was updated to include an oral RfD of 1 x 10"4 mg/kg/d based on developmental
neurological effects in human infants. An oral RfD of 3 x 10"4 mg/kg/d for chronic systemic effects of
methylmercury among the general adult population was available in IRIS until May 1, 1995; however,
it was not listed in the IRIS update on that date. For the purposes of calculating an SV for methylmercury
that is protective of developing fetuses and nursing infants, EPA's Office of Water has chosen to continue
to use the general adult population RfD of 3 x 104 mg/kg/d for chronic systemic effects of methylmercury
until a value is relisted in IRIS, and to reduce this value by a factor of 5 to derive an RfD of 6 x 10"5
mg/kg/d for developmental effects among fetuses and nursing infants. The protective factor of 5 is based
on experimental results that suggest a possible 5-fold increase in fetal sensitivity to methylmercury
exposure. This more protective approach recommended by the Office of Water was deemed to be most
prudent at this time. This approach should be considered interim until such time as the Agency has
reviewed new studies on the chronic and developmental effects of methylmercury.
Oral Slope Factor: - Carcinogenic Classification: C [3]
Wildlife
Partitioning Factors: Over 90 percent of methylmercury is absorbed from the gastrointestinal tract in
animals, and following such absorption most accumulates in erythrocytes, giving red cell to plasma ratios
of up to 300 to 1 [4]. This allows for efficient transport through the body and results in a generally
uniform pattern of distribution in tissues and organs—blood, kidney, and brain concentrations are within
a range of one to three by ratio [5]. There is an exceptional ability of methylmercury to pass the blood-
brain barrier, and injury to the central nervous system then arises by strong binding of methylmercury to
sulfhydryl residues and subsequent release of mercuric ions to binding sites in the central nervous system.
The slow elimination of methylmercury from the body is a result of the high erythrocyte-plasma ratio [4].
Mercury will accumulate in both cerebellum and also cerebral cortex, where it will be tightly bound by
sulfhydryl groups. Inside the cell, methylmercury will inhibit protein synthesis and RNA synthesis [6,7].
The effects are particularly important in the developing fetal and young brain of most animals. The ability
485
-------
BIOACCUMULATION SUMMARY METHYLMERCURY
of methylmercury to penetrate the placental barrier leads to accumulation in the fetus. The rate of
transport across the placental barrier is 10-fold higher than for inorganic mercury. It appears that fetal
tissue has a greater binding ability for methylmercury than does the pregnant mother. Exposure via milk
is also important for feeding babies. It does appear that pregnant animals may detoxify themselves by
transferences to their fetuses [8].
Food Chain Multipliers: In birds, there is a tendency for mercury concentrations to be highest in species
feeding on fish (or on other seabirds) [9]. However, when one compares mercury levels among
predominantly fish-eating species, levels apparently do not show clear patterns or any evident association
with diet composition [10]. Particularly high concentrations have been found in some species of
procellariiforms [11]. There is an inverse relationship between total mercury and percent methylmercury
in tissues of various avian species [12,13]. Overall, the form of mercury in seabirds is predominantly
inorganic, suggesting that biotransformation of ingested methylmercury is an important mechanism by
which long-lived and slow-moulting seabirds avoid the toxic effects of accumulating large quantities of
methylmercury [14,15]. Among furbearers, mecury burdens are higher in fish-eating species than in
herbivorous ones [16]. Mink and river otter accumulate about 10 times more mercury than predatory
fishes from the same areas [17]. Nonmarine mammals with mercury concentrations in the liver and
kidney in excess of approximately 30 mg/kg of wet weight were likely to suffer mercury intoxification.
The results of laboratory studies support this value and indicate that a dietary methylmercury
concentration of aproximately 2 to 6 mg/kg of wet weight produced mercury poisoning in feeding
experiments using a range of mammalian species [18].
Aquatic Organisms
Partitioning Factors: Concentrations of total mercury in water are usually low, typically on the order
of a few nanograms per liter. Elemental mercury adsorbs to sediments, where methylmercury can be
produced and destroyed by microbial processes. This complex process is affected by environmental
factors [1]. A significant fraction of the total mercury in water is found in the form of methylmercury,
the species predominantly accumulated by aquatic organisms [19]. In the Onondaga Lake food web, the
percent of total mercury occurring as methylmercury was determined as follows [20]:
Lake water 5%
Interstitial water 37%
Phytoplankton 24%
Zooplankton 40%
Benthic macroinvertebrates 26%
Fishes 96%
Bioconcentration factors (BCFs) for methylmercury are highly variable. Log BCFs for methylmercury
in brook trout range from 4.84 to 5.80, depending on the tissue analyzed. Methylmercury concentrations
and bioaccumulation factors (BAFs) increased with higher trophic levels in both the pelagic and benthic
components of aquatic food webs [20].
Food Chain Multipliers: Fish bioconcentrate methylmercury directly from water by uptake across the
gills [21,22,23] and piscivores, such as walleye, readily accumulate mercury from dietary sources [24,25].
Methylmercury accumulation from either source may be substantial, but the relative contribution of each
486
-------
BIOACCUMULATION SUMMARY METHYLMERCURY
pathway may vary with fish species [26,27,28,29]. In addition, invertebrates generally have a lower
percentage of methylmercury in their tissues than fish or marine mammals [30]. The percentage of
methylmercury increases with age in both fish and invertebrates [30].
Mercury is accumulated by all trophic levels with biomagnification occurring up the food web. While
sediment is usually the primary source of methylmercury in most aquatic systems, the food web is the
main pathway for accumulation [24,25]. High concentrations of organic substances and reduced sulfur
can complex free mercury ions in the sediment and reduce the availability to organisms [31,32].
Methylmercury can be accumulated directly from the water by uptake across the gills [21,22,23]. High-
trophic-level species tend to accumulate the most methylmercury, with concentrations highest in fish-
eating predators. Methylmercury concentrations in higher trophic species often do not correlate with
concentrations in environmental media. Correlations have been made between sediment and lower
trophic species that typically have a high percentage of inorganic mercury, and between mercury
concentrations in higher trophic species and their prey items. The best measure of bioavailability of
mercury in any system can be obtained through analysis of mercury concentrations in the biota at the
specific site.
The transfer efficiency of mercury through the food web is affected by the form of mercury. Although
inorganic mercury is the dominant form in the environment and easily accumulated, it is also depurated
quickly. Methylmercury accumulates quickly, depurates very slowly, and therefore has a greater potential
to biomagnify in higher-trophic-level species. Pharmacologic half-lives of total mercury in tissues of
aquatic organisms have been estimated at approximately 2 months to 1 year in saltwater mussels, 1 to
more than 3 years in fishes, and 1.4 to 2.7 years in pinnipeds and dolphins [33]. As the concentration of
methylmercury increases in prey items, the transfer efficiency also increases [34]. Methylmercury
accumulation from either the water column or food sources might be substantial, but the relative
contribution of each pathway varies from species to species [26,27,28,29]. Invertebrates generally have
a lower percentage of methylmercury in their tissues than fish or marine mammals, but the percentage can
vary greatly, from 1 percent in deposit-feeding polychaetes to almost 100 percent in crabs.
The amount of methylmercury in animal tissues increases proportionately with the age of the organism,
with the exception of marine mammals. Because marine mammals feed primarily on fish, they have the
greatest potential for the highest tissue concentrations of methylmercury compared to other marine
organisms. Contrary to other species or groups of animals, the tissue concentrations of methylmercury
are higher in juvenile marine mammals than in adults because the adults can mineralize methylmercury
into inorganic mercury [33].
Toxicity/Bioaccumulation Assessment Profile
Methylmercury is the most hazardous mercury species due to its high stability, its lipid solubility, and its
ionic properties that lead to a high ability to penetrate the membranes of living organisms [35]. Because
methylmercury is lipid-soluble, it can rapidly penetrate the blood-brain barrier [36,37,38,39,40]. Injury
to the central nervous system arises by accumulation in the cerebellum and cerebral cortex, where
methylmercury binds tightly to sulfhydryl groups, resulting in pathological changes [41]. Inside the cell,
methylmercury inhibits protein synthesis and RNA synthesis [6,7].
487
-------
BIOACCUMULATION SUMMARY METHYLMERCURY
The early developmental stages of organisms are the most sensitive to the toxic effects of mercury, with
methylmercury being more toxic than inorganic mercury. Mercury adversely affects reproduction,
growth, behavior, osmoregulation, and oxygen exchange in aquatic organisms. In birds and mammals,
comparatively low concentrations of mercury have adverse effects on growth and development, behavior,
motor coordination, vision, hearing, histology, and metabolism [33].
Toxicity of methylmercury is dependent on temperature [42], oxygen conditions [43], salinity [44], and
the presence of other metals such as zinc and lead [45]. The complex behavior of methylmercury in
sediments makes it difficult to predict toxicity from bulk sediment chemistry. Toxicity of mercury has
been linked with bioaccumulation, but the situation is complicated by the fact that some animals exposed
to low concentrations of mercury can build up a tolerance to this contaminant, as well as detoxify the free
metal within their cells via the production of metailothioneins and other metal-binding proteins. Brown
et al. [46] propose that toxic effects occur as the binding capacity of these metal-binding proteins becomes
saturated.
488
-------
Summary of Biological Effects Tissue Concentrations for Methylmercury
Species:
Taxa
Invertebrates
Phytoplankton
Concentration, Units in1: Toxicity:
Sediment Water Tissue (Sample Type) Effects
Interstitial 32 |ig/kg
water:
0.003 ng/L
Lake water:
0.0003 |ig/L
Ability to Accumulate2:
Log Log
BCF BAF BSAF
5.00
Source:
Reference Comments3
[20] F; estimated from
chart; chart reported
log BAF values
Crepidula fornicata,
Slipper limpet
9.00045013427734
mg/kg (whole body)5
Growth, ED25
15.0007495880126
mg/kg (whole body)5
Reproduction,
LOED
[62] L; approximate 25%
reduction in growth
at lowest test
concentration; algal
food contained
mercury at
approximatley 2.9
|ig/L in addition to
water concentration
[62] L; significant effect
on fecundity
(number of
gametes); exposure
includes mercury in
food at
approximately 9.5
-------
Summary of Biological Effects Tissue Concentrations for Methylmercury
Species:
Taxa
Concentration, Units in1:
Toxicity:
Ability to Accumulate2:
Source:
Log Log
Sediment Water Tissue (Sample Type) Effects BCF BAF BSAF Reference Comments3
30.0014991760253 Development,
mg/kg (whole body)5 NOED
[62] L; no significant
effect on number of
live spat at peak
settlement; exposure
includes mercury in
food at
approximately 3 1
30.0014991760253
mg/kg (whole body)5
Reproduction,
NOED
[62] L; no significant
effect on ability to
produce gametes;
exposure includes
mercury in food at
approximately 3 1
9.00045013427734
mg/kg (whole body)5
Reproduction,
NOED
[62] L; no significant
effect on fecundity
(number of
gametes); exposure
includes mercury in
food at
approximately 2.9
-------
Summary of Biological Effects Tissue Concentrations for Methylmercury
Species: Concentration, Units in1:
Taxa Sediment Water
Elliptic complanata,
Freshwater mussel
Rangia cuneata,
Marsh clam
Zooplankton, Interstitial
Cladocerans water:
0.003 ng/L
Lake water:
0.0003 ng/L
Tissue (Sample Type)
43 ng/kg
12 mg/kg
(whole body)5
28 mg/kg
(whole body)5
73.1399993896484
mg/kg (whole body)5
6 mg/kg
(whole body)5
260 |ig/kg
Toxicity: Ability to Accumulate2:
Log Log
Effects BCF BAF BSAF
Relative to least
contaminated
station (17.9
mg/kg, dry total
Hg in sediment
vs. 0.07 mg/kg,
dry), whole
animal ww was
reduced by 97
percent
Mortality, ED50
Mortality, ED50
Mortality,
LOED
Mortality,
NOED
5.94
Source:
Reference Comments3
[48] F; 42 and 84 days
exposure;
probable effects at
tissue
concentrations >34
|ig/kg, ww
[54] L; lethal to 50% of
clams in 7 days
[54] L; lethal to 50% of
clams in 7 days
[54] L; lethal body
burden
[54] L; no effect on
mortality
[20] F; estimated from
chart; chart reported
log BAF values
-------
Summary of Biological Effects Tissue Concentrations for Methylmercury
Species: Concentration, Units in1: Toxicity: Ability to Accumulate2: Source:
Log Log
Taxa Sediment Water Tissue (Sample Type) Effects BCF BAF BSAF Reference Comments3
Diaptomus
oregonensis
Diaptomus minutus,
Zooplankton
Holopedium
gibberum,
Zooplankton
Unfiltered 22-66 |ig/kg (dw) 7.10
water:
total Hg =
0.43-4.79 ng/L
MeHg = 0.04-
2.20 ng/L
Filtered water: 4.04
total Hg =
0.27-4.50 ng/L
MeHg =
0.03- 1.95 ng/L
Unfiltered 40-419 |ig/kg (dw)
water:
total Hg =
0.43-4.79 ng/L
MeHg = 0.04-
2.20 ng/L
Filtered water:
total Hg =
0.27-4.50 ng/L
MeHg =
0.03- 1.95 ng/L
[47] F; results were
summarized for
zooplankton and
water samples taken
from 12 lakes -
ranges are given
[47] F; results were
summarized for
zooplankton and
water samples taken
from 12 lakes -
ranges are given
[47] F; results were
summarized for
biota and water
samples taken from
12 lakes - ranges are
given
-------
Summary of Biological Effects Tissue Concentrations for Methylmercury
Species: Concentration, Units in1: Toxicity: Ability to Accumulate2: Source:
Log Log
Taxa Sediment Water Tissue (Sample Type) Effects BCF BAF BSAF Reference Comments3
Bosmina
longirostris,
Cladoceran
Daphnia pulex
Daphnia galeatra
mendotae
Daphnia ambigua,
Cladocerans
Unfiltered 479 |ig/kg (dw)
water:
total Hg =
0.43-4.79 ng/L
MeHg = 0.04-
2.20 ng/L
Filtered water:
total Hg =
0.27-4.50 ng/L
MeHg =
0.03- 1.95 ng/L
Unfiltered 1-211 |ig/kg (dw)
water:
total Hg =
0.43-4.79 ng/L
MeHg4 = 0.04-
2.20 ng/L
Filtered water:
total Hg =
0.27-4.50 ng/L
MeHg =
0.03- 1.95 ng/L
[47] F; results were
summarized for
biota and water
samples taken from
12 lakes - ranges are
given
[47] F; results were
summarized for
biota and water
samples taken from
12 lakes - ranges are
given
Daphnia magna,
Cladoceran
18.3999996185302
mg/kg (whole body)5
Mortality, ED25
[51] L; 25% reduction in
survival compared
to controls in 21
days
-------
Summary of Biological Effects Tissue Concentrations for Methylmercury
Species:
Taxa
Concentration, Units in1:
Toxicity:
Ability to Accumulate2:
Log Log
Sediment Water Tissue (Sample Type) Effects BCF BAF BSAF
Source:
Reference Comments3
2.32800006866455
mg/kg (whole body)5
Reproduction,
NA
1.63999998569488 Reproduction,
mg/kg (whole body)5 NA
4.67000007629394 Reproduction,
mg/kg (whole body)5 NA
7.57000017166137 Reproduction,
mg/kg (whole body)5 NA
18.3999996185302 Reproduction,
mg/kg (whole body)5 NA
0.859000027179718
mg/kg (whole body)5
1.52600002288818
mg/kg (whole body)5
2.32800006866455
mg/kg (whole body)5
1.63999998569488
mg/kg (whole body)5
4.67000007629394
mg/kg (whole body)5
Mortality,
NOED
Mortality,
NOED
Mortality,
NOED
Mortality,
NOED
Mortality,
NOED
[51] L; 32% reduction in
number of neonates
produced in 21 days
[51] L; 35% reduction in
number of neonates
produced in 21 days
[51] L; 62% reduction in
number of neonates
produced in 21 days
[51] L; 63% reduction in
number of neonates
produced in 21 days
[51] L; 99% reduction in
number of neonates
produced in 21 days
[51] L; no effect on
mortality
[51] L; no effect on
mortality
[51] L; no effect on
mortality
[51] L; no effect on
mortality
[51] L; no effect on
mortality
-------
Summary of Biological Effects Tissue Concentrations for Methylmercury
Species:
Taxa
Daphnia magna,
Cladoceran
Concentration, Units in1:
Sediment Water Tissue (Sample Type)
7.57000017166137
mg/kg (whole body)5
0.859000027179718
mg/kg (whole body)5
1.52600002288818
mg/kg (whole body)5
0.790000021457672
mg/kg (whole body)5
91.3000030517578
Toxicity: Ability to Accumulate2:
Log Log
Effects BCF BAF BSAF
Mortality,
NOED
Reproduction,
NOED
Reproduction,
NOED
Reproduction,
ED10
Mortality, ED50
Source:
Reference
[51]
[51]
[51]
[55]
[55]
Comments3
L; no effect on
mortality
L; no significant
reproductive
impairment
L; no significant
reproductive
impairment
L; 10% reduction in
number of offspring
L; lethal body
mg/kg (whole body)
burden after 21 day
exposure
Benthic
invertebrates
Scientific names not
given
(amphipods and
chironomids)
Interstitial
water:
0.003 |ig/L
Lake water:
0.0003 |ig/L
25 |ig/kg
8.3xl04
[20]
Palaemonetes
pugio, Grass shrimp
1.09399998188018 Behavior,
mg/kg (whole body)5 LOED
[50] L; decreased
sensitivity to
physical disturbance
-------
Summary of Biological Effects Tissue Concentrations for Methylmercury
Species:
Taxa
Concentration, Units in1:
Toxicity:
Ability to Accumulate2:
Log Log
Sediment Water Tissue (Sample Type) Effects BCF BAF BSAF
Source:
Reference Comments3
2.12299990653991 Mortality,
mg/kg (whole body)5 NOED
[50] L; no statistically
significant increase
in mortality
Uca pugnax,
Fiddler crab
12.329999923706 Development,
mg/kg (whole body)5 LOED
19.4200000762939 Development,
mg/kg (whole body)5 LOED
[53] L; inhibition of limb
regeneration and
molting in male
crabs
[53] L; inhibition of limb
regeneration and
molting in female
crabs
Fishes
Squalus acanthias,
Spiny dogfish
0.0930000022053719 Mortality,
mg/kg (whole body)5 NOED
[57]
L; no effect on
mortality in 24
hours
-------
Summary of Biological Effects Tissue Concentrations for Methylmercury
Species:
Concentration, Units in1:
Toxicity:
Ability to Accumulate2:
Source:
Taxa
Oncorhynchus
mykiss,
Rainbow trout
Sediment Water
Exposure
concentrations
(CH3HgCl):
4|ig/L
Exposure
concentrations
Log
Tissue (Sample Type) Effects BCF
kidney = 74±30 58 .2 d±2 1 .4
(16-1 16 mg/kg)
liver = 76± 19
(32-1 14 mg/kg)
spleen = 89±38
(32-1 18 mg/kg)
brain = 19±8
(7-32 mg/kg)
muscle = 31±12
(9-52 mg/kg)
gill = 66±15
(42-93 mg/kg)
whole fish =11.2±6.1 24.2 d±5.6
(4.0-27.3 mg/kg)
Log
BAF BSAF Reference Comments3
[49] L; d = mean days to
death ± SD; n = 20
fish per treatment.
[49]
(CH3HgCl):
9|ig/L
Exposure
concentrations
(CH3HgCl):
lO^g/L
kidney = 64±20
(40-116 mg/kg)
liver = 47±10
(27-65 mg/kg)
spleen = 72±22
(37-112 mg/kg)
brain = 13±3
(7-19 mg/kg)
muscle = 18±5
(9-27 mg/kg)
gill = 51±12
(34-85 mg/kg)
21.7d±6.0
[49] L; n = 20 per
treatment; d = days
to death; n = 20 per
treatment.
-------
Summary of Biological Effects Tissue Concentrations for Methylmercury
Species: Concentration, Units in1:
Taxa Sediment Water
Exposure
concentrations
(CH3HgCl):
13ng/L
Exposure
concentrations
(CH3HgCl):
34|ig/L
Toxicity:
Tissue (Sample Type) Effects
kidney =39±21 7.6d±5.1
(19-91 mg/kg)
liver = 42±27
(16- 129 mg/kg)
spleen = 51 ±3 8
(19-194 mg/kg)
brain = 7.7±5.6
(2.3-22 mg/kg)
muscle = 6.2±7.7
(1.2-26 mg/kg)
gill = 64±15
(36-98 mg/kg)
kidney = 6.2±2.7 l.Od
(2.3-10 mg/kg)
liver = 7.2±2.8
(3. 0-1 2 mg/kg)
spleen = 6.4±3.2
(2.7- 14 mg/kg)
brain = 1.1±0.3
(0.6-1. 5 mg/kg)
muscle = 0.7±0.3
(2.7- 14 mg/kg)
gill = 56±12
(29-73 mg/kg)
Ability to Accumulate2: Source:
Log Log
BCF BAF BSAF Reference Comments3
[49] L; n = 20 per
treatment; d = days
to death; n = 20 per
treatment.
[49] L; d = mean days to
death (no SD
reported)
Oncorhynchus
mykiss, Rainbow
trout
1.60000002384185 Growth, NOED
mg/kg (blood)5
0.100000001490116 Growth, NOED
mg/kg (blood)5
[52
[52
L; no effect on
growth
L; no effect on
growth
-------
Summary of Biological Effects Tissue Concentrations for Methylmercury
Species: Concentration, Units in1:
Taxa Sediment Water Tissue (Sample Type)
0.5 mg/kg (brain)5
0.100000001490116
mg/kg (brain)5
0.400000005960464
mg/kg (gill)5
0.100000001490116
mg/kg (gill)5
1.60000002384185
mg/kg (kidney)5
0.200000002980232
mg/kg (kidney)5
1 mg/kg (liver)5
0.100000001490116
mg/kg (liver)5
0.5 mg/kg (muscle)5
0.100000001490116
mg/kg (muscle)5
1.60000002384185
mg/kg (posterior
Toxicity: Ability to Accumulate2:
Log Log
Effects BCF BAF BSAF
Growth, NOED
Growth, NOED
Growth, NOED
Growth, NOED
Growth, NOED
Growth, NOED
Growth, NOED
Growth, NOED
Growth, NOED
Growth, NOED
Growth, NOED
Source:
Reference
[52]
[52]
[52]
[52]
[52]
[52]
[52]
[52]
[52]
[52]
[52]
Comments3
L; no effect on
growth
L; no effect on
growth
L; no effect on
growth
L; no effect on
growth
L; no effect on
growth
L; no effect on
growth
L; no effect on
growth
L; no effect on
growth
L; no effect on
growth
L; no effect on
growth
L; no effect on
growth
intestine)5
-------
o
Summary of Biological Effects Tissue Concentrations for Methylmercury
Species: Concentration, Units in1:
Taxa Sediment Water Tissue (Sample Type)
6 mg/kg (posterior
intestine)5
1.29999995231628
mg/kg (spleen)5
0.300000011920929
mg/kg (spleen)5
0.140000000596046
mg/kg (whole body)5
0.469999998807907
mg/kg (whole body)5
1.60000002384185
mg/kg (blood)5
0.100000001490116
mg/kg (blood)5
0.5 mg/kg (brain)5
0.100000001490116
mg/kg (brain)5
0.400000005960464
mg/kg (gill)5
0.100000001490116
mg/kg (gill)5
1.60000002384185
mg/kg (kidney)5
Toxicity: Ability to Accumulate2:
Log Log
Effects BCF BAF BSAF
Growth, NOED
Growth, NOED
Growth, NOED
Growth, NOED
Growth, NOED
Mortality,
NOED
Mortality,
NOED
Mortality,
NOED
Mortality,
NOED
Mortality,
NOED
Mortality,
NOED
Mortality,
NOED
Source:
Reference
[52]
[52]
[52]
[52]
[52]
[52]
[52]
[52]
[52]
[52]
[52]
[52]
Comments3
L; no effect on
growth
L; no effect on
growth
L; no effect on
growth
L; no effect on
growth
L; no effect on
growth
L; no effect on
mortality
L; no effect on
mortality
L; no effect on
mortality
L; no effect on
mortality
L; no effect on
mortality
L; no effect on
mortality
L; no effect on
mortality
-------
Summary of Biological Effects Tissue Concentrations for Methylmercury
Species: Concentration, Units in1:
Taxa Sediment Water Tissue (Sample Type)
0.200000002980232
mg/kg (kidney)5
1 mg/kg (liver)5
0.100000001490116
mg/kg (liver)5
0.5 mg/kg (muscle)5
0.100000001490116
mg/kg (muscle)5
1.60000002384185
mg/kg
(posterior intestine)5
6 mg/kg (posterior
intestine)5
1.29999995231628
mg/kg (spleen)5
0.300000011920929
mg/kg (spleen)5
0.140000000596046
mg/kg (whole body)5
0.469999998807907
mg/kg (whole body)5
Toxicity:
Effects
Mortality,
NOED
Mortality,
NOED
Mortality,
NOED
Mortality,
NOED
Mortality,
NOED
Mortality,
NOED
Mortality,
NOED
Mortality,
NOED
Mortality,
NOED
Mortality,
NOED
Mortality,
NOED
Ability to Accumulate2: Source:
Log Log
BCF BAF BSAF Reference
[52]
[52]
[52]
[52]
[52]
[52]
[52]
[52]
[52]
[52]
[52]
Comments3
L; no effect on
mortality
L; no effect on
mortality
L; no effect on
mortality
L; no effect on
mortality
L; no effect on
mortality
L; no effect on
mortality
L; no effect on
mortality
L; no effect on
mortality
L; no effect on
mortality
L; no effect on
survival
L; no effect on
survival
-------
LAl
o
Summary of Biological Effects Tissue Concentrations for Methylmercury
Species: Concentration, Units in1:
Taxa Sediment Water Tissue (Sample Type)
Oncorhynchus 15 mg/kg
mykiss, (whole body)5
Rainbow trout
20 mg/kg
(whole body)5
6 mg/kg
(whole body)5
4.76000022888183
mg/kg (whole body)5
5.69999980926513
mg/kg (whole body)5
3.91000008583068
mg/kg (whole body)5
2.02999997138977
mg/kg (whole body)5
10 mg/kg
(whole body)5
2 mg/kg
(whole body)5
5 mg/kg
(whole body)5
8 mg/kg
(whole body)5
Toxicity: Ability to Accumulate2:
Log Log
Effects BCF BAF BSAF
Mortality,
ED 100
Mortality,
ED 100
Mortality, ED50
Mortality, ED50
Mortality, ED50
Mortality, ED50
Mortality, ED50
Mortality,
LOED
Mortality,
LOED
Mortality,
LOED
Mortality,
LOED
Source:
Reference
[58]
[58]
[58]
[58]
[58]
[58]
[58]
[58]
[58]
[58]
[58]
Comments3
L; 100% mortality
in 15 days
L; 100% mortality
in 15 days
L; 50% mortality in
15 days
L; 30 day ED50 for
brain
L; 15dayED50for
single
intraperitoneal
injection
L; 30 day ED50 for
muscle
L; 30 day ED50 for
eye
L; 83% mortality in
15 days
L; 33% mortality in
15 days
L; 83% mortality in
15 days
L; 67% mortality in
15 days
-------
Summary of Biological Effects Tissue Concentrations for Methylmercury
Species: Concentration, Units in1:
Taxa Sediment Water
Salvelinus fontinalis,
Brook trout
Salvelinus fontinalis,
Brook trout
Tissue (Sample Type)
4 mg/kg
(whole body)5
2 mg/kg
(whole body)5
46.2000007629394
mg/kg (blood cells)5
16.8999996185302
mg/kg (brain)5
4.40000009536743
mg/kg (carcass)5
22.2000007629394
mg/kg (gill)5
12.3000001907348
mg/kg (gonad)5
26.8999996185302
mg/kg (kidney)5
24.3999996185302
mg/kg (liver)5
10.1999998092651
mg/kg (muscle)5
38.7000007629394
mg/kg (spleen)5
46.2000007629394
Toxicity: Ability to Accumulate2:
Log Log
Effects BCF BAF BSAF
Mortality,
LOED
Mortality,
NOED
Development,
LOED
Development,
LOED
Development,
LOED
Development,
LOED
Development,
LOED
Development,
LOED
Development,
LOED
Development,
LOED
Development,
LOED
Growth, LOED
Source:
Reference
[58]
[58]
[38]
[38]
[38]
[38]
[38]
[38]
[38]
[38]
[38]
[38]
Comments3
L; 13% mortality in
15 days
L; no mortality in
15 days
L; affected embryo
development
L; affected embryo
development
L; affected embryo
development
L; affected embryo
development
L; affected embryo
development
L; affected embryo
development
L; affected embryo
development
L; affected embryo
development
L; affected embryo
development
L; decreased weight
mg/kg (blood cells)5
-------
Summary of Biological Effects Tissue Concentrations for Methylmercury
Species: Concentration, Units in1:
Taxa Sediment Water Tissue (Sample Type)
16.8999996185302
mg/kg (brain)5
4.40000009536743
mg/kg (carcass)5
22.2000007629394
mg/kg (gill)5
12.3000001907348
mg/kg (gonad)5
26.8999996185302
mg/kg (kidney)5
24.3999996185302
mg/kg (liver)5
Salvelinusfontinalis, 10.1999998092651
Brook trout mg/kg (muscle)5
38.7000007629394
mg/kg (spleen)5
9.39999961853027
mg/kg (whole body)5
46.2000007629394
mg/kg (blood cells)5
16.8999996185302
mg/kg (brain)5
4.40000009536743
mg/kg (carcass)5
Toxicity: Ability to Accumulate2:
Log Log
Effects BCF BAF BSAF
Growth, LOED
Growth, LOED
Growth, LOED
Growth, LOED
Growth, LOED
Growth, LOED
Growth, LOED
Growth, LOED
Mortality,
LOED
Reproduction,
LOED
Reproduction,
LOED
Reproduction,
LOED
Source:
Reference
[38]
[38]
[38]
[38]
[38]
[38]
[38]
[38]
[38]
[38]
[38]
[38]
Comments3
L; decreased weight
L; decreased weight
L; decreased weight
L; decreased weight
L; decreased weight
L; decreased weight
L; decreased weight
L; decreased weight
L; mortality of
offspring
L; reduced
reproduction
L; reduced
reproduction
L; reduced
reproduction
-------
Summary of Biological Effects Tissue Concentrations for Methylmercury
Species: Concentration, Units in1:
Taxa Sediment Water Tissue (Sample Type)
22.2000007629394
mg/kg (gill)5
12.3000001907348
mg/kg (gonad)5
26.8999996185302
mg/kg (kidney)5
24.3999996185302
mg/kg (liver)5
10.1999998092651
mg/kg (muscle)5
38.7000007629394
mg/kg (spleen)5
3.40000009536743
mg/kg (whole body)5
2.70000004768371
mg/kg (whole body)5
Salvelinusfontinalis, 21.3999996185302
Brook trout mg/kg (blood cells)5
5.19999980926513
mg/kg (blood cells)5
2.29999995231628
mg/kg (blood cells)5
5.30000019073486
mg/kg (brain)5
Toxicity: Ability to Accumulate2:
Log Log
Effects BCF BAF BSAF
Reproduction,
LOED
Reproduction,
LOED
Reproduction,
LOED
Reproduction,
LOED
Reproduction,
LOED
Reproduction,
LOED
Reproduction,
LOED
Development,
NOED
Growth, NOED
Growth, NOED
Growth, NOED
Growth, NOED
Source:
Reference
[38]
[38]
[38]
[38]
[38]
[38]
[38]
[38]
[38]
[38]
[38]
[38]
Comments3
L; reduced
reproduction
L; reduced
reproduction
L; reduced
reproduction
L; reduced
reproduction
L; reduced
reproduction
L; reduced
reproduction
L; reduction in
reproduction
L; no physical
abnormalities
L; decreased weight
L; decreased weight
L; decreased weight
L; decreased weight
-------
o
ON
Summary of Biological Effects Tissue Concentrations for Methylmercury
Species: Concentration, Units in1:
Taxa Sediment Water Tissue (Sample Type)
1.70000004768371
mg/kg (brain)5
0.800000011920928
mg/kg (brain)5
1.60000002384185
mg/kg (carcass)5
0.589999973773956
mg/kg (carcass)5
0.400000005960464
mg/kg (carcass)5
6.19999980926513
mg/kg (gill)5
1.60000002384185
mg/kg (gill)5
0.699999988079071
mg/kg (gill)5
2.90000009536743
mg/kg (gonad)5
0.899999976158142
mg/kg (gonad)5
Salvelinusfontinalis, 0.200000002980232
Brook trout mg/kg (gonad)5
8.89999961853027
mg/kg (kidney)5
Toxicity: Ability to Accumulate2:
Log Log
Effects BCF BAF BSAF
Growth, NOED
Growth, NOED
Growth, NOED
Growth, NOED
Growth, NOED
Growth, NOED
Growth, NOED
Growth, NOED
Growth, NOED
Growth, NOED
Growth, NOED
Growth, NOED
Source:
Reference
[38]
[38]
[38]
[38]
[38]
[38]
[38]
[38]
[38]
[38]
[38]
[38]
Comments3
L; decreased weight
L; decreased weight
L; decreased weight
L; decreased weight
L; decreased weight
L; decreased weight
L; decreased weight
L; decreased weight
L; decreased weight
L; decreased weight
L; decreased weight
L; decreased weight
-------
Summary of Biological Effects Tissue Concentrations for Methylmercury
o
-J
Species: Concentration, Units in1:
Taxa Sediment Water Tissue (Sample Type)
2.5 mg/kg (kidney)5
1.20000004768371
mg/kg (kidney)5
8.30000019073486
mg/kg (liver)5
2.20000004768371
mg/kg (liver)5
0.699999988079071
mg/kg (liver)5
4.90000009536743
mg/kg (muscle)5
1.89999997615814
mg/kg (muscle)5
1 mg/kg (muscle)5
11.8000001907348
mg/kg (spleen)5
3.20000004768371
mg/kg (spleen)5
1.20000004768371
mg/kg (spleen)5
2.70000004768371
mg/kg (whole body)5
Salvelinusfontinalis, 21.3999996185302
Brook trout mg/kg (blood cells)5
Toxicity: Ability to Accumulate2:
Log Log
Effects BCF BAF BSAF
Growth, NOED
Growth, NOED
Growth, NOED
Growth, NOED
Growth, NOED
Growth, NOED
Growth, NOED
Growth, NOED
Growth, NOED
Growth, NOED
Growth, NOED
Mortality,
NOED
Reproduction,
NOED
Source:
Reference
[38]
[38]
[38]
[38]
[38]
[38]
[38]
[38]
[38]
[38]
[38]
[38]
[38]
Comments3
L; decreased weight
L; decreased weight
L; decreased weight
L; decreased weight
L; decreased weight
L; decreased weight
L; decreased weight
L; decreased weight
L; decreased weight
L; decreased weight
L; decreased weight
L; no effect on
mortality
L; reduced
reproduction
-------
o
oo
Summary of Biological Effects Tissue Concentrations for Methylmercury
Species: Concentration, Units in1:
Taxa Sediment Water Tissue (Sample Type)
5.19999980926513
mg/kg (blood cells)5
2.29999995231628
mg/kg (blood cells)5
5.30000019073486
mg/kg (brain)5
1.70000004768371
mg/kg (brain)5
0.800000011920928
mg/kg (brain)5
1.60000002384185
mg/kg (carcass)5
0.589999973773956
mg/kg (carcass)5
0.400000005960464
mg/kg (carcass)5
6.19999980926513
mg/kg (gill)5
1.60000002384185
mg/kg (gill)5
0.699999988079071
mg/kg (gill)5
2.90000009536743
mg/kg (gonad)5
Toxicity: Ability to Accumulate2:
Log Log
Effects BCF BAF BSAF
Reproduction,
NOED
Reproduction,
NOED
Reproduction,
NOED
Reproduction,
NOED
Reproduction,
NOED
Reproduction,
NOED
Reproduction,
NOED
Reproduction,
NOED
Reproduction,
NOED
Reproduction,
NOED
Reproduction,
NOED
Reproduction,
NOED
Source:
Reference
[38]
[38]
[38]
[38]
[38]
[38]
[38]
[38]
[38]
[38]
[38]
[38]
Comments3
L; reduced
reproduction
L; reduced
reproduction
L; reduced
reproduction
L; reduced
reproduction
L; reduced
reproduction
L; reduced
reproduction
L; reduced
reproduction
L; reduced
reproduction
L; reduced
reproduction
L; reduced
reproduction
L; reduced
reproduction
L; reduced
reproduction
-------
Summary of Biological Effects Tissue Concentrations for Methylmercury
Species: Concentration, Units in1:
Taxa Sediment Water Tissue (Sample Type)
0.899999976158142
mg/kg (gonad)5
Salvelinusfontinalis, 0.200000002980232
Brook trout mg/kg (gonad)5
8.89999961853027
mg/kg (kidney)5
2.5 mg/kg (kidney)5
1.20000004768371
mg/kg (kidney)5
8.30000019073486
mg/kg (liver)5
2.20000004768371
mg/kg (liver)5
0.699999988079071
mg/kg (liver)5
4.90000009536743
mg/kg (muscle)5
1.89999997615814
mg/kg (muscle)5
1 mg/kg (muscle)5
11.8000001907348
mg/kg (spleen)5
Toxicity: Ability to Accumulate2:
Log Log
Effects BCF BAF BSAF
Reproduction,
NOED
Reproduction,
NOED
Reproduction,
NOED
Reproduction,
NOED
Reproduction,
NOED
Reproduction,
NOED
Reproduction,
NOED
Reproduction,
NOED
Reproduction,
NOED
Reproduction,
NOED
Reproduction,
NOED
Reproduction,
NOED
Source:
Reference
[38]
[38]
[38]
[38]
[38]
[38]
[38]
[38]
[38]
[38]
[38]
[38]
Comments3
L; reduced
reproduction
L; reduced
reproduction
L; reduced
reproduction
L; reduced
reproduction
L; reduced
reproduction
L; reduced
reproduction
L; reduced
reproduction
L; reduced
reproduction
L; reduced
reproduction
L; reduced
reproduction
L; reduced
reproduction
L; reduced
reproduction
-------
Summary of Biological Effects Tissue Concentrations for Methylmercury
Species:
Taxa
Concentration, Units in1:
Toxicity:
Ability to Accumulate2:
Log Log
Sediment Water Tissue (Sample Type) Effects BCF BAF BSAF
Source:
Reference Comments3
3.20000004768371
mg/kg (spleen)5
1.20000004768371
mg/kg (spleen)5
Reproduction,
NOED
Reproduction,
NOED
[38]
[38]
L; reduced
reproduction
L; reduced
reproduction
Esox lucius,
Northern pike
7 mg/kg
(whole body)5
Physiological,
LOED
[60] F; lowered blood
alkaline
phosphatase, serum
cortisol, emaciation
Planktivores:
Dorosoma
cepedianum,
Gizzard shad
Interstitial
water:
0.003 |ig/L
Lake water:
0.0003|ig/L
680 |ig/kg
6.40
[20] F; mean
methylmercury
concentrations in
whole bodies of fish
were slightly lower
than concentrations
in fillets for 4
species evaluated
(white perch,
smallmouth bass,
bluegill, and gizzard
shad); differences
were significant
(P<0.05, t-test) for
bluegill only; BAF
value estimated
from chart as log
BAF
-------
Summary of Biological Effects Tissue Concentrations for Methylmercury
Species: Concentration, Units in1: Toxicity:
Taxa Sediment Water Tissue (Sample Type) Effects
Benthivores: Interstitial 480 |ig/kg
Cyprinus carpio; water:
Carp; 0.003 |ig/L
Ictalurus punctatus,
Channel catfish; Lake water:
and 0.0003 |ig/L
Lepomis
macrochirus,
Bluegill
Ability to Accumulate2: Source:
Log Log
BCF BAF BSAF Reference Comments3
6.20 [20] F; mean
methylmercury
concentrations in
whole bodies of fish
were slightly lower
than concentrations
in fillets for 4
species evaluated
(white perch,
smallmouth bass,
bluegill, and gizzard
shad); differences
were significant
(P<0.05, t-test) for
bluegill only; BAF
value estimated
from chart as log
BAF
Oryzias latipes,
Japanese medaka
54 mg/kg
(whole body)5
56 mg/kg
(whole body)5
54 mg/kg
(whole body)5
56 mg/kg
(whole body)5
Development,
ED 100
Development,
ED100
Morphology,
ED 100
Morphology,
ED 100
[59]
[59]
[59]
[59]
L; complete failure
of eggs to hatch
L; complete failure
of eggs to hatch
L; subcutaneous
hemorrhage,
deformed vertebrae
-------
Summary of Biological Effects Tissue Concentrations for Methylmercury
Species: Concentration, Units in1:
Taxa Sediment Water Tissue (Sample Type)
29 mg/kg
(whole body)5
29 mg/kg
(whole body)5
29 mg/kg
(whole body)5
16 mg/kg
(whole body)5
16 mg/kg
(whole body)5
Toxicity: Ability to Accumulate2:
Log Log
Effects BCF BAF BSAF
Behavior,
LOED
Development,
LOED
Morphology,
LOED
Development,
NOED
Morphology,
NOED
Source:
Reference
[59]
[59]
[59]
[59]
[59]
Comments3
L; hatchlings unable
to control fin
movement, loss of
equilibrium
L; over 50%
reduction in number
of eggs which
hatched
L; subcutaneous
hemorrhage,
deformed vertebrae
L; no effect on
hatchability of eggs
compared to
controls
L; no observations
of subcutaneous
hemorrhage or
deformed vertebrae
-------
Summary of Biological Effects Tissue Concentrations for Methylmercury
Species:
Concentration, Units in1:
Toxicity:
Ability to Accumulate2:
Source:
Taxa
Morone americana,
White perch
Sediment Water
Interstitial
water:
0.003 |ig/L
Tissue (Sample Type) Effects
680 ng/kg
Log
BCF
Log
BAF
6.40
BSAF Reference
[20]
Comments3
F; mean
methylmercury
concentrations in
Lake water:
0.0003 |ig/L
Percaflavescens,
Yellow perch
0.135000005364418
mg/kg (whole body)5
Growth, NOED
[63]
whole bodies of fish
were slightly lower
than concentrations
in fillets for 4
species evaluated
(white perch,
smallmouth bass,
bluegill, and gizzard
shad); differences
were significant
(P<0.05, t-test) for
bluegill only; BAF
value estimated
from chart as log
BAF
F, controlled field
study; two years but
only 1 -year-old fish
analyzed; basin
treated by reducing
pH from about 6 to
5.6
-------
Summary of Biological Effects Tissue Concentrations for Methylmercury
Species:
Concentration, Units in1:
Toxicity:
Ability to Accumulate2:
Source:
Taxa Sediment Water Tissue (Sample Type) Effects
Piscivores: Interstitial l,100|ig/kg
Microplerus water:
dolomieui, 0.003 |j,g/L
Smallmouth bass;
and Lake water:
Stizostedion vitreum, 0.0003 |ig/L
Walleye
Log Log
BCF BAF BSAF Reference Comments3
3.7xl06 [20] F; mean
methylmercury
concentrations in
whole bodies of fish
were slightly lower
than concentrations
in fillets for 4
species evaluated
(white perch,
smallmouth bass,
bluegill, and gizzard
shad); differences
were significant
(P<0.05, t-test) for
bluegill only; BAF
value estimated
from chart as log
BAF
Stizostedion vitreum,
Walleye
0.25 mg/kg
(whole body)5
2.36999988555908
mg/kg (whole body)5
0.25 mg/kg
(whole body)5
2.36999988555908
mg/kg (whole body)5
Cellular, LOED
Cellular, LOED
Development,
LOED
Development,
LOED
[56]
[56]
[56]
[56]
L; multifocal cell
atrophy, testicular
atrophy
L; decreased
testicular
development,
lowered
gonadosomatic
index
-------
Summary of Biological Effects Tissue Concentrations for Methylmercury
Species: Concentration, Units in1:
Taxa Sediment Water
Pseiidopleiironectes
americanus, Winter
flounder
Tissue (Sample Type)
2.36999988555908
mg/kg (whole body)5
0.25 mg/kg
(whole body)5
0.25 mg/kg
(whole body)5
0.25 mg/kg
(whole body)5
2.36999988555908
mg/kg (whole body)5
2.36999988555908
mg/kg (whole body)5
5 mg/kg
(whole body)5
2 mg/kg
(whole body)5
Toxicity: Ability to Accumulate2:
Log Log
Effects BCF BAF BSAF
Growth, LOED
Physiological,
LOED
Growth, NOED
Mortality,
NOED
Mortality,
NOED
Physiological,
NOED
Mortality,
LOED
Physiological,
LOED
Source:
Reference
[56]
[56]
[56]
[56]
[56]
[56]
[61]
[61]
Comments3
L; significant
reduction in length
and weight of
males, but not
females
L; reduced cortisol
levels
L; no effect on
length or weight
L; no statistically
significant increase
in mortality
L; no effect on
cortisol levels
L; increased
mortality
L; increased
ornithine
decarboxylase
activity
-------
Summary of Biological Effects Tissue Concentrations for Methylmercury
Species:
Taxa
Wildlife
Lams californicus,
California gull
Pelecaniis
occidentalis,
Brown pelican
Phalacrocorax
penicillatus,
Brandts cormorant
Concentration, Units in1:
Sediment Water Tissue (Sample Type)
0.404000014066696
mg/kg (brain)5
0.828999996185302
mg/kg (breast)5
1.08000004291534
mg/kg (liver)5
0.202999994158745
mg/kg (brain)5
0.347499996423721
mg/kg (breast)5
0.806500017642974
mg/kg (liver)5
0.648999989032745
mg/kg (brain)5
0.986000001430511
mg/kg (breast)5
2.94000005722045
mg/kg (liver)5
3.06999993324279
Toxicity: Ability to Accumulate2:
Log Log
Effects BCF BAF BSAF
Mortality, NA
Mortality, NA
Mortality, NA
Mortality, NA
Mortality, NA
Mortality, NA
Mortality, NA
Mortality, NA
Mortality, NA
Mortality, NA
Source:
Reference
[64]
[64]
[64]
[64]
[64]
[64]
[64]
[64]
[64]
[64]
Comments3
L
L
L
L
L
L
L
L
L
L
mg/kg (liver)5
-------
1 Concentration units based on wet weight unless otherwise noted.
2 BCF = bioconcentration factor, BAF = bioaccumulation factor, BSAF = biota-sediment accumulation factor.
3 L = laboratory study, spiked sediment, single chemical; F = field study, multiple chemical exposure; other unusual study conditions or observations noted.
4 MeHg = methylmercury.
5 This entry was excerpted directly from the Environmental Residue-Effects Database (ERED, www.wes.army.mil/el/ered, U.S. Army Corps of Engineers and U.S.
Environmental Protection Agency). The original publication was not reviewed, and the reader is strongly urged to consult the publication to confirm the information
presented here.
-------
BIOACCUMULATION SUMMARY METHYLMERCURY
References
1. USEPA. 1996. Hazardous Substances Data Bank (HSDB). National Library of Medicine online
(TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental
Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. March.
2. USEPA. 1989. Chemical fate rate constants for SARA section 313 chemicals and Superfund
Health Evaluation Manual chemicals. Prepared by Chemical Hazard Assessment Division,
Syracuse Research Corporation, for U.S. Environmental Protection Agency, Office of Toxic
Substances, Exposure Evaluation Division, Washington, DC, and Environmental Criteria and
Assessment Office, Cincinnati, OH. August 11.
3. USEPA. 1995. Integrated Risk Information System (IRIS). National Library of Medicine online
(TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental
Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. September.
4. Norseth, T., and T.W. Clarkson. 1970. Studies on the biotransformation of mercury-203-labeled
methyl mercury chloride in rats. Arch. Environ. Health. 21:717-27.
5. Swensson, A., and U. Ulfvarson. 1968. Distribution and excretion of various mercury
compounds after single injections in poultry. Acta Pharmacol. Toxicol. 26:259-72.
6. Yoshino, Y., T. Mozai, and K. Nakao. 1966. Biochemical changes in the brain in rats poisoned
with an alkymercury compound, with special reference to the inhibition of protein synthesis in
brain cortex slices. /. Neurochem. 13:397-406.
7. Chang, L.W., A.H. Martin, and H.A. Hartmann. 1972. Quantitative autoradiographic study on
the RNA synthesis in the neurons after mercury and toxication. Exp. Neurol. 37:62-67.
8. Syverson. 1974. Distribution of mercury in enzymaticaily characterized subcellular fractions
from the developing rat brain after injections of methyl mercuric chloride and diethyl mercury.
Biochem. Pharmacol. 23:2999-3007.
9. Braune, B.M. 1987. Mercury accumulation in relation to size and age of Atlantic herring Clupea
harengus harengus from the southwestern Bay of Fundy, Canada. Arch. Environ. Contain.
Toxicol. 16:217-224.
10. Elliott, J.E., A.M. Scheuhammer, F.A. Leighton, and P.A. Pearce. 1992 Heavy metal and
metallothionein concentrations in Atlantic Canadian seabirds. Arch. Environ. Contam. Toxicol.
22:63-73.
11. Muirhead, S.J., and R.W. Furness. 1988. Heavy metal concentrations in the tissues of seabirds
from Gough Island South Atlantic Ocean. Mar. Pollut. Bull. 19:278-283.
12. Norheim, G., L. Somme, and G. Holt. 1982. Mercury and persistent chlorinated hydrocarbons
in Antarctic birds from Bouvetoya and Dronning Maud Land. Environ. Pollut. 28A:233-240.
518
-------
BIOACCUMULATION SUMMARY METHYLMERCURY
13. Karlog, O., and B. Clausen. 1983. Mercury and methylmercury in liver tissue from ringed
herring gulls collected in three Danish localities. Nord. Vet. Med. 35:245-250.
14. Thompson, D.R., and R.W. Furness. 1989. The chemical form of mercury stored in south
Atlantic seabirds. Environ. Pollut. 60:305-317.
15. Honda, K., J.E. Marcovecchio, S. Kan, R. Tatsukawa, and H. Ogi. 1990. Metal concentrations
in pelagic seabirds from the north Pacific Ocean. Arch. Environ. Contain. Toxicol. 19:704-711.
16. Sheffy, T.B., and J.R. St. Amant. 1982. Mercury burdens in furbearers in Wisconsin. J.Wildl.
Manage. 46:1117-1120.
17. Kucera, E. 1983. Mink and otter as indicators of mercury in Manitoba waters. Canad. J. Zool.
61:2250-2256.
18. Thompson, D.R. 1996. Chapter 14: Mercury in birds and terrestrial mammals. In
Environmental contaminants in wildlife: Interpreting tissue concentrations, ed. W.N. Beyer, G.H.
Heinz, and A.W. Redmon-Norwood, pp. 341-356. Lewis Publishers, Boca Raton, FL.
19. St. Louis, V., J.W.M. Rudd, C.A. Kelly, K.G. Beaty, N.S. Bloom, and RJ. Flett. 1994.
Importance of wetlands as sources of methyl mercury to boreal forest ecosystems. Can. J. Fish.
Aquat. Sci. 51(5): 1065-1076.
20. Becker, D.S., and G.N. Bigham. 1995. Distribution of mercury in the aquatic food web of
Onondaga Lake, New York. (Water Air Soil Pollut. 80:563-571.) In Mercury as a global
pollutant, ed. D.B. Porcella, J.W. Huckabee, and B. Wheatley, pp. 563-571. Kluwer Academic
Publishers, New York, NY.
21. Rodgers, D.W., and F.W.H. Beamish. 1981. Uptake of waterborne methylmercury by rainbow
trout (Salmo gairdneri) in relation to oxygen consumption and methylmercury concentration.
Can. J. Fish. Aquat. Sci. 38:1309-1315.
22. Wren, C.D., H.R. MacCrimmon, and B.R. Loescher. 1983. Examination of bioaccumulation and
biomagnification of metals in a Precambrian shield lake. Water Air Soil Pollut. 19:277-291.
23. Xun, L., N.E.R. Campbell, and J.W.M. Rudd. 1987. Measurements of specific rates of net
methylmercury production in the water column and surface sediment of acidified circumneutral
lakes. Can. J. Fish. Aquat. Sci. 44:750-757.
24. Mathers, R., and P. Johansen. 1985. The effects of feeding ecology on mercury accumulation
in walleye (Stizostedion vitreum) and pike (Esox lucius) in Lake Simcoe. Can. J. Zool. 63:2006-
2012.
25. Wiener, J.G., and DJ. Spry. 1996. Toxicological significance of mercury in freshwater fish. In
Interpreting concentrations of environmental contaminants in wildlife tissues, ed. G. Heinz and
N. Beyer, pp. 297-339. Lewis Publishers, Chelsea, MI.
519
-------
BIOACCUMULATION SUMMARY METHYLMERCURY
26. Huckabee, J.W., S.A. Janzen, E.G. Blaylock, Y. Talmi, and JJ. Beauchamp. 1978. Methylated
mercury in brook trout (Salvelinus fontinalis): Absence of in vivo methylating process. Trans.
Amer. Fish. Soc. 107:848-852.
27. Norstrom, R.J., A.F. McKinnon, and A.S.W. DeFreitas. 1976. A bioenergetics based model for
pollutant bioaccumulation by fish: Simulation of PCB and methylmercury residues in Ottawa
River perch (Percaflavescens). J. Fish. Res. Board Can. 33:248-267.
28. Phillips, G.R., T.E. Lenhart, and R.W. Gregory. 1980. Relation between trophic position and
mercury accumulation among fishes from the Tongue River, Montana. Environ. Res. 22:73-80.
29. Rodgers, D.W., and S.U. Qadri. 1982. Growth and mercury accumulation in yearling yellow
perch, Percaflavescens, in Ottawa River, Ontario. Environ. Biol. Fish. 7:377-383.
30. Beckvar, N., J. Field, S. Salazar, and R. Hoff. 1996. Contaminants in aquatic habitats at
hazardous waste sites: Mercury. National Oeanic and Atmospheric Administration and EVS
Consultants, Seattle, WA.
31. Luoma, S.N. 1977. The dynamics of biologically available mercury in a small estuary. Estuar.
Coast. Mar. Sci. 5:643-652.
32. Rubinstein, N.I., E. Lores, and N.R. Gregory. 1983. Accumulation of PCBs, mercury and
cadmium by Nereis virens, Mercenaria mercenaria and Palaemonetes pugio from contaminated
harbor sediments. Aquat. Toxicol. 3:249-260.
33. Eisler, R. 1987. Mercury hazards to fish, wildlife, and invertebrates: A synoptic review. U.S.
Fish Wildl. Serv. Biol. Rep. 85(1.10). 90pp.
34. Windom, H.L., and D. R. Kendall. 1979. Accumulation and biotransformation of mercury in
coastal and marine biota. In The bio geochemistry of mercury in the environment, ed. J.O. Nriagu,
pp. 277-302. Elsevier/North-Holland Biomedical Press, New York, NY.
35. USEPA. 1985. Ambient water quality criteria for mercury - 1984. EPA 440/5-84-026. U.S.
Environmental Protection Agency, Office of Water, Washington, DC.
36. Peltier, J.S., E. Kahn, B. Salick, F.C. Van Natta, and M.W. Whitehouse. 1972. Heavy metal
poisoning: Mercury and lead. Ann. Intern. Med. 76:779-792.
37. Giblin, F.J., and E.J. Massaro. 1973. Pharmacodynamics of methyl mercury in rainbow trout
(Salmo gairdneri): Tissue uptake, distribution and excretion. Toxicol. Appl. Pharmacol.
24:81-91.
38. McKim, J.M., G.F. Olson, G.W. Holcombe, and E.P. Hunt. 1976. Long-term effects of
methylmercuric chloride on three generations of brook trout (Salvelinus fontinalis): Toxicity,
accumulation, distribution, and elimination. /. Fish. Res. B. Can. 33:2726-2739.
520
-------
BIOACCUMULATION SUMMARY METHYLMERCURY
39. Olson, K R., K.S. Squibb, and RJ. Cousins. 1978. Tissue uptake, subcellular distribution, and
metabolism of 14CH3HgCl and CH3203 HgCl by rainbow trout, Salmo gairdneri. J. Fish. Res.
Board Can. 35:381-90.
40. Beijer, K., and A. Jernelov. 1979. Methylation of mercury in aquatic environments. In The
biogeochemistry of mercury in the environment, ed. J.O. Nriagu, pp. 203-210. Elsevier/North-
Holland Biomedical Press, New York, NY.
41. Sastry, K.V., and K. Sharma. 1980. Effects of mercuric chloride on the activities of brain
enzymes in a freshwater teleost, Ophiocephalus (Channa) punctatus. Arch. Environ. Contain.
Toxicol. 9:425-430.
42. Armstrong, F.A.J. 1979. Effects of mercury compounds on fish. In The biogeochemistry of
mercury in the environment, ed. J.O. Nriagu, pp. 657-670. Elsevier/North-Holland Biomedical
Press, New York, NY.
43. Slooff, W., P.F.H. Bont, M. van Ewijk, and J.A. Janus. 1991. Exploratory report mercury.
Report no. 710401006. National Institute of Public Health and Environmental Protection,
Bilthoven, The Netherlands.
44. McKenney, C.L., Jr., and J.D. Costlow, Jr. 1981. The effects of salinity and mercury on
developing megalopae and early crab stages of the blue crab Callinectes sapidus Rathbun. In
Biological monitoring of marine pollutants, ed. F.J. Vernberg, A. Calabrese, F.P. Thurberg, and
W.B. Vernberg, pp. 241-262. Academic Press, New York, NY.
45. Parker, J.G. 1979. Toxic effects of heavy metals upon cultures of Uronema marinum
(Ciliophora:Uronematidae). Mar. Biol. 54:17-24.
46. Brown, D.A., R.W. Gosset, P. Hershelman, H.A. Schaefer, K.D. Jenkins, and E.M. Perkins.
1983. Bioaccumulation and detoxification of contaminants in marine organisms from Southern
California coastal waters. In Waste disposal in the oceans, ed. D.F. Soule and D. Walsh, p. 171.
Westview Press, Boulder, CO.
47. Back, R.C., and C.J. Watras. 1995. Mercury in zooplankton of Northern Wisconsin lakes:
Taxonomic and site-specific trends. (Water Air Soil Pollut. 80:931-9381.) In Mercury as a global
pollutant, ed. D.B. Porcella, J.W. Huckabee, and B. Wheatley, pp. 931-938. Kluwer Academic
Publishers, Hingham, MA.
48. Salazar, S.M., N. Beckvar, M.H. Salazar, and K. Finkelstein. 1995. An in situ assessment of
mercury contamination in the Sudbury River, Massachusetts, using bioaccumulation and growth
in transplanted freshwater mussels. NOAA Technical Report. Submitted to U.S. Environmental
Protection Agency, Massachusettes Superfund Program Region 1, Boston, MA.
49. Niimi, A.J., and G.P. Kissoon. 1994. Evaluation of the critical body burden concept based on
inorganic and organic mercury toxicity to rainbow trout (Oncorhynchus mykiss). Arch. Environ.
Contam. Toxicol. 26:169-178.
521
-------
BIOACCUMULATION SUMMARY METHYLMERCURY
50. Barthalmus, G.T. 1977. Behavioral effects of mercury on grass shrimp. Mar. Pollut. Bull. 8:87-
90.
51. Biesinger, K.E., L.E. Anderson, and J.G. Eaton. 1982. Chronic effects of inorganic and organic
mercury on Daphnia magna: Toxicity, accumulation, and loss. Arch. Environ. Contam. Toxicol.
11:769-774.
52. Boudou, A., and F. Ribeyre. 1985. Experimental study of trophic contamination of Salmo
gairdneri by two mercury compounds - HgCl2 and CH3HgCl - Analysis at the organism and organ
levels. Water Air Soil Pollut. 26:137-148.
53. Callahan, P., and J.S. Weis. 1983. Methylmercury effects on regeneration and ecdysis in fiddler
crabs (Uca pugilator, U. pugnax) after short-term and chronic pre-exposure. Arch. Environ.
Contam. Toxicol. 12:707-714.
54. Dillon, T.M. 1977. Mercury and the estuarine marsh clam, Rangia cuneata Gray. I. Toxicity.
Arch. Environ. Contam. Toxicol. 6:249-255.
55. Enserink, E.L., J.L. Maas-Diepeveen, and C.J. Van Leeuwen. 1991. Combined effects of metals;
an ecotoxicological evaluation. Water Res. 25:679-687.
56. Friedmann, A.S., M.C. Watzin, T. Brinck-Johnsen, and J.C. Leiter. 1996. Low levels of dietary
methylmercury inhibit growth and gonadal development in juvenile walleye (Stizostedion
vitreum). Aquat. Toxicol. 35:265-278.
57. Guarino, A.M., and S.T. Arnold. 1979. Xenobiotic transport mechanisms and pharmacokinetics
in the dogfish shark. In Pesticide and xenobiotic metabolism in aquatic organisms, ed. M.A.Q.
Khan, JJ. Lech, and JJ. Menn, pp. 233-258. American Chemical Society, Washington, DC.
58. Hawryshyn, C.W., and W.C. Mackay. 1979. Toxicity and tissue uptake of methylmercury
administered interperitoneally to rainbow trout (Salmo gairdneri Richardson). Bull. Environ.
Contam. Toxicol. 23:79-86.
59. Heisinger, J.F., and W. Green. 1975. Mercuric chloride uptake by eggs of the ricefish and
resulting teratogenic effects. Bull. Environ. Contam. Toxicol. 14:665-673.
60. Lockhart, W.L., J.F. Uthe, A.R. Kenney, and P.M. Mehrle. 1972. Methylmercury in northern pike
(Esox lucius): Distribution, elimination, and some biochemical characteristics of contaminated
fish. /. Fish. Res. Bd. Can. 29:1519-1523.
61. Manen, C.A., B. Schmidt-Nielsen, and D.N. Russell. 1976. Polyamine synthesis in liver and
kidney of flounder in response to methylmercury. Amer. J. Physiol. 231:560-564.
62. Thain, J.E. 1984. Effects of mercury on the prosobranch mollusc Crepidula fornicata: Acute
lethal toxicity and effects on growth and reproduction of chronic exposure. Mar. Environ. Res.
12: 285-309.
-------
BIOACCUMULATION SUMMARY METHYLMERCURY
63. Weiner, J.G., W.F. Fitzgerald, CJ. Watras, and R.G. Rada. 1990. Partitioning and bioavailability
of mercury in an experimentally acidified Wisconsin lake. Environ. Toxicol. Chem. 9: 909-918.
64. Young, D.R., and T.C. Heeson. 1977. Marine bird deaths at the Los Angeles Zoo. Coastal Water
Research Program annual report. Southern California Coastal Water Research Project, El
Segundo, CA.
523
-------
-------
BIOACCUMULATION SUMMARY NICKEL
Chemical Category: METAL
Chemical Name (Common Synonyms): NICKEL ASRN: 7440-02-0
Chemical Characteristics
Solubility in Water: Insoluble [1] Half-Life: Not applicable, stable [1]
LogKow: - LogKoc: -
Human Health
Oral RfD: 2 x 10"2 mg/kg/day [2] Confidence: Medium uncertainty factor = 300
Critical Effect: Decreased body and organ weights
Oral Slope Factor: Not available [2] Carcinogenic Classification: A [2]
Wildlife
Partitioning Factors: Partitioning factors for nickel in wildlife were not found in the literature.
Food Chain Multipliers: Food chain multipliers for nickel in wildlife were not found in the literature.
Aquatic Organisms
Partitioning Factors: Nickel in the aquatic environment can partition to dissolved and particulate
organic carbon. Also, the bioavailability of nickel can be influenced to some extent by the concentrations
of calcium and magnesium in water. The bioavailability of nickel in sediments is controlled by the
concentration of acid-volatile sulfides (AVS) [8].
Food Chain Multipliers: Little evidence exists to support the general occurrence of biomagnification
of nickel in the aquatic environment [9 and 10].
Toxicity/Bioaccumulation Assessment Profile
Bioaccumulation of nickel is most pronounced in sediments when the ratio of simultaneously extracted
metals to acid-volatile sulfide (SEM/AVS) is greater than 1. Although nickel concentrations in animals
from sediments with SEM/AVS ratios >1 were approximately 2- to 10-fold greater than nickel
concentrations in benthic organisms from sediments with SEM/AVS ratio <1, nickel uptake (tissue
concentration) was proportional to the concentration in sediment. Ankley et al. [3] have shown that
bioaccumulation of nickel from the sediment by Lumbriculus variegatus was not predictable based on
total sediment metal concentration, but was related to the sediment SEM/AVS ratio.
525
-------
Summary of Biological Effects Tissue Concentrations for Nickel
Species:
Taxa
Invertebrates
Lumbriculus
variegatus,
Oligochaete worm
Tiibificidae
Concentration, Units in1:
Sediment Water
0.58 |imol/L
16.44 |imol/L
38.24 |imol/L
31.40|imol/L
4.53 |imol/L
32.77 |imol/L
8.58 |imol/L
14.43 |imol/L
3.72 |imol/L
17.96 |imol/L
0.52 |imol/L
2.75 |imol/L
0.50 |imol/L
3.51 |imol/L
16.67 |imol/L
17.20 |imol/L
51 M-g/g
50 ng/g
93 |ig/g
76 |ig/g
75 |ig/g
Toxicity: Ability to Accumulate2: Source:
Log Log
Tissue (Sample Type) Effects BCF BAF BSAF Reference Comments3
0.10|imol/g [3] F
5.00 |imol/g
3.32 |imol/g
0.87 |imol/g
0.07 |imol/g
0.33 |imol/g
1.88|imol/g
0.97 |imol/g
3.59 |imol/g
2.77 |imol/g
0.10|imol/g
0.29 |imol/g
1.41 |imol/g
1.91 |imol/g
7.79 |imol/g
0.95 |imol/g
7.20 mg/g [6] L
3.19 mg/g
6.96 mg/g
12.04 mg/g
9.45 mg/g
-------
Summary of Biological Effects Tissue Concentrations for Nickel
Species: Concentration, Units in1:
Taxa Sediment Water
Neanthes
arenaceodentata,
Polychaete worm
Cerastoderma
edule, Clam
<0.28 |imol/L
0.42 |imol/L
2.62 |imol/L
0.16 |imol/L
<0.74 |imol/L
3.72 |imol/L
0.37 |imol/L
0.80 |imol/L
54.30 |imol/L
1.28|imol/L
64.8 |imol/L
67.4 |imol/L
36.4 |imol/L
0.86 |imol/L
73.1 |imol/L
52.4 |imol/L
449 |imol/L
Tissue (Sample Type)
<0.002 |imol/g
0.01 |imol/g
0.01 |imol/g
<0.002 |imol/g
<0.001 |imol/g
0.01 |imol/g
0.02 |imol/g
<0.006 |imol/g
0.12 |imol/g
<0.002 |imol/g
0.05 |imol/g
0.06 |imol/g
0.12 |imol/g
0.02 |imol/g
0.10 |imol/g
0.21 |imol/g
1.69 |imol/g
56.6 mg/kg
(whole body)4
Toxicity: Ability to Accumulate2: Source:
Log Log
Effects BCF BAF BSAF Reference Comments3
3% mortality [4] F
13% mortality
0% mortality
3% mortality
7% mortality
13% mortality
0% mortality
0% mortality
20% mortality
7% mortality
10% mortality
0% mortality
3% mortality
0% mortality
0% mortality [5] F
0% mortality
3% mortality
Mortality, [12] L; estimated body
ED50 residue by regression
from other data
values, number of
replicates is 2 to 5
-------
to Summary of Biological Effects Tissue Concentrations for Nickel
oo
Species: Concentration, Units in1:
Taxa Sediment Water Tissue (Sample Type)
128 mg/kg (adductor
muscle)4
140 mg/kg (foot)4
209 mg/kg (gill)4
274 mg/kg (mantle)4
138 mg/kg (visceral
tissue)4
167 mg/kg
(whole body)4
Toxicity: Ability to Accumulate2: Source:
Log Log
Effects BCF BAF
Physiological,
NOED
Physiological,
NOED
Physiological,
NOED
Physiological,
NOED
Physiological,
NOED
Physiological,N
OED
BSAF Reference Comments3
[12]
[12]
[12]
[12]
[12]
[12]
L; no significant
effect on respiration
rate at 100 |ig/L
(highest test
concentration at
which body residues
were measured),
number of replicates
is 2 to 5
Mytilus
galloprovincialis,
Mussel
1.1-1.4 mg/kg
0.22
[11]
Lamellidans
marginalis, HOmg/L
Freshwater mussel
Day 4:
1456.1 |ig/g
(ctenidium)
432.7 |ig/g (mantle)
468.3 ng/g
(hepatopancreas)
328.4 |ig/g (foot)
373.9 |ig/g (adductor
muscle)
[5]
L
-------
Summary of Biological Effects Tissue Concentrations for Nickel
Species:
Taxa
Concentration, Units in1:
Sediment Water
Toxicity:
Tissue (Sample Type) Effects
Ability to Accumulate2:
BSAF
Log
BCF
Log
BAF
Source:
Reference Comments3
Lamellidans
marginalis, 22 mg/L
Freshwater mussel
Day 15:
569.8 (j.g/g (ctenidium)
277.1 ng/g (mantle)
327.1 ng/g
(hepatopancreas)
218.6 ng/g (foot)
186.7 |ig/g (adductor
muscle)
[5]
L
Daphnia magna,
Cladoceran
223 mg/kg
(whole body)4
Mortality,
ED50
[6] L; lethal body burden
after 21-day
exposure
Fishes
Cypriniis carpio,
Carp
Day 4:
40 mg/L 202.8 mg/L (gill)
226.3 mg/L (kidney)
82.2 mg/L (liver)
97.1 mg/L (brain)
118.1 mg/L
(white muscle)
8 mg/L Day 15:
103.0 mg/L (gill)
80.3 mg/L (kidney)
97.1 mg/L (liver)
40.6 mg/L (brain)
58.0 mg/L (white)
muscle)
[5]
L
-------
Summary of Biological Effects Tissue Concentrations for Nickel
Species:
Taxa
Pimephales
promelas,
Fathead minnow
Concentration, Units in1:
Sediment Water
31 Hg/g
51 M-g/g
50 ng/g
57 |ig/g
93 ng/g
73 |ig/g
76 |ig/g
60 |ig/g
75 |ig/g
53 |ig/g
Toxicity: Ability to Accumulate2: Source:
Log Log
Tissue (Sample Type) Effects BCF BAF BSAF Reference Comments3
8.69 mg/g [7] F
8.19 mg/g
5.66 mg/g
4.02 mg/g
10.72 mg/g
10. 10 mg/g
11. 51 mg/g
13.32 mg/g
11. 75 mg/g
10.90 mg/g
1 Concentration units based on wet weight unless otherwise noted.
2 BCF = bioconcentration factor, BAF = bioaccumulation factor, BSAF = biota-sediment accumulation factor.
3 L = laboratory study, spiked sediment, single chemical; F = field study, multiple chemical exposure; other unusual study conditions or observations noted.
4 This entry was excerpted directly from the Environmental Residue-Effects Database (ERED, www.wes.army.mil/el/ered, U.S. Army Corps of Engineers and U.S.
Environmental Protection Agency). The original publication was not reviewed, and the reader is strongly urged to consult the publication to confirm the information
presented here.
-------
BIOACCUMULATION SUMMARY NICKEL
References
1. Weast handbook of chemistry and physics, 68th edition, 1987-1988, B-110. (Cited in: USEPA.
1995. Hazardous Substances Data Bank (HSDB). National Library of Medicine online (TOXNET).
U.S. Environmental Protection Agency, Office of Health and Environmental Assessment,
Environmental Criteria and Assessment Office, Cincinnati, OH. September).
2. USEPA. 1995. Integrated Risk Information System (IRIS). National Library of Medicine online
(TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental
Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. September.
3. Ankley, .T., G.L. Phipps, E.N. Leonard, D.A. Benoit, V.R. Mattson, P.A. Kosian, A.M. Cotter, J.R.
Dierkes, DJ. Hansen, and J.D.Mahony. 1991. Acid-volatile sulfide as a factor mediating cadmium
and nickel bioavailability in contaminated sediments. Environ. Set Tech. 10:1299-1307.
4. Pesch, C.E., DJ. Hansen, W.S. Boothman, WJ. Berry, and J.D. Mahony. 1995. The role of acid-
volatile sulfide and interstitial water metal concentrations in determining bioavailability of cadmium
and nickel from contaminated sediments to the marine polychaete Neanthes arenaceodentata.
Environ. Toxicol. Chem. 14:129-141.
5. Sreedevi, P., A. Suresh, B. Sivaramakrishna, B. Prabhavathi, and K. Radhakrishnaiah. 1992.
Biaccumulation of nickel in the organs of the freshwater fish, Cyprinus carpio, and the freshwater
mussel Lamellidens margina, under lethal/sublethal nickel stress. Chemosphere 24:29-36.
6. Enserink, E.L., J.L. Mass-Diepeveen, and CJ. Van Leeuwen. 1991. Combined effects of metals:
An ecotoxicological evaluation. Water Res. 25:679-687.
7. Krantzberg, G. 1994. Spatial and temporal variability in metal bioavailability and toxicity of
sediment from Hamilton Harbour, Lake Ontario. Environ. Toxicol. Chem. 13:1685-1698.
8. Di Toro, D.M., J.D. Mahony, DJ. Hansen, KJ. Scott, M.B. Hicks, S.M. Mayr, and M.S. Redmond.
1990. Toxicity of cadmium in sediments: The role of acid volatile sulfide. Environ. Toxicol. Chem.
9:1487-1502.
9. Krantzberg, G., and D. Boyd. 1992. The biological significance of contaminants in sediment from
Hamilton Harbor, Lake Ontario.
10. Nriagu, J.O. 1980. Global cycle and properties of nickel. In Nickel in the environment, pp. 1-26,
Wiley, New York, NY.
11. Houkal, D., B. Rummel, and B. Shephard. 1996. Results of an in situ mussel bioassay in the Puget
Sound. Abstract, 17th Annual Meeting, Society of Environmental Toxicology and Chemistry,
Washington, DC. November 17-21, 1996
531
-------
BIOACCUMULATION SUMMARY NICKEL
12. Wilson, J.G. 1983. The uptake and accumulation of Ni by Cerastoderma edule and its effect on
mortality, body condition and respiration rate. Mar. Environ. Res 8:129-148.
532
-------
BIOACCUMULATION SUMMARY OXYFLUORFEN
Chemical Category: PESTICIDE (CHLOROPHENOXY)
Chemical Name (Common Synonyms): OXYFLUORFEN CASRN: 42874-03-3
Chemical Characteristics
Solubility in Water: No data [1] Half-Life: No data [2]
Log Kow: No data [3] Log Koc: —
Human Health
Oral RfD: 3 x 10"3 mg/kg/day [4] Confidence: High, uncertainty factor =100
Critical Effect: Increased absolute liver weight and nonneoplastic lesions in mice
Oral Slope Factor: 1.3 x 10"1 per (mg/kg)/day [5] Carcinogenic Classification: C [5]
Wildlife
Partitioning Factors: Partitioning factors for in wildlife were not found in the literature.
Food Chain Multipliers: Food chain multipliers for oxyfluorfen in wildlife were not found in the
literature.
Aquatic Organisms
Partitioning Factors: Partitioning factors for oxyfluorfen in aquatic organisms were not found in the
literature.
Food Chain Multipliers: Food chain multipliers for oxyfluorfen in aquatic organisms were not found
in the literature.
Toxicity/Bioaccumulation Assessment Profile
A light activated herbicide, oxyfluorfen at 10"2 mM increased cell membrane permeability in Lemna minor
[6]. The screening tissue value for fish for oxyfluorfen presented by the Chesapeake Bay Program is 800
ng/g [7].
533
-------
Summary of Biological Effects Tissue Concentrations for Oxyfluorfen
Species:
Taxa
Concentration, Units in1:
Sediment
Water
Toxicity:
Tissue (Sample Type) Effects
Ability to Accumulate2:
Log
BCF
Log
BAF
BSAF
Source:
Reference Comments3
Invertebrates
[NO DATA]
Fishes
[NO DATA]
Wildlife
[NO DATA]
1 Concentration units based on wet weight unless otherwise noted.
2 BCF = bioconcentration factor, BAF = bioaccumulation factor, BSAF = biota-sediment accumulation factor.
3 L = laboratory study, spiked sediment, single chemical; F = field study, multiple chemical exposure; other unusual study conditions or observations noted.
-------
BIOACCUMULATION SUMMARY OXYFLUORFEN
References
1. USEPA. 1995. Hazardous Substances Data Bank (HSDB). National Library of Medicine online
(TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental
Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. September.
2. USEPA. 1989. Chemical fate rate constants for SARA section 313 chemicals and Superfund Health
Manual chemicals. Prepared by Chemical Hazard Assessment Division, Syracuse Research
Corporation, for U.S. Environmental Protection Agency, Office of Toxic Substances, Exposure
Evaluation Division, Washington, DC, and Environmental Criteria and Assessment Office,
Cincinnati, OH. August 11.
3. Karickhoff, S.W., and J.M. Long, 1995. Internal report on summary of measured, calculated, and
recommended log values. Draft. Prepared by U.S. Environmental Protection Agency, Office of
Research and Development, Environmental Research Laboratory-Athens, for E. Southerland, Office
of Water, Office of Science and Technology, Standards and Applied Science Division, Washington,
DC. April 10.
4. USEPA. 1997. Integrated Risk Information System (IRIS). National Library of Medicine online
(TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental
Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. January.
5. USEPA. 1992. Classification list of chemicals evaluated for carcinogenicity potential. U.S.
Environmental Protection Agency, Office of Pesticide Programs, Washington, DC.
6. O'Brien, M.C., and G.N. Prendeville. 1979. Effect of herbicides on cell membrane permeability in
Lemna minor. Weed Res. 19:331-334.
7. Chesapeake Bay Program. 1996. Finfish/'shellfish tissue human health consumption thresholds
compendium. CBP/TRS 96/XX. Chesapeake Bay Program Office, Annapolis, MD.
535
-------
BIOACCUMULATION SUMMARY
PCB28
Chemical Category: BIPHENYLS
Chemical Name (Common Synonyms): 2,4,4'-TRICHLOROBIPHENYL CASRN: 7012-37-5
Chemical Characteristics
Solubility in Water: No data [1], 160 ug/L [2]
Log Kow: 5.60 [2]
Half-Life: No data [3,4]
Log Koc: 5.51 L/kg organic carbon
Human Health
Oral RfD: No data [5]
Critical Effect: —
Oral Slope Factor: No data [5]
Confidence:
Carcinogenic Classification: No data [5]
Wildlife
Partitioning Factors: No partitioning factors were identified for wildlife.
Food Chain Multipliers: For PCBs as a class the most toxic congeners have been shown to be
selectively accumulated from organisms at one trophic level to the next [6]. At least three studies have
concluded that PCBs have the potential to biomagnify in food webs based on aquatic organisms and
predators that feed primarily on aquatic organisms [7,8,9]. The results from Biddinger and Gloss [7] and
USAGE [9] generally agreed that highly water-insoluble compounds (including PCBs) have the potential
to biomagnify in these types of food webs. Thomann's [10] model also indicated that highly water-
insoluble compounds (log Kow values 5 to 7) showed the greatest potential to biomagnify. Log
biomagnification factors of 1.07 and 1.97 were determined for total PCBs from alewife to herring gull
eggs and from alewife to whole body herring gull, respectively [11]. No specific food chain multipliers
were identified for PCB 28.
Aquatic Organisms
Partitioning Factors: Biota-sediment accumulation factors (BSAFs) range from 1.5 to 18.2 for aquatic
invertebrate species. The highest BSAF was provided for marine crustaceans.
Food Chain Multipliers: Polychlorinated biphenyls as a class have been demonstrated to biomagnify
through the food web. Oliver and Niimi [12], studying accumulation of PCBs in various organisms in
the Lake Ontario food web, reported concentrations of total PCBs in phytoplankton, zooplankton, and
several species of fish. Their data indicated a progressive increase in tissue PCB concentrations moving
from organisms lower in the food web to top aquatic predators. In a study of PCB accumulation in lake
trout (Salvelinus namaycush) of Lake Ontario, Rasmussen et al. [13] reported that each trophic level
536
-------
BIOACCUMULATION SUMMARY PCS 28
contributed about a 3.5-fold biomagnification factor to the PCB concentrations in the trout. No specific
food chain multipliers were identified for PCB 28 or other trichlorobiphenyls.
Toxicity/Bioaccumulation Assessment Profile
PCBs are a group (209 congeners/isomers) of organic chemicals, based on various substitutions of
chlorine atoms on a basic biphenyl molecule. These manufactured chemicals have been widely used in
various processes and products because of the extreme stability of many isomers, particularly those with
five or more chlorines [14]. A common use of PCBs was as dielectric fluids in capacitors and
transformers. In the United States, Aroclor is the most familiar registered trademark of commercial PCB
formulations. Generally, the first two digits in the Aroclor designation indicate that the mixture contains
biphenyls, and the last two digits give the weight percent of chlorine in the mixture
As a result of their stability and their general hydrophobic nature, PCBs released to the environment have
dispersed widely throughout the ecosystem [14]. PCBs are among the most stable organic compounds
known, and chemical degradation rates in the environment are thought to be slow. As a result of their
highly lipophilic nature and low water solubility, PCBs are generally found at low concentrations in water
and at relatively high concentrations in sediment [15]. Individual PCB congeners have different physical
and chemical properties based on the degree of chlorination and position of chlorine substitution,
although differences with degree of chlorination are more significant [15]. Solubilities and octanol-water
partition coefficients for PCB congeners range over several orders of magnitude [16]. Octanol-water
partition coefficients, which are often used as estimators of the potential for bioconcentration, are highest
for the most chlorinated PCB congeners.
Dispersion of PCBs in the aquatic environment is a function of their solubility [15], whereas PCB
mobility within and sorption to sediment are a function of chlorine substitution pattern and degree of
chlorination [17]. The concentration of PCBs in sediments is a function of the physical characteristics
of the sediment, such as grain size [18,19] and total organic carbon content [18,19,20,21]. Fine sediments
typically contain higher concentrations of PCBs than coarser sediments because of more surface area [15].
Mobility of PCBs in sediment is generally quite low for the higher chlorinated biphenyls [17]. Therefore,
it is common for the lower chlorinated PCBs to have a greater dispersion from the original point source
[15]. Limited mobility and high rates of sedimentation could prevent some PCB congeners in the
sediment from reaching the overlying water via diffusion [17].
The persistence of PCBs in the environment is a result of their general resistance to degradation [16]. The
rate of degradation of PCB congeners by bacteria decreases with increasing degree of chlorination [22];
other structural characteristics of the individual PCBs can affect susceptibility to microbial degradation
to a lesser extent [16]. Photochemical degradation, via reductive dechlorination, is also known to occur
in aquatic environments; the higher chlorinated PCBs appear to be most susceptible to this process [21].
Toxicity of PCB congeners is dependent on the degree of chlorination as well as the position of chlorine
substitution. Lesser chlorinated congeners are more readily absorbed, but are metabolized more rapidly
than higher chlorinated congeners [23]. PCB congeners with no chlorine substituted in the ortho (2 and
2') positions but with four or more chlorine atoms at the meta (3 and 3') and para (4 and 4') positions can
assume a planar conformation that can interact with the same receptor as the highly toxic 2,3,7,8-
tetrachlorodibenzo-j?-dioxin (TCDD) [24]. Examples of these more toxic, coplanar congeners are
537
-------
BIOACCUMULATION SUMMARY
PCB28
3,3',4,4'-trachlorobiphenyl (PCB 77), 3,3',4,4',5-pentachlorobiphenyl (PCB 126), and 3,3',4,4',5,5'-
hexachlorobiphenyl (PCB 169). A method that has been proposed to estimate the relative toxicity of
mixtures is to use toxic equivalency factors (TEFs) [25]. With this method, relative potencies for
individual congeners are calculated by expressing their potency in relation to 2,3,7,8-TCDD. The
following TEFs have been recommended [25,26]:
Congener Class
3,3',4,4',5-PentaCB
3,3',4,4',5,5'-HexaCB
3,3'4,4'-TetraCB
Monoortho coplanar PCBs
Diortho coplanar PCBs
Recommended TEF
0.1
0.05
0.01
0.001
0.00002
Due to the toxicity, high Kow values, and highly persistent nature of many PCBs, they possess a high
potential to bioaccumulate and exert reproductive effects in higher-trophic-level organisms. Aquatic
organisms have a strong tendency to accumulate PCBs from water and food sources. The log
bioconcentration factor for fish is approximately 4.70 [27]. This factor represents the ratio of
concentration in tissue to the ambient water concentration. Aquatic organisms living in association with
PCB-contaminated sediments generally have tissue concentrations equal to or greater than the
concentration of PCB in the sediment [27]. Once taken up by an organism, partition primarily into lipid
compartments [15]. Thus, differences in PCB concentration between species and between different
tissues within the same species may reflect differences in lipid content [15]. PCB concentrations in
polychaetes and fish have been strongly correlated to their lipid content [28]. Elimination of PCBs from
organisms is related to the characteristics of the specific PCB congeners present. It has been shown that
uptake and depuration rates in mussels are high for lower-chlorinated PCBs and much lower for higher-
chlorinated congeners [29, 30]. In some species, tissue concentrations of in females can be reduced
during gametogenesis because of PCB transfer to the more lipophilic eggs. Therefore, the transferred are
eliminated from the female during spawning [31,32]. Fish and other aquatic organisms biotransform
PCBs more slowly than other species, and they appear less able to metabolize, or excrete, the higher
chlorinated PCB congeners [31]. Consequently, fish and other aquatic organisms may accumulate more
of the higher chlorinated PCB congeners than is found in the environment [16].
The acute toxicity of PCBs appears to be relatively low, but results from chronic toxicity tests indicate
that PCB toxicity is directly related to the duration of exposure [33]. Toxic responses have been noted
to occur at concentrations of 0.03 and 0.014 |ig/L in marine and freshwater environments, respectively
[33]. The LC50 for grass shrimp exposed to PCBs in marine waters for 4 days was 6.1 to 7.8 |ig/L [33].
Chronic toxicity of PCBs presents a serious environmental concern because of their resistance to
degradation [34], although the acute toxicity of PCBs is relatively low compared to that of other
chlorinated hydrocarbons. Sediment contaminated with PCBs has been shown to elicit toxic responses
at relatively low concentrations. Sediment bioassays and benthic community studies suggest that chronic
effects generally occur in sediment at total PCB concentrations exceeding 370 [35].
A number of field and laboratory studies provide evidence of chronic sublethal effects on aquatic
organisms at low tissue concentrations [16]. Field and Dexter [16] suggest that a number of marine and
538
-------
BIOACCUMULATION SUMMARY PCS 28
freshwater fish species have experienced chronic toxicity at PCB tissue concentrations of less than 1.0
mg/kg and as low as 0.1 mg/kg. Spies et al. [36] reported an inverse relationship between PCB
concentrations in starry flounder eggs in San Francisco Bay and reproductive success, with an effective
PCB concentration in the ovaries of less than 0.2 mg/kg. Monod [37] also reported a significant
correlation between PCB concentrations in eggs and total egg mortality in Lake Geneva char. PCBs have
also been shown to cause induction of the mixed function oxidase (MFO) system in aquatic animals, with
MFO induction by PCBs at tissue concentrations within the range of environmental exposures [16].
539
-------
Summary of Biological Effects Tissue Concentrations for PCB 28
Species:
Taxa
Concentration, Units in1:
Sediment Water
Toxicity: Ability to Accumulate2: Source:
Tissue (Sample Type) Effects
Log Log
BCF BAF BSAF
Reference Comments
Invertebrates
Microcystis 1.35±0.9ng/g
aeruginosa, dw (n = 11)
Daphnia longispina, (0-20 cm)
Plankton
0.23 ± 0.22 ng/g
(n=14)
3.3 [38] F; Amsterdam; value is
mean ± SD; mean sediment
TOC = 9.7%; mean lipid =
0.65%
Plankton, 1.9494(mean) 0.0084 (mean) 0.3504 (mean)
Species not reported SD = 0.7309 SD = 0.0031 SD = 0.2353
(n = 9) |ig/kg (n = 3) ng/L (n = 5) |ig/kg
dw
[39] F; collected in western Lake
Erie (offshore Middle Sister
Island); sediment TOC =
7.4% (SD= 1.78), lipid =
1.2%(mean)SD = 0.24
Dreissena
polymorpha,
Zebra mussel
1.9494(mean)
SD = 0.7309
(n = 9)
|ig/kg dw
0.0084(mean) 0.4314(mean)
SD = 0.0031 SD = 0.4642
(n = 3) (n = 20) |ig/kg
ng/L
lipid =1.3% (mean)
SD = 0.34
Dreissena
polymorpha,
Zebra mussel
1.35 ± 0.9 ng
dw(n= 11)
(0-20 cm)
0.52 ± 0.36 ng/g
(n = 5)
2.8 [38] F; Amsterdam; value is
mean ± SD; mean sediment
TOC = 9.7%; mean lipid =
1.74%
Corbicula fluminea, Station B6:
Bivalve 0.44 ng/g dw 1.14 ng/L
Station CIO:
0.034 ng/g dw
-------
Summary of Biological Effects Tissue Concentrations for PCB 28
Species:
Taxa
Crustaceans
Gammarus tigriniis,
Assellus aquaticus,
Orchestra carimana
Gammarus
fasciatus,
Amphipod
Orconectes
propinquus,
Crayfish
Hydropsyche
alterans,
Caddisfly larva
Fishes
Prochilodiis
platensis, Fish
Concentration,
Sediment
1.35±0.9ng/g
dw(n= 11)
(0-20 cm)
1.9494(mean)
SD = 0.7309
(n = 9)
|ig/kg dw
1.9494(mean)
SD = 0.7309
(n = 9)
|ig/kg dw
1.9494(mean)
SD = 0.7309
(n = 9)
|ig/kg dw
Station F17:
0.084 ng/g dw
Units in1:
Water
0.0084 (mean)
SD = 0.0031
(n = 3) ng/L
0.0084 (mean)
SD = 0.0031
(n = 3)
ng/L
0.0084 (mean)
SD = 0.0031
(n = 3)
ng/L
-------
Summary of Biological Effects Tissue Concentrations for PCB 28
Species:
Taxa
Anguilla anguilla,
Eel
Concentration, Units in1: Toxicity:
Sediment Water Tissue (Sample Type) Effects
1.35 d
dw (n
(0-20
1 0.9 ng/g 3.98 ± 3.42 ng/g
= 11) (n = 6)
cm)
Ability to Accumulate2: Source:
Log Log
BCF BAF BSAF Reference Comments3
1.5 [38] F; Amsterdam; value is
mean ± SD; mean sediment
TOC = 9.7%;
mean lipid = 14.9%
1 Concentration units based on wet weight unless otherwise noted.
2 BCF = bioconcentration factor, BAF = bioaccumulation factor, BSAF = biota-sediment accumulation factor.
3 L = laboratory study, spiked sediment, single chemical; F = field study, multiple chemical exposure; other unusual study conditions or observations noted.
4 Reported concentrations reflect both congeners 28 and 31.
5 Not clear from reference if concentration is based on wet or dry weight.
-------
BIOACCUMULATION SUMMARY PCS 28
References
1. USEPA. 1996. Hazardous Substances Data Bank (HSDB). National Library of Medicine online
(TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental
Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. February.
2. Shiw, W.Y., and D. Mac Kay. 1986. A critical review of aqueous solubilities, vapor pressures,
Henrys' Law Constants, and octanol-water partition coefficients of the polychlorinated biphenyls.
/. Phys. Chem. Data 15: 911-929.
3. MacKay, D.M., W.Y. Shiw, and K.C. Ma. 1992. Illustrated handbook of physical-chemical
properties and environmental fate for organic chemicals. Vol. I, Monoaromatic hydrocarbons,
chlorobenzenes and PCBs. Lewis Publishers, Boca Raton, FL.
4. USEPA. 1989. Chemical fate rate constants for SARA section 313 chemicals and Superfund
Health Evaluation Manual chemicals. Prepared by Chemical Hazard Assessment Division,
Syracuse Research Corporation, for U.S. Environmental Protection Agency, Office of Toxic
Substances, Exposure Evaluation Division, Washington, DC, and Environmental Criteria and
Assessment Office, Cincinnati, OH. August 11.
5. USEPA. 1996. Integrated Risk Information System (IRIS). National Library of Medicine online
(TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental
Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. September.
6. Jones, P.O., J.P. Giesy, TJ. Kubiak, D.A. Verbrugge, J.C. Newstead, J.P. Ludwig, D.E. Tillit, R.
Crawford, N. De Galan, and G.T. Ankley. 1993. Biomagnification of bioassay-derived 2, 3, 7, 8-
tetrachlorodibenzo-p-dioxin equivalents. Chemosphere 26:1203-1212.
7. Biddinger, G.R., and S.P. Gloss. 1984. The importance of trophic transfer in the bioaccumulation
of chemical contaminants in aquatic ecosystems. Residue Rev. 91:103-145.
8. Kay, 1984. Potential for biomagniflcation of contaminants within marine and freshwater food
webs. Technical Report D-84-7. U.S. Army Corps of Engineers, Waterways Experiment Station,
Vicksburg, MS.
9. USAGE. 1995. Trophic transfer and biomagnification potential of contaminants in aquatic
ecosystems. Environmental Effects of Dredging, Technical Notes EEDP-01-33. U.S. Army Corps
of Engineers, Waterways Experiment Station, Vicksburg, MS.
10. Thomann, R.V. 1989. Bioaccumulation model of organic chemical distribution in aquatic food
chains. Environ. Sci. Technol. 23:699.
11. Braune, B.M., andR. J. Norstrom. 1989. Dynamics of organochlorine compounds in herring gulls:
III. Tissue distribution and bioaccumulation in Lake Ontario Gulls. Environ. Toxicol. Chem.
8:957-968.
543
-------
BIOACCUMULATION SUMMARY PCS 28
12. Oliver, E.G., and AJ. Niimi. 1988. Trophodynamic analysis of polychlorinated biphenyl
congeners and other chlorinated hydrocarbons in the Lake Ontario ecosystem. Environ. Set
Technol. 22:388-397.
13. Rasmussen, J.B., DJ. Rowan, D.R.S. Lean, and J.H. Carey. 1990. Food chain structure in Ontario
lakes determines PCB levels in lake trout (Salvelinus namaycush) and other pelagic fish. Can. J.
Fish. Aquat. Sci. 47:2030-2038.
14. Rand, G. M., P. G. Wells, and L. S. McCarty. 1995. Chapter 1. Introduction to aquatic toxicology.
In: Fundamentals of aquatic toxicology: Effects, environmental fate, and risk assessment, ed. G.M.
Rand, pp. 3-67. Taylor and Francis. Washington, DC.
15. Phillips, D.J.H. 1986. Use of organisms to quantify PCBs in marine and estuarine environments.
In PCBs and the environment, ed. J.S. Waid, pp. 127-182. CRC Press, Inc., Boca Raton, FL.
16. Field, L. J., and R. N. Dexter. 1998. A discussion of PCB target levels in aquatic sediments.
Unpublished document. January 11, 1988.
17. Fisher, J.B., R.L. Petty, and W. Lick. 1983. Release of polychlorinated biphenyls from
contaminated lake sediments: Flux and apparent diffusivities of four individual PCBs. Environ.
Pollut. 5B: 121-132.
18. Pavlou, S.P., and R.N. Dexter. 1979. Distribution of polychlorinated biphenyls (PCB) in estuarine
ecosystems: Testing the concept of equilibrium partitioning in the marine environment. Environ.
Sci. Technol. 13:65-71.
19. Lynch, T.R., and H.E. Johnson. 1982. Availability of hexachlorobiphenyl isomer to benthic
amphipods from experimentally contaminated sediments. In Aquatic Toxicology and Hazard
Assessment: Fifth Conference, ASTM STP 766, ed. J.G. Pearson, R.B. Foster, and W.E. Bishop,
pp. 273-287. American Society of Testing and Materials, Philadelphia, PA.
20. Chou, S.F.J., and R.A. Griffin. 1986. Solubility and soil mobility of polychlorinated biphenyls.
In: PCBs and the Environment, ed. J. S. Waid, Vol. 1, pp. 101-120. CRC Press, Inc. Boca Raton,
FL.
21. Sawhney, B.L. 1986. Chemistry and properties of PCBs in relation to environmental effects. In
PCBs and the environment, ed. J.S. Waid,. pp. 47-65. CRC Press, Inc., Boca Raton, FL.
22. Furukawa, K. 1986. Modification of PCBs by bacteria and other microorganisms. In PCBs and
the environment, ed. J.S. Waid,. Vol. 2, pp. 89-100. CRC Press, Inc., Boca Raton, FL.
23. Bolger, M. 1993. Overview of PCB toxicology. In Proceedings of the U.S. Environmental
Protection Agency's National Technical Workshop, "PCBs in Fish Tissue," May 10-11, 1993, pp.
3-9. EPA/823-R-93-003, U.S. Environmental Protection Agency, Office of Water, Washington,
DC.
24. Erickson, M.D. 1993. Introduction to PCBs and analytical methods. In Proceedings of the U.S.
Environmental Protection Agency's National Technical Workshop "PCBs in Fish Tissue," May 10-
544
-------
BIOACCUMULATION SUMMARY PCS 28
11, 1993, pp. 3-9. EPA/823-R-93-003, U.S. Environmental Protection Agency, Office of Water,
Washington, DC.
25. Safe, S. 1990. Polychlorinated biphenyls (PCBs), dibenzo-p-dioxins (PCDDs), dibenzofurans
(PCDFs), and related compounds: Environmental and mechanistic considerations which support
the development of toxic equivalency factors (TEFs). Crit. Rev. Toxicol 21(l):51-88.
26. USEPA. 1991. Workshop report on toxicity equivalency factors for poly chlorinate d biphenyl
congeners. EPA/625/3-91/020. U.S. Environmental Protection Agency. (Eastern Research Group,
Inc., Arlington, MA.)
27. Neff, J.M. 1984. Bioaccumulation of organic micropollutants from sediments and suspended
particulates by aquatic animals. Fres. Z. Anal. Chem. 319:132-136.
28. Shaw, G. R., and D. W. Connell. 1982. Factors influencing concentrations of polychlorinated
biphenyls in organisms from an estuarine ecosystem. Aust. J. Mar. Freshw. Res. 33:1057-1070.
29. Tanabe, S., R. Tatsukawa, and D.J.H. Phillips. 1987. Mussels as bioindicators of PCB pollution:
A case study on uptake and release of PCB isomers and congeners in green-lipped mussels (Perna
viridis) in Hong Kong waters. Environ. Pollut. 47:41-62.
30. Pruell, R. J., J. L. Lake, W. R. Davis, and J. G. Quinn. 1986. Uptake and depuration of organic
contaminants by blue mussels (Mytilus edulis) exposed to environmentally contaminated sediments.
Mar.Biol 91:497-508.
31. Lech, J.J., and R.E. Peterson. 1983. Biotransformation and persistence of polychlorinated
biphenyls (PCBs) in fish. In PCBs: Human and environmental hazards, ed. P.M. D'ltri and M.A.
Kamrin, pp. 187-201. Ann Arbor Science Publishers, Inc., Ann Arbor, MI.
32. Stout, V.F. 1986. What is happening to PCBs? Elements of effective environmental monitoring
as illustrated by an analysis of PCB trends in terrestrial and aquatic organisms. In PCBs and the
Environment, ed. J.S. Waid. CRC Press, Inc., Boca Raton, FL.
33. Eisler, R. 1986. Polychlorinated biphenyl hazards to fish, wildlife, and invertebrates: A synoptic
review. U.S. Fish Wildl. Serv. Biol. Rep. 85(1.7).
34. Mearns, A.J., M. Malta, G. Shigenaka, D. MacDonald, M. Buchman, H. Harris, J. Golas, and G.
Lauenstein. 1991. Contaminant trends in the Southern California Bight: Inventory and
assessment. Technical Memorandum NOAA ORCA 62. National Oceanic and Atmospheric
Administration. Seattle, WA.
35. 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. NOAA Tech. Memo. NOS OMA
52. National Oceanic and Atmospheric Administration, Seattle, WA.
36. Spies, R. B., D. W. Rice, Jr., P. A. Montagna, and R. R. Ireland. 1985. Reproductive success,
xenobiotic contaminants and hepatic mixed-function oxidase (MFO) activity in Platichthys stellatus
populations from San Francisco Bay. Mar. Environ. Res. 17:117-121.
545
-------
BIOACCUMULATION SUMMARY PCS 28
37. Monod, G. 1985. Egg mortality of Lake Geneva char (Salvelinus alpinus) contaminated by PCB
and DDT derivatives. Bull Environ. Contain. Toxicol. 35:531-536.
38. Van der Oost, R., H. Heida, and A. Opperhuizen. 1988. Polychlorinated biphenyl congeners in
sediments, plankton, molluscs, crustaceans, and eel in a freshwater lake: Implications of using
reference chemicals and indicator organisms in bioaccumulation studies. Arch. Environ. Contam.
Toxicol. 17:721-729.
39. Morrison, H.A., F.A.P.C. Gobas, R. Lazar, and G.D. Haffner. 1996. Development and verification
of a bioaccumulation model for organic contaminants in benthic invertebrates. Environ. Sci.
Technol. 30:3377-3384.
40. Columbo, J.C., M.F. Khalil, M. Arnac, and A.C. Horth. 1990. Distribution of chlorinated
pesticides and individually polychlorinated biphenyls in biotic and abiotic compartments of the Rio
de la Plata, Argentina. Environ. Sci. Technol 24:498-505.
546
-------
BIOACCUMULATION SUMMARY
PCB77
Chemical Category: POLYCHLORINATED BIPHENYLS
Chemical Name (Common Synonyms): 3,3',4,4'-TETRACHLOROBIPHENYL CASRN: 32598-13-3
Chemical Characteristics
Solubility in Water: 0.18 mg/L [1]
Log Kow: No data [4], 6.1 [5]
Half-Life: No data [2,3]
Log Koc: —
Human Health
Oral RfD: No data [6]
Critical Effect: —
Oral Slope Factor: No data [6]
Confidence:
Carcinogenic Classification: No data [6]
Wildlife
Partitioning Factors: Bioaccumulation factors (BAFs) were determined for mink. The mink had less
PCB-77 in their tissues than was measured in their diet. BAF values ranged from 0.1 to 0.2.
Food Chain Multipliers: For PCBs as a class the most toxic congeners have been shown to be
selectively accumulated from organisms at one trophic level to the next [7]. At least three studies have
concluded that PCBs have the potential to biomagnify in food webs based on aquatic organisms and
predators that feed primarily on aquatic organisms [8,9,10]. The results from Biddinger and Gloss [8]
and USAGE [10] generally agreed that highly water-insoluble compounds (including PCBs) have the
potential to biomagnify in these types of food webs. Thomann's [11] model also indicated that highly
water-insoluble compounds (log Kow values 5 to 7) showed the greatest potential to biomagnify. Log
biomagnification factors (BMFs) for tetrachlorobiphenyls from ale wife to herring gulls ranged from 1.52
to 1.83, but were not measured specifically for PCB 77 [12]. A study of arctic marine food chains
measured log biomagnification factors for tetrachlorobiphenyls that ranged from 0.08 to 0.40 for fish to
seal, <-0.40 for seal to bear, and <-0.30 for fish to bear [13]. Log BMFs calculated for mink fed PCB
77-contaminated feed ranged from -1.00 to -0.70 [40].
Aquatic Organisms
Partitioning Factors: Log bioconcentration factors (BCFs) for blue mussels deployed in New Bedford
Harbor, MA, were approximately 6.40 and 6.60 during two years of the study, as reported in the attached
summary table [42].
547
-------
BIOACCUMULATION SUMMARY PCS 77
Food Chain Multipliers: Polychlorinated biphenyls as a class have been demonstrated to biomagnify
through the food web. Oliver and Niimi [14], studying accumulation of PCBs in various organisms in
the Lake Ontario food web, reported concentrations of total PCBs in phytoplankton, zooplankton, and
several species of fish. Their data indicated a progressive increase in tissue PCB concentrations moving
from organisms lower in the food web to top aquatic predators. In a study of PCB accumulation in lake
trout (Salvelinus namaycush) of Lake Ontario, Rasmussen et al. [15] reported that each trophic level
contributed about a 3.5-fold biomagnification factor to the PCB concentrations in the trout. No specific
food chain multipliers were identified for PCB 77 or other tetrachlorobiphenyls.
Toxicity/Bioaccumulation Assessment Profile
PCBs are a group (209 congeners/isomers) of organic chemicals, based on various substitutions of
chlorine atoms on a basic biphenyl molecule. These manufactured chemicals have been widely used in
various processes and products because of the extreme stability of many isomers, particularly those with
five or more chlorines [16]. A common use of PCBs was as dielectric fluids in capacitors and
transformers. In the United States, Aroclor is the most familiar registered trademark of commercial PCB
formulations. Generally, the first two digits in the Aroclor designation indicate that the mixture contains
biphenyls, and the last two digits give the weight percent of chlorine in the mixture.
As a result of their stability and their general hydrophobic nature, PCBs released to the environment have
dispersed widely throughout the ecosystem [16]. PCBs are among the most stable organic compounds
known, and chemical degradation rates in the environment are thought to be slow. As a result of their
highly lipophilic nature and low water solubility, PCBs are generally found at low concentrations in water
and at relatively high concentrations in sediment [17]. Individual PCB congeners have different physical
and chemical properties based on the degree of chlorination and position of chlorine substitution,
although differences with degree of chlorination are more significant [17]. Solubilities and octanol-water
partition coefficients for PCB congeners range over several orders of magnitude [18]. Octanol-water
partition coefficients, which are often used as estimators of the potential for bioconcentration, are highest
for the most chlorinated PCB congeners.
Dispersion of PCBs in the aquatic environment is a function of their solubility [17] , whereas PCB
mobility within and sorption to sediment are a function of chlorine substitution pattern and degree of
chlorination [19]. The concentration of PCBs in sediments is a function of the physical characteristics
of the sediment, such as grain size [20,21] and total organic carbon content [20,21,22,23]. Fine sediments
typically contain higher concentrations of PCBs than coarser sediments because of more surface area [17].
Mobility of PCBs in sediment is generally quite low for the higher chlorinated biphenyls [19]. Therefore,
it is common for the lower chlorinated PCBs to have a greater dispersion from the original point source
[17]. Limited mobility and high rates of sedimentation could prevent some PCB congeners in the
sediment from reaching the overlying water via diffusion [19].
The persistence of PCB s in the environment is a result of their general resistance to degradation [18]. The
rate of degradation of PCB congeners by bacteria decreases with increasing degree of chlorination [24];
other structural characteristics of the individual PCBs can affect susceptibility to microbial degradation
to a lesser extent [18]. Photochemical degradation, via reductive dechlorination, is also known to occur
in aquatic environments; the higher chlorinated PCBs appear to be most susceptible to this process [23].
548
-------
BIOACCUMULATION SUMMARY
PCB77
Toxicity of PCB congeners is dependent on the degree of chlorination as well as the position of chlorine
substitution. Lesser chlorinated congeners are more readily absorbed, but are metabolized more rapidly
than higher chlorinated congeners [25]. PCB congeners with no chlorine substituted in the ortho (2 and
2') positions but with four or more chlorine atoms at the meta (3 and 3') and para (4 and 4') positions can
assume a planar conformation that can interact with the same receptor as the highly toxic 2,3,7,8-
tetrachlorodibenzo-j?-dioxin (TCDD) [26]. Examples of these more toxic, coplanar congeners are
3,3',4,4'-tetrachlorobiphenyl (PCB 77), 3,3',4,4',5-pentachlorobiphenyl (PCB 126), and 3,3',4,4',5,5'-
hexachlorobiphenyl (PCB 169). A method that has been proposed to estimate the relative toxicity of
mixtures is to use toxic equivalency factors (TEFs) [27]. With this method, relative potencies for
individual congeners are calculated by expressing their potency in relation to 2,3,7,8-TCDD. The
following TEFs have been recommended [27,28]:
Congener Class
3,3',4,4',5-PentaCB
3,3',4,4',5,5'-HexaCB
3,3'4,4'-TetraCB
Monoortho coplanar PCBs
Diortho coplanar PCBs
Recommended TEF
0.1
0.05
0.01
0.001
0.00002
Due to the toxicity, high Kow values, and highly persistent nature of many PCBs, they possess a high
potential to bioaccumulate and exert reproductive effects in higher-trophic-level organisms. Aquatic
organisms have a strong tendency to accumulate PCBs from water and food sources. The log
bioconcentration factor for fish is approximately 4.70 [29]. This factor represents the ratio of
concentration in tissue to the ambient water concentration. Aquatic organisms living in association
with PCB-contaminated sediments generally have tissue concentrations equal to or greater than the
concentration of PCB in the sediment [29]. Once taken up by an organism, PCBs partition primarily
into lipid compartments [17]. Thus, differences in PCB concentration between species and between
different tissues within the same species may reflect differences in lipid content [17]. PCB
concentrations in polychaetes and fish have been strongly correlated to their lipid content [30].
Elimination of PCBs from organisms is related to the characteristics of the specific PCB congeners
present. It has been shown that uptake and depuration rates in mussels are high for lower-chlorinated
PCBs and much lower for higher-chlorinated congeners [31,32]. In some species, tissue
concentrations of PCBs in females can be reduced during gametogenesis because of PCB transfer to
the more lipophilic eggs. Therefore, the transferred PCBs are eliminated from the female during
spawning [33,34]. Fish and other aquatic organisms biotransform PCBs more slowly than other
species, and they appear less able to metabolize, or excrete, the higher chlorinated PCB congeners
[33]. Consequently, fish and other aquatic organisms may accumulate more of the higher chlorinated
PCB congeners than is found in the environment [18].
The acute toxicity of PCBs appears to be relatively low, but results from chronic toxicity tests indicate
that PCB toxicity is directly related to the duration of exposure [35]. Toxic responses have been
noted to occur at concentrations of 0.03 and 0.014 |ig/L in marine and freshwater environments,
respectively [35]. The LC50 for grass shrimp exposed to PCBs in marine waters for 4 days was 6.1 to
7.8 |ig/L [35]. Chronic toxicity of PCBs presents a serious environmental concern because of their
resistance to degradation [36], although the acute toxicity of PCBs is relatively low compared to that
549
-------
BIOACCUMULATION SUMMARY PCS 77
of other chlorinated hydrocarbons. Sediment contaminated with PCBs has been shown to elicit toxic
responses at relatively low concentrations. Sediment bioassays and benthic community studies
suggest that chronic effects generally occur in sediment at total PCB concentrations exceeding 370
Hg/kg [37].
A number of field and laboratory studies provide evidence of chronic sublethal effects on aquatic
organisms at low tissue concentrations [18]. Field and Dexter [18] suggest that a number of marine
and freshwater fish species have experienced chronic toxicity at PCB tissue concentrations of less
than 1.0 mg/kg and as low as 0.1 mg/kg. Spies et al [38] reported an inverse relationship between
PCB concentrations in starry flounder eggs in San Francisco Bay and reproductive success, with an
effective PCB concentration in the ovaries of less than 0.2 mg/kg. Monod [39] also reported a
significant correlation between PCB concentrations in eggs and total egg mortality in Lake Geneva
char. PCBs have also been shown to cause induction of the mixed function oxidase (MFO) system in
aquatic animals, with MFO induction by PCBs at tissue concentrations within the range of
environmental exposures [18].
550
-------
Summary of Biological Effects Tissue Concentrations for PCB 77
Species:
Taxa
Invertebrates
Mytilus edulis,
Blue mussel
Mytilus edulis,
Blue mussel
Concentration, Units in1: Toxicity:
Sediment Water Tissue (Sample Type) Effects
1993:
Particulate
1.7jig/L
±0.5
n = 9
Dissolved
l.Ong/L
±0.1
n = 9
1994: -360ng/gdw
Particulate (whole body)
2.3 |ig/L
±0.9
n = 3
Dissolved
0.9 |ig/L
±0.1
n = 3
Ability to Accumulate2: Source:
Log Log
BCF BAF BSAF Reference Comments3
-6.60 [42] F; New Bedford
Harbor, MA;
deployment study;
tissue concen-
trations were only
presented for 1994
samples; BCF and
tissue concen-
trations are
approximations (~)
as data were taken
from figure
-6.40 [42] Presented for 1994
samples; BCF and
tissue concen-
trations are
approximations (~)
as data were taken
from figure
-------
Summary of Biological Effects Tissue Concentrations for PCB 77
Species:
Taxa
Daphnia magna,
Freshwater
cladoceran
My sis relicta,
Epibenthic
freshwater shrimp
Concentration, Units in1:
Sediment Water Tissue (Sample Type)
exposure -6.5 ng/mg dw
water (n = 3)
0.1 |ig/L
l.Ong/L -55 ng/mg dw
(n = 3)
1 18.47 ng/kg Screened mysids:
dw (TOC = o.72 |ig/kg
22.8%)
Toxicity: Ability to Accumulate2:
Log Log
Effects BCF BAF BSAF
No significant
effect on
survival or
reproduction;
increased
biomass
No significant
effect on
survival or
reproduction;
decreased
biomass
Source:
Reference Comments3
[40] L; 21 -day static
renewal tests; tissue
concentrations are
approximations (~),
as data were taken
from figures
[41] L; mysids exposed
to field
contaminated
Unscreened mysids:
8.74 jig/kg
sediments from
Lake Champlain,
NY; 24-day
exposure; screened
mysids were
screened from
direct contact with
sediments (% lipid
= 5.94 ± 0.27)
whole body;
unscreened mysids
were allowed to
burrow into
sediment.(% lipid =
5.80 ±0.18)
whole body
-------
Summary of Biological Effects Tissue Concentrations for PCB 77
Species:
Taxa
Concentration, Units in1:
Sediment
Water
Toxicity:
Tissue (Sample Type) Effects
Ability to Accumulate2:
Log Log
BCF BAF BSAF
Source:
Reference Comments
Strongylocentrotus 0.050 nŁ
droebachiensis,
Sea urchin
0.087 ng/g
[43] F; sediment and
biota collected near
or in Hamlet in
Cambridge Bay,
NW Territories,
Canada.
Fishes
Myoxocephalus
quadricornis,
Fourhorn sculpin
0.050 ng/g dw
0.056 ng/g (liver)
O.llng/g
(whole body)
[43] F; sediment and
biota collected near
or in Hamlet in
Cambridge Bay,
NW Territories,
Canada.
Salmonids
0.29
[47]
Wildlife
Falco peregrinus,
Peregrine falcon
1.5 ng/g (eggs) (n = 6) 11.4% eggshell
thinning
[46] F; Kola Peninsula,
Russia
White leghorn
chicken
(embryo)
2.6 ng/kg (egg)
8.6 ng/kg (egg)
LD50
LD50
[44] L; PCBs were
injected into the air
cell of eggs
-------
Summary of Biological Effects Tissue Concentrations for PCB 77
Species:
Taxa
Mustela vison,
Mink
Concentration, Units in1: Toxicity:
Sediment Water Tissue (Sample Type) Effects
Diet:
1 1 pg/g4 50 pg/g4 (liver) NOAEL
300 pg/g4 45 pg/g4 (liver) LOAEL;
reduced kit body
weights
followed by
reduced survival
600 pg/g4 50 pg/g4 (liver) Reduced kit
body weights
followed by
reduced survival
1,100 pg/g4 90 pg/g4 (liver) Significant
decrease in
number of live
kits whelped per
female
Ability to Accumulate2: Source:
Log Log
BCF BAF BSAF Reference Comments3
[45] L;BMF= lipid-
No BMP normalized
reported concentration in the
liver divided by the
Log lipid-normalized
BMP = dietary
-0.70 concentration
Log
BMF =
-1.00
Log
BMF =
-1.00
1 Concentration units expressed in wet weight unless otherwise noted.
2 BCF = bioconcentration factor, BAF = bioaccumulation factor, BSAF = biota-sediment accumulation factor.
3 L = laboratory study, spiked sediment, single chemical; F = field study, multiple chemical exposure; other unusual study conditions or observations noted.
4 Not clear whether units are in dry or wet weight.
-------
BIOACCUMULATION SUMMARY PCB 77
References
1. National Academy of Science. 1979. Polychlorinated biphenyls (report), p. 154. (Cited in USEPA.
1996. Hazardous Substances Data Bank (HSDB). National Library of Medicine online
(TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental
Assessment, Environmental Criteria and Assessment Office, Cinncinati, OH. February.)
2. MacKay, D.M., W.Y. Shiw, and K.C. Ma. 1992. Illustrated handbook of physical-chemical
properties and environmental fate for organic chemicals, Vol. I, Monoaromatic hydrocarbons,
chlorobenzenes and PCBs. Lewis Publishers, Boca Raton, FL.
3. USEPA. 1989. Chemical fate rate constants for SARA section 313 chemicals and Superfund
Health Evaluation Manual chemicals. Prepared by Chemical Hazard Assessment Division,
Syracuse Research Corporation, for U.S. Environmental Protection Agency, Office of Toxic
Substances, Exposure Evaluation Division, Washington, DC, and Environmental Criteria and
Assessment Office, Cincinnati, OH. August 11.
4. Karickhoff, S.W., and J.M. Long. 1995. Internal report on summary of measured, calculated
and recommended log Kow values. Draft. Prepared by U.S. Environmental Protection Agency,
Office of Research and Development, Environmental Research Laboratory-Athens, for E.
Southerland, Office of Water, Office of Science and Technology, Standards and Applied Science
Division, Washington, DC. April 10.
5. Shiw, W.Y., and D. MacKay. 1986. A critical review of aqueous solubilities, vapor pressures,
Henrys' Law Constants, and octanol-water partition coefficients of the polychlorinated biphenyls.
/. Phys. Chem. Data 15:911-929.
6. USEPA. 1996. Integrated Risk Information System (IRIS). National Library of Medicine online
(TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental
Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. September.
7. Jones, P.O., J.P. Giesy, T.J. Kubiak, D.A. Verbrugge, J.C. Newstead, J.P. Ludwig, D.E. Tillit,
R. Crawford, N. De Galan, and G.T. Ankley. 1993. Biomagnification of bioassay-derived 2, 3,
7, 8-tetrachlorodibenzo-j?-dioxin equivalents. Chemosphere 26:1203-1212.
8. Biddinger, G.R., and S.P. Gloss. 1984. The importance of trophic transfer in the
bioaccumulation of chemical contaminants in aquatic ecosystems. Residue Rev. 91:103-145.
9. Kay, S.H. 1984. Potential for biomagnification of contaminants within marine and freshwater
food webs. Technical Report D-84-7, U.S. Army Corps of Engineers, Waterways Experiment
Station, Vicksburg, MS.
10. USAGE. 1995. Trophic transfer and biomagnification potential of contaminants in aquatic
ecosystems. Environmental Effects of Dredging, Technical Notes EEDP-01-33. U.S. Army
Corps of Engineers, Waterways Experiment Station, Vicksburg, MS.
555
-------
BIOACCUMULATION SUMMARY PCB 77
11. Thomann, R.V. 1989. Bioaccumulation model of organic chemical distribution in aquatic food
chains. Environ. Sci. Technol. 23:699.
12. Braune, B.M., and R. J. Norstrom. 1989. Dynamics of organochlorine compounds in herring
gulls: HI. Tissue distribution and bioaccumulation in Lake Ontario Gulls. Environ. Toxicol.
Chem. 8:957-968.
13. Muir, D.C.G., R.J. Norstrom, and M. Simon. 1988. Organochlorine contaminants in arctic
marine food chains: Accumulation of specific polychlorinated biphenyls and chlordane-related
compounds. Environ. Sci. Technol. 22:1071-1079.
14. Oliver, E.G., and AJ. Niimi. 1988. Trophodynamic analysis of polychlorinated biphenyl
congeners and other chlorinated hydrocarbons in the Lake Ontario ecosystem. Environ. Sci.
Technol. 22:388-397.
15. Rasmussen, J.B., DJ. Rowan, D.R.S. Lean, and J.H. Carey. 1990. Food chain structure in
Ontario lakes determines PCB levels in lake trout (Salvelinus namaycush) and other pelagic fish.
Can. J. Fish. Aquat. Sci. 47:2030-2038.
16. Rand, G. M., P. G. Wells, and L. S. McCarty. 1995. Chapter 1. Introduction to aquatic
toxicology. In Fundamentals of aquatic toxicology: Effects, environmental fate, and risk
assessment, ed. G.M. Rand, pp. 3-67. Taylor and Francis, Washington, DC.
17. Phillips, DJ.H. 1986. Use of organisms to quantify PCB s in marine and estuarine environments.
In PCBs and the environment, ed. J.S. Waid, pp.127-182. CRC Press, Inc., Boca Raton, FL.
18. Field, L. J. and R. N. Dexter. 1998. A discussion of PCB target levels in aquatic sediments.
Unpublished document. January 11, 1988.
19. Fisher, J.B., R.L. Petty, and W. Lick. 1983. Release of polychlorinated biphenyls from
contaminated lake sediments: Flux and apparent diffusivities of four individual PCBs. Environ.
Pollut. 5B: 121-132.
20. Pavlou, S.P., and R.N. Dexter. 1979. Distribution of polychlorinated biphenyls (PCB) in
estuarine ecosystems: Testing the concept of equilibrium partitioning in the marine environment.
Environ. Sci. Technol. 13:65-71.
21. Lynch, T.R., and H.E. Johnson. 1982. Availability of hexachlorobiphenyl isomer to benthic
amphipods from experimentally contaminated sediments. In Aquatic Toxicology and Hazard
Assessment: Fifth Conference, ASTM STP 766, ed. J.G. Pearson, R.B. Foster, and W.E. Bishop,
pp. 273-287. American Society of Testing and Materials, Philadelphia, PA.
22. Chou, S.F.J., and R.A. Griffin. 1986. Solubility and soil mobility of polychlorinated biphenyls.
In PBS and the Environment, ed. J. S. Waid, Vol. 1, pp. 101-120. CRC Press, Inc. Boca Raton,
FL.
556
-------
BIOACCUMULATION SUMMARY PCB 77
23. Sawhney, B.L. 1986. Chemistry and properties of PCBs in relation to environmental effects.
In PCBs and the environment, ed. J.S. Waid, pp. 47-65. CRC Press, Inc., Boca Raton, FL.
24. Furukawa, K. 1986. Modification of PCBs by bacteria and other microorganisms. In PCBs and
the environment, ed. J.S. Waid, Vol. 2, pp. 89-100. CRC Press, Inc., Boca Raton, FL.
25. Bolger, M. 1993. Overview of PCB toxicology. In Proceedings of the U.S. Environmental
Protection Agency's National Technical Workshop "PCBs in Fish Tissue," May 10-11, 1993,
pp. 37-53. EPA/823-R-93-003, U.S. Environmental Protection Agency, Office of Water,
Washington, DC.
26. Erickson, M.D. 1993. Introduction to PCBs and analytical methods. In Proceedings of the U.S.
Environmental Protection Agency's National Technical Workshop "PCBs in Fish Tissue," May
10-11, 1993, pp. 3-9. EPA/823-R-93-003. U.S. Environmental Protection Agency, Washington,
DC.
27. Safe, S. 1990. Polychlorinated biphenyls (PCBs), dibenzo-/?-dioxins (PCDDs), dibenzofurans
(PCDFs), and related compounds: Environmental and mechanistic considerations which support
the development of toxic equivalency factors (TEFs). Crit. Rev. Toxicol. 21(l):51-88.
28. USEPA. 1991. Workshop report on toxicity equivalency factors for polychlorinated biphenyl
congeners. EPA/625/3-91/020. U.S. Environmental Protection Agency. (Eastern Research
Group, Inc., Arlington, MA.)
29. Neff, J.M. 1984. Bioaccumulation of organic micropollutants from sediments and suspended
particulates by aquatic animals. Fres. Z. Anal. Chem. 319:132-136.
30. Shaw, G. R. and D. W. Connell. 1982. Factors influencing concentrations of polychlorinated
biphenyls in organisms from an estuarine ecosystem. Aust. J. Mar. Freshw. Res. 33:1057-1070.
31. Tanabe, S., R. Tatsukawa, and DJ.H. Phillips. 1987. Mussels as bioindicators of PCB pollution:
A case study on uptake and release of PCB isomers and congeners in green-lipped mussels
(Perna viridis) in Hong Kong waters. Environ. Pollut. 47:41-62.
32. Pruell, R.J., J.L. Lake, W.R. Davis, and J.G. Quinn. 1986. Uptake and depuration of organic
contaminants by blue mussels (Mytilus edulis) exposed to environmentally contaminated
sediments. Mar. Biol. 91:497-508.
33. Lech, J.J., and R.E. Peterson. 1983. Biotransformation and persistence of polychlorinated
biphenyls (PCBs) in fish. In PCBs: Human and environmental hazards, ed. P.M. D'ltri and M.A.
Kamrin, pp. 187-201. Ann Arbor Science Publishers, Inc., Ann Arbor, MI.
34. Stout, V.F. 1986. What is happening to PCBs? Elements of effective environmental monitoring
as illustrated by an analysis of PCB trends in terrestrial and aquatic organisms. In PCBs and the
environment, ed. J.S. Waid. CRC Press, Inc., Boca Raton, FL.
557
-------
BIOACCUMULATION SUMMARY PCB 77
35. USEPA. 1980. Ambient water quality criteria document: Poly chlorinated biphenyls. EPA
440/5-80-068. (Cited in USEPA. 1996. Hazardous Substances Data Bank (HSDB). National
Library of Medicine online (TOXNET). U.S. Environmental Protection Agency, Office of Health
and Environmental Assessment, Environmental Criteria and Assessment Office, Cinncinati, OH.
February.)
36. Mearns, A.J., M. Malta, G. Shigenaka, D. MacDonald, M. Buchman, H. Harris, J. Golas, and G.
Lauenstein. 1991. Contaminant trends in the Southern California Bight: Inventory and
assessment. Technical Memorandum NOAA ORCA 62. National Oceanic and Atmospheric
Administration. Seattle, WA.
37. 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. NOAA Technical
Memorandum NOS OMA 52. National Oceanic and Atmospheric Administration, Seattle, WA.
38. Spies, R. B., D. W. Rice, Jr., P. A. Montagna, and R. R. Ireland. 1985. Reproductive success,
xenobiotic contaminants and hepatic mixed-function oxidase (MFO) activity in Platichthys
stellatus populations from San Francisco Bay. Mar. Environ. Res. 17:117-121.
39. Monod, G. 1985. Egg mortality of Lake Geneva char (Salvelinus alpinus) contaminated by PCB
and DDT derivatives. Bull. Environ. Contam. Toxicol. 35:531-536.
40. Van der Oost, R., H. Heida, and A. Opperhuizen. 1988. Polychlorinated biphenyl congeners in
sediments, plankton, molluscs, crustaceans, and eel in a freshwater lake: Implications of using
reference chemicals and indicator organisms in bioaccumulation studies. Arch. Environ. Contam.
Toxicol. 17:721-729.
41. Lester, D.C., and A. Mclntosh. 1994. Accumulation of polychlorinated biphenyl congeners from
Lake Champlain sediments by Mysis relicta. Environ. Toxicol. Chem. 13:1825-1841.
42. Bergen, B.J., W.G. Nelson, and RJ.Pruell. 1996. Comparison of nonplanar and coplanar PCB
congener partitioning in seawater and bioaccumulation in blue mussels (Mytilus edulis). Environ.
Toxicol. Chem. 15:1517-1523.
43. Bright, D.A., S.L. Grundy, and K.J. Reimer. 1995. Differential bioaccumulation of non-ortho
substituted and other PCB congeners in coastal arctic invertebrates and fish. Environ. Sci.
Technol. 29:2504-2512.
44. Brunstrom, B., and L. Andersson. 1988. Toxicity and 7-ethoxyresorufin O-deethylase-inducing
potency of coplanar polychlorinated biphenyls (PCBs) in chick embryos. Arch. Toxicol. 62:263-
266.
45. Tillitt, D.E., R.W. Gale, J.C. Meadows, J.L. Zajicek, P.H. Peterman, S.N. Heaton, P.O. Jones, S.J.
Bursian, T.J. Kubiak, J.P. Giesy, and R.J. Aulerich. 1996. Dietary exposure of mink to carp
from Saginaw Bay. 3. Characterization of dietary exposure to planar halogenated hydrocarbons,
dioxin equivalents, and biomagnification. Environ. Sci. Technol. 30:283-291.
558
-------
BIOACCUMULATION SUMMARY PCB 77
46. Henny, C.J., S.A. Ganusevich, P.P. Ward, and T.R. Schwartz. 1994. Organochlorine pesticides,
chlorinated dioxins and furans, and PCBs in peregrine falcon Falco peregrinus eggs from the
Kola Penninsula, Russia. In Raptor conservation today, ed. B.U. Meyburg and R.D. Chancellor,
pp. 739-749. WWGPB/The Pica Press.
47. USEPA. 1995. Great Lakes Water Quality Initiative technical support document for the
procedure to determine bio accumulation factors. EPA-820-B-95-005. U.S. Environmental
Protection Agency, Office of Water, Washington, DC.
559
-------
560
-------
BIOACCUMULATION SUMMARY
PCB81
Chemical Category: POLYCHLORINATED BIPHENYLS
Chemical Name (Common Synonyms): 3,4,4',5-TETRACHLOROBIPHENYL CASRN: 70362-50-4
Chemical Characteristics
Solubility in Water: No data [1,2]
Log Kow: No data [2,4]
Half-Life: No data [2,3]
Log Koc: —
Human Health
Oral RfD: No data [5]
Critical Effect: —
Oral Slope Factor: No data [5]
Confidence: —
Carcinogenic Classification: No data [5]
Wildlife
Partitioning Factors: Bioaccumulation factors were determined for mink. At PCB 81 concentration
> 66 pg/g, the mink had less PCB 81 in their tissues (liver) than was measured in their diet. At low PCB
81 concentrations (e.g., 27 pg/g), there was an increase in the tissue burden. Log BAF values ranged from
-0.10 to 0.23.
Food Chain Multipliers: For PCBs as a class the most toxic congeners have been shown to be
selectively accumulated from organisms at one trophic level to the next [6]. At least three studies have
concluded that PCBs have the potential to biomagnify in food webs based on aquatic organisms and
predators that feed primarily on aquatic organisms [7,8,9]. The results from Biddinger and Gloss [7] and
USAGE [9] generally agreed that highly water-insoluble compounds (including PCBs) have the potential
to biomagnify in these types of food webs. Thomann's [10] model also indicated that highly water-
insoluble compounds (log Kow values 5 to 7) showed the greatest potential to biomagnify. Log
biomagnification factors for tetrachlorobiphenyls from alewife to herring gulls ranged from 1.52 to 1.83,
but were not measured specifically for PCB 81 [11]. A study of arctic marine food chains measured log
biomagnification factors for tetrachlorobiphenyls that ranged from 0.08 to 0.40 for fish to seal, <-0.4 for
seal to bear, and <-0.3 for fish to bear [12]. No specific food chain multipliers were identified for PCB
81.
Aquatic Organisms
Partitioning Factors: No partitioning factors were identified for aquatic organisms.
Food Chain Multipliers: Polychlorinated biphenyls as a class have been demonstrated to biomagnify
through the food web. Oliver and Niimi [13], studying accumulation of PCBs in various organisms in
561
-------
BIOACCUMULATION SUMMARY PCB 81
the Lake Ontario food web, reported concentrations of total PCBs in phytoplankton, zooplankton, and
several species of fish. Their data indicated a progressive increase in tissue PCB concentrations moving
from organisms lower in the food web to top aquatic predators. In a study of PCB accumulation in lake
trout (Salvelinus namaycush) of Lake Ontario, Rasmussen et al. [14] reported that each trophic level
contributed about a 3.5-fold biomagnification factor to the PCB concentrations in the trout. No specific
food chain multipliers were identified for PCB 81.
Toxicity/Bioaccumulation Assessment Profile
PCBs are a group (209 congeners/isomers) of organic chemicals, based on various substitutions of
chlorine atoms on a basic biphenyl molecule. These manufactured chemicals have been widely used in
various processes and products because of the extreme stability of many isomers, particularly those with
five or more chlorines [15]. A common use of PCBs was as dielectric fluids in capacitors and
transformers. In the United States, Aroclor is the most familiar registered trademark of commercial PCB
formulations. Generally, the first two digits in the Aroclor designation indicate that the mixture contains
biphenyls, and the last two digits give the weight percent of chlorine in the mixture.
As a result of their stability and their general hydrophobic nature, PCBs released to the environment have
dispersed widely throughout the ecosystem [15]. PCBs are among the most stable organic compounds
known, and chemical degradation rates in the environment are thought to be slow. As a result of their
highly lipophilic nature and low water solubility, PCBs are generally found at low concentrations in water
and at relatively high concentrations in sediment [16]. Individual PCB congeners have different physical
and chemical properties based on the degree of chlorination and position of chlorine substitution,
although differences with degree of chlorination are more significant [16]. Solubilities and octanol-water
partition coefficients for PCB congeners range over several orders of magnitude [17]. Octanol-water
partition coefficients, which are often used as estimators of the potential for bioconcentration, are highest
for the most chlorinated PCB congeners.
Dispersion of PCBs in the aquatic environment is a function of their solubility [16], whereas PCB
mobility within and sorption to sediment are a function of chlorine substitution pattern and degree of
chlorination [18]. The concentration of PCBs in sediments is a function of the physical characteristics
of the sediment, such as grain size [19,20] and total organic carbon content [19,20,21,22]. Fine sediments
typically contain higher concentrations of PCB s than coarser sediments because of more surface area [16].
Mobility of PCBs in sediment is generally quite low for the higher chlorinated biphenyls [18]. Therefore,
it is common for the lower chlorinated PCBs to have a greater dispersion from the original point source
[16]. Limited mobility and high rates of sedimentation could prevent some PCB congeners in the
sediment from reaching the overlying water via diffusion [18].
The persistence of PCB s in the environment is a result of their general resistance to degradation [17]. The
rate of degradation of PCB congeners by bacteria decreases with increasing degree of chlorination [23];
other structural characteristics of the individual PCBs can affect susceptibility to microbial degradation
to a lesser extent [17]. Photochemical degradation, via reductive dechlorination, is also known to occur
in aquatic environments; the higher chlorinated PCBs appear to be most susceptible to this process [22].
Toxicity of PCB congeners is dependent on the degree of chlorination as well as the position of chlorine
substitution. Lesser chlorinated congeners are more readily absorbed, but are metabolized more rapidly
than higher chlorinated congeners [24]. PCB congeners with no chlorine substituted in the ortho (2 and
562
-------
BIOACCUMULATION SUMMARY
PCB81
2') positions but with four or more chlorine atoms at the meta (3 and 3') and para (4 and 4') positions can
assume a planar conformation that can interact with the same receptor as the highly toxic 2,3,7,8-
tetrachlorodibenzo-p-dioxin (TCDD) [25]. Examples of these more toxic, coplanar congeners are
3,3',4,4'-tetrachlorobiphenyl (PCB 77), 3,3',4,4',5-pentachlorobiphenyl (PCB 126), and 3,3',4,4'5,5'-
hexachlorobiphenyl (PCB 169). A method that has been proposed to estimate the relative toxicity of
mixtures is to use toxic equivalency factors (TEFs) [26]. With this method, relative potencies for
individual congeners are calculated by expressing their potency in relation to 2,3,7,8-TCDD. The
following TEFs have been recommended [26,27]:
Congener Class
3,3',4,4',5-PentaCB
3,3',4,4',5,5'-HexaCB
3,3'4,4'-TetraCB
Monoortho coplanar PCBs
Diortho coplanar PCBs
Recommended TEF
0.1
0.05
0.01
0.001
0.00002
Due to the toxicity, high Kow values, and highly persistent nature of many PCBs, they possess a high
potential to bioaccumulate and exert reproductive effects in higher-trophic-level organisms. Aquatic
organisms have a strong tendency to accumulate PCBs from water and food sources. The log
bioconcentration factor for fish is approximately 4.70 [28]. This factor represents the ratio of
concentration in tissue to the ambient water concentration. Aquatic organisms living in association with
PCB-contaminated sediments generally have tissue concentrations equal to or greater than the
concentration of PCB in the sediment [28]. Once taken up by an organism, PCBs partition primarily into
lipid compartments [16]. Thus, differences in PCB concentration between species and between different
tissues within the same species may reflect differences in lipid content [16]. PCB concentrations in
polychaetes and fish have been strongly correlated to their lipid content [29]. Elimination of PCBs from
organisms is related to the characteristics of the specific PCB congeners present. It has been shown that
uptake and depuration rates in mussels are high for lower-chlorinated PCBs and much lower for higher-
chlorinated congeners [30, 31]. In some species, tissue concentrations of PCBs in females can be reduced
during gametogenesis because of PCB transfer to the more lipophilic eggs. Therefore, the transferred
PCBs are eliminated from the female during spawning [32,33]. Fish and other aquatic organisms
biotransform PCBs more slowly than other species, and they appear less able to metabolize, or excrete,
the higher chlorinated PCB congeners [32]. Consequently, fish and other aquatic organisms may
accumulate more of the higher chlorinated PCB congeners than is found in the environment [17].
The acute toxicity of PCBs appears to be relatively low, but results from chronic toxicity tests indicate
that PCB toxicity is directly related to the duration of exposure [34]. Toxic responses have been noted
to occur at concentrations of 0.03 and 0.014 |ig/L in marine and freshwater environments, respectively
[34]. The LC50 for grass shrimp exposed to PCBs in marine waters for 4 days was 6.1 to 7.8 |ig/L [34].
Chronic toxicity of PCBs presents a serious environmental concern because of their resistance to
degradation [35], although the acute toxicity of PCBs is relatively low compared to that of other
chlorinated hydrocarbons. Sediment contaminated with PCBs has been shown to elicit toxic responses
at relatively low concentrations. Sediment bioassays and benthic community studies suggest that chronic
effects generally occur in sediment at total PCB concentrations exceeding 370 |ig/kg [36].
563
-------
BIOACCUMULATION SUMMARY PCB 81
A number of field and laboratory studies provide evidence of chronic sublethal effects on aquatic
organisms at low tissue concentrations [17]. Field and Dexter [17] suggest that a number of marine and
freshwater fish species have experienced chronic toxicity at PCB tissue concentrations of less than 1.0
mg/kg and as low as 0.1 mg/kg. Spies et al. [37] reported an inverse relationship between PCB
concentrations in starry flounder eggs in San Francisco Bay and reproductive success, with an effective
PCB concentration in the ovaries of less than 0.2 mg/kg. Monod [38] also reported a significant
correlation between PCB concentrations in eggs and total egg mortality in Lake Geneva char. PCBs have
also been shown to cause induction of the mixed function oxidase (MFO) system in aquatic animals, with
MFO induction by PCBs at tissue concentrations within the range of environmental exposures [17].
564
-------
Summary of Biological Effects Tissue Concentrations for PCB 81
Species:
Taxa
Invertebrates
Tiibifex sp,
Oligochaetes
Fishes
Cyprinus carpio,
Carp
Salmonids
Wildlife
Bucephala clangula,
Goldeneye
Aythya affinis,
Lesser scaup
Aythya marila,
Greater scaup
Falco peregriniis,
Peregrine falcon
Concentration, Units in1:
Sediment Water
0.0006 mg/kg
(n=l)
0.0006 mg/kg
(n=l)
0.0006 mg/kg
(n=l)
0.0006 mg/kg
(n=l)
0.0006 mg/kg
(n=l)
Toxicity: Ability to Accumulate2:
Log Log
Tissue (Sample Type) Effects BCF BAF BSAF
0.0003 mg/kg
(one composite)
0.021±0.012 mg/kg
(n = 9)
0.67
0.017±0.0002 mg/kg
(n = 3)
0.31±0.017 mg/kg
(n = 7)
0.046±0.016 mg/kg
(n = 3)
0.14 ng/g (eggs) 1 1 .4% eggshell
(n = 6) thinning
Source:
Reference
[39]
[39]
[42]
[39]
[39]
[39]
[40]
Comments3
F; lower Detroit
River
F; lower Detroit
River
F
F; lower Detroit
River
F; lower Detroit
River
F; lower Detroit
River
F; Kola Peninsula,
Russia
-------
ON
ON
Summary of Biological Effects Tissue Concentrations for PCB 81
Species: Concentration, Units in1: Toxicity:
Taxa Sediment Water Tissue (Sample Type) Effects
Miistela vison, Mink Diet: 2 pg/g4 50 pg/g4 (liver) NOAEL
27pg/g4 45 pg/g4 (liver) LOAEL;
reduced kit
body weights
followed by
66 pg/g4 50 pg/g4 (liver) reduced
survival
150 pg/g4
100 pg/g4 (liver) Reduced kit
body weights
followed by
reduced
survival
Significant
decrease in
number of live
kits whelped
per female
Ability to Accumulate2:
Log Log
BCF BAF BSAF
No BMP
reported
Log
BMF =
0.23
Log
BMF =
-0.10
Log
BMF =
0.00
Source:
Reference Comments3
[41] L; BMP = lipid-
normalized
concentration in
the liver divided
by the lipid-
normalized dietary
concentration
1 Concentration units in wet weight unless otherwise noted.
2 BCF = bioconcentration factor, BAF = bioaccumulation factor, BSAF = biota-sediment accumulation factor.
3 L = laboratory study, spiked sediment, single chemical; F = field study, multiple chemical exposure; other unusual study conditions or observations noted.
4 Not clear whether units are in dry or wet weight.
-------
BIOACCUMULATION SUMMARY PCS 81
References
1. USEPA. 1995. Hazardous Substances Data Bank (HSDB). National Library of Medicine online
(TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental
Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. February.
2. MacKay, D.M., W.Y. Shiw, and K.C. Ma. 1992. Illustrated handbook of physical-chemical
properties and environmental fate for organic chemicals. Vol. I, Monoaromatic hydrocarbons,
chlorobenzenes and PCBs. Lewis Publishers, Boca Raton, FL.
3. USEPA. 1989. Chemical fate rate constants for SARA section 313 chemicals and Superfund
Health Evaluation Manual chemicals. Prepared by Chemical Hazard Assessment Division,
Syracuse Research Corporation, for U.S. Environmental Protection Agency, Office of Toxic
Substances, Exposure Evaluation Division, Washington, DC, and Environmental Criteria and
Assessment Office, Cincinnati, OH. August 11.
4 Karickhoff, S.W., and J.M. Long. 1995. Internal report on summary of measured, calculated
and recommended log Kow values. Draft. Prepared by U.S. Environmental Protection Agency,
Office of Research and Development, Environmental Research Laboratory-Athens, for E.
Southerland, Office of Water, Office of Science and Technology, Standards and Applied Science
Division, Washington, DC. April 10.
5. USEPA. 1996. Integrated Risk Information System (IRIS). National Library of Medicine online
(TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental
Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. September.
6. Jones, P.O., J.P. Giesy, T.J. Kubiak, D.A. Verbrugge, J.C. Newstead, J.P. Ludwig, D.E. Tillit,
R. Crawford, N. De Galan, and G.T. Ankley. 1993. Biomagnification of bioassay-derived 2, 3,
7, 8-tetrachlorodibenzo-p-dioxin equivalents. Chemosphere 26:1203-1212.
7. Biddinger, G.R., and S.P. Gloss. 1984. The importance of trophic transfer in the
bioaccumulation of chemical contaminants in aquatic ecosystems. Residue Rev. 91:103-145.
8. Kay, S.H. 1984. Potential for biomagnification of contaminants within marine and freshwater
food webs. Technical Report D-84-7. U.S. Army Corps of Engineers, Waterways Experiment
Station, Vicksburg, MS.
9. USAGE. 1995. Trophic transfer and biomagnification potential of contaminants in aquatic
ecosystems. Environmental Effects of Dredging, Technical Notes EEDP-01-33. U.S. Army
Corps of Engineers, Waterways Experiment Station, Vicksburg, MS.
10. Thomann, R.V. 1989. Bioaccumulation model of organic chemical distribution in aquatic food
chains. Environ. Sci. Technol. 23:699.
11. Braune, B.M., and R.J. Norstrom. 1989. Dynamics of organochlorine compounds in herring
gulls: III. Tissue distribution and bioaccumulation in Lake Ontario gulls. Environ. Toxicol.
Chem. 8:957-968.
567
-------
BIOACCUMULATION SUMMARY PCS 81
12. Muir, D.C.G., RJ. Norstrom, and M. Simon. 1988. Organochlorine contaminants in arctic
marine food chains: Accumulation of specific polychlorinated biphenyls and chlordane-related
compounds. Environ. Set Technol 22:1071-1079.
13. Oliver, E.G., and AJ. Niimi. 1988. Trophodynamic analysis of polychlorinated biphenyl
congeners and other chlorinated hydrocarbons in the Lake Ontario ecosystem. Environ. Sci.
Technol. 22:388-397.
14. Rasmussen, J.B., DJ. Rowan, D.R.S. Lean, and J.H. Carey. 1990. Food chain structure in
Ontario lakes determines PCB levels in lake trout (Salvelinus namaycush) and other pelagic fish.
Can. J. Fish. Aquat. Sci. 47:2030-2038.
15. Rand, G.M., P.O. Wells, and L.S. McCarty. 1995. Chapter 1. Introduction to aquatic toxicology.
In Fundamentals of aquatic toxicology: Effects, environmental fate, and risk assessment, ed.
G.M. Rand, pp. 3-67. Taylor and Francis, Washington, DC.
16. Phillips, DJ.H. 1986. Use of organisms to quantify PCB s in marine and estuarine environments.
In PCBs and the environment, ed. J.S. Waid, pp.127-182. CRC Press, Inc., Boca Raton, FL.
17. Field, L.J., and R.N. Dexter. 1998. A discussion of PCB target levels in aquatic sediments.
Unpublished document. January 11, 1988.
18. Fisher, J.B., R.L. Petty, and W. Lick. 1983. Release of polychlorinated biphenyls from
contaminated lake sediments: Flux and apparent diffusivities of four individual PCBs. Environ.
Pollut. 5B: 121-132.
19. Pavlou, S.P., and R.N. Dexter. 1979. Distribution of polychlorinated biphenyls (PCB) in
estuarine ecosystems: Testing the concept of equilibrium partitioning in the marine environment.
Environ. Sci. Technol. 13:65-71.
20. Lynch, T.R., and H.E. Johnson. 1982. Availability of hexachlorobiphenyl isomer to benthic
amphipods from experimentally contaminated sediments. In Aquatic Toxicology and Hazard
Assessment: Fifth Conference, ASTM STP 766, ed. J.G. Pearson, R.B. Foster, and W.E. Bishop,
pp. 273-287. American Society of Testing and Materials, Philadelphia, PA.
21. Chou, S.F.J., and R.A. Griffin. 1986. Solubility and soil mobility of polychlorinated biphenyls.
In PCBs and the environment, ed. J.S. Waid, Vol.1, pp. 101-120. CRC Press, Inc. Boca Raton,
FL.
22. Sawhney, B.L. 1986. Chemistry and properties of PCBs in relation to environmental effects.
In PCBs and the environment, ed. J.S. Waid, pp. 47-65. CRC Press, Inc., Boca Raton, FL.
23. Furukawa, K. 1986. Modification of PCBs by bacteria and other microorganisms. In PCBs and
the environment, ed. J.S. Waid, Vol. 2., pp. 89-100. CRC Press, Inc., Boca Raton, FL.
24. Bolger, M. 1993. Overview of PCB toxicology. In Proceedings of the U.S. Environmental
Protection Agency's National Technical Workshop "PCBs in Fish Tissue," May 10-11, 1993,
568
-------
BIOACCUMULATION SUMMARY PCS 81
pp. 37-53. EPA/823-R-93003, U.S. Environmental Protection Agency, Office of Water,
Washington, DC.
25. Erickson, M.D. 1993. Introduction to PCBs and analytical methods. In Proceedings of the U.S.
Environmental Protection Agency's National Technical Workshop "PCBs in Fish Tissue" May
10-11, 1993, pp. 3-9. EPA/823-R-93003, U.S. Environmental Protection Agency, Office of
Water, Washington, DC.
26. Safe, S. 1990. Polychlorinated biphenyls (PCBs), dibenzo-p-dioxins (PCDDs), dibenzofurans
(PCDFs), and related compounds: Environmental and mechanistic considerations which support
the development of toxic equivalency factors (TEFs). Crit. Rev. Toxicol 21(l):51-88.
27. USEPA. 1991. Workshop report on toxicity equivalency factors for poly chlorinated bipheny I
congeners. EPA/625/3-91/020. U.S. Environmental Protection Agency. (Eastern Research
Group, Inc., Arlington, MA.)
28. Neff, J.M. 1984. Bioaccumulation of organic micropollutants from sediments and suspended
particulates by aquatic animals. Fres. Z. Anal. Chem. 319:132-136.
29. Shaw, G.R., and D.W. Connell. 1982. Factors influencing concentrations of polychlorinated
biphenyls in organisms from an estuarine ecosystem. Aust. J. Mar. Freshw. Res. 33:1057-1070.
30. Tanabe, S., R. Tatsukawa, and DJ.H. Phillips. 1987. Mussels as bioindicators of PCB pollution:
A case study on uptake and release of PCB isomers and congeners in green-lipped mussels
(Perna viridis) in Hong Kong waters. Environ. Pollut. 47:41-62.
31. Pruell, R. J., J.L. Lake, W.R. Davis, and J.G. Quinn. 1986. Uptake and depuration of organic
contaminants by blue mussels (Mytilus edulis) exposed to environmentally contaminated
sediments. Mar. Biol. 91:497-508.
32. Lech, J.J., and R.E. Peterson. 1983. Biotransformation and persistence of polychlorinated
biphenyls (PCBs) in fish. In PCBs: Human and environmental hazards, ed. P.M. D'ltri and M.A.
Kamrin, pp. 187-201. Ann Arbor Science Publishers, Inc., Ann Arbor, MI.
33. Stout, V.F. 1986. What is happening to PCBs? Elements of effective environmental monitoring
as illustrated by an analysis of PCB trends in terrestrial and aquatic organisms. In PCBs and the
environment, ed. J.S. Waid. CRC Press, Inc., Boca Raton, FL.
34. USEPA. 1980. Ambient water quality criteria document: Polychlorinated biphenyls. EPA
440/5-80-068. (Cited in USEPA. 1996. Hazardous Substances Data Bank (HSDB). National
Library of Medicine online (TOXNET). U.S. Environmental Protection Agency, Office of Health
and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH.
February.)
35. Mearns, A.J., M. Malta, G. Shigenaka, D. MacDonald, M. Buchman, H. Harris, J. Golas, and G.
Lauenstein. 1991. Contaminant trends in the Southern California Bight: Inventory and
569
-------
BIOACCUMULATION SUMMARY PCS 81
assessment. Technical Memorandum NOAA ORCA 62. National Oceanic and Atmospheric
Administration. Seattle, WA.
36. 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. NOAA Technical
Memorandum NOS OMA 52. National Oceanic and Atmospheric Administration, Seattle, WA.
37. Spies, R. B., D.W. Rice, Jr., P.A. Montagna, and R.R. Ireland. 1985. Reproductive success,
xenobiotic contaminants and hepatic mixed-function oxidase (MFO) activity in Patichthys
stellatus populations from San Francisco Bay. Mar. Environ. Res. 17:117-121.
38. Monod, G. 1985. Egg mortality of Lake Geneva char (Salvelinus alpinus) contaminated by PCB
and DDT derivatives. Bull. Environ. Contain. Toxicol. 35:531-536.
39. Smith, E.V., J.M. Spurr, J.C. Filkins, and JJ. Jones. 1985. Organochlorine contaminants of
wintering ducks foraging on Detroit River sediments. /. Great Lakes Res. 11(3):231-246.
40. Henny, C.J., S.A. Ganusevich, F.P. Ward, and T.R. Schwartz. 1994. Organochlorine pesticides,
chlorinated dioxins and furans, and PCBs in peregrine falcon Falco peregrinus eggs from the
Kola Penninsula, Russia. In Raptor conservation today, ed. B.U. Meyburg and R.D. Chancellor,
pp. 739-749. WWGPB/The Pica Press.
41. Tillitt, D.E., R.W. Gale, J.C. Meadows, J.L. Zajicek, P.M. Peterman, S.N. Heaton, P.O. Jones, S.J.
Bursian, T.J. Kubiak, J.P. Giesy, and R.J. Aulerich. 1996. Dietary exposure of mink to carp
from Saginaw Bay. 3. Characterization of dietary exposure to planar halogenated hydrocarbons,
dioxin equivalents, and biomagnification. Environ. Sci. Technol. 30:283-291.
42. USEPA. 1995. Great Lakes Water Quality Initiative technical support document for the
procedure to determine bioaccumulation factors. EPA-820-B-95-005. U.S. Environmental
Protection Agency, Office of Water, Washington, DC.
570
-------
BIOACCUMULATION SUMMARY
PCB 105
Chemical Category: POLYCHLORINATED BIPHENYLS
Chemical Name (Common Synonyms):
2,3,3 ',4,4'-PENT ACHLOROBIPHENYL
CASRN: 32598-14-4
Chemical Characteristics
Solubility in Water: No data [1],
0.0008-0.17mg/L[2]
Log Kow: 5.6 - 6.5 [2], No data [4]
Half-Life: No data [2,3]
Log Koc: 5.51 - 6.39 L/kg organic carbon
Human Health
Oral RfD: No data [5]
Critical Effect: —
Oral Slope Factor: No data [5]
Confidence:
Carcinogenic Classification: No data [5]
Wildlife
Partitioning Factors: One study reported biomagnification factors (BMFs) for mink exposed to PCB-
contaminated food. The lipid-normalized BMFs ranged from 3.8 to 6.8 indicating an accumulation of
this PCB congener in the liver.
Food Chain Multipliers: For PCBs as a class the most toxic congeners have been shown to be
selectively accumulated from organisms at one trophic level to the next [6]. At least three studies have
concluded that PCBs have the potential to biomagnify in food webs based on aquatic organisms and
predators that feed primarily on aquatic organisms [7,8,9]. The results from Biddinger and Gloss [7] and
USAGE [9] generally agreed that highly water-insoluble compounds (including PCBs) have the potential
to biomagnify in these types of food webs. Thomann's [10] model also indicated that highly water-
insoluble compounds (log Kow values 5 to 7) showed the greatest potential to biomagnify. The log
biomagnification factor for PCB 105 from alewife to herring gulls in Lake Ontario was 2.01 [11]. A
study of arctic marine food chains measured log biomagnification factors for pentachlorobiphenyls that
ranged from 0.71 to 1.05 for fish to seal, 0.28 to 0.49 for seal to bear, and 1.14 for fish to bear [12].
Aquatic Organisms
Partitioning Factors: Two studies were found that reported laboratory-measured data to calculate non-
normalized log bioaccumulation factors (BAFs) and biota-sediment accumulation factors (BSAFs). In
the first study the log BAFs determined for marine clams ranged from 0.86 to 1.35 [41]. The BSAFs
ranged from 1.63 to 3.85, with the highest BSAF value associated with the lowest BAF. In the second
571
-------
BIOACCUMULATION SUMMARY PCS 105
study, only BSAF for marine clams were reported. These values ranged from 0.22 to 0.68 [42]. A BSAF
of 4.49 was determined for salmonids [46].
Food Chain Multipliers: Polychlorinated biphenyls as a class have been demonstrated to biomagnify
through the food web. Oliver and Niimi [13], studying accumulation of PCBs in various organisms in
the Lake Ontario food web, reported concentrations of total PCBs in phytoplankton, zooplankton, and
several species of fish. Their data indicated a progressive increase in tissue PCB concentrations moving
from organisms lower in the food web to top aquatic predators. In a study of PCB accumulation in lake
trout (Salvelinus namaycush) of Lake Ontario, Rasmussen et al. [14] reported that each trophic level
contributed about a 3.5-fold biomagnification factor to the PCB concentrations in the trout. No specific
food chain multipliers were identified for PCB 105 or other pentachlorobiphenyls.
Toxicity/Bioaccumulation Assessment Profile
PCBs are a group (209 congeners/isomers) of organic chemicals, based on various substitutions of
chlorine atoms on a basic biphenyl molecule. These manufactured chemicals have been widely used in
various processes and products because of the extreme stability of many isomers, particularly those with
five or more chlorines [15]. A common use of PCBs was as dielectric fluids in capacitors and
transformers. In the United States, Aroclor is the most familiar registered trademark of commercial PCB
formulations. Generally, the first two digits in the Aroclor designation indicate that the mixture contains
biphenyls, and the last two digits give the weight percent of chlorine in the mixture.
As a result of their stability and their general hydrophobic nature, PCBs released to the environment have
dispersed widely throughout the ecosystem [15]. PCBs are among the most stable organic compounds
known, and chemical degradation rates in the environment are thought to be slow. As a result of their
highly lipophilic nature and low water solubility, PCBs are generally found at low concentrations in water
and at relatively high concentrations in sediment [16]. Individual PCB congeners have different physical
and chemical properties based on the degree of chlorination and position of chlorine substitution,
although differences with degree of chlorination are more significant [16]. Solubilities and octanol-water
partition coefficients for PCB congeners range over several orders of magnitude [17]. Octanol-water
partition coefficients, which are often used as estimators of the potential for bioconcentration, are highest
for the most chlorinated PCB congeners.
Dispersion of PCBs in the aquatic environment is a function of their solubility [16], whereas PCB
mobility within and sorption to sediment are a function of chlorine substitution pattern and degree of
chlorination [18]. The concentration of PCBs in sediments is a function of the physical characteristics
of the sediment, such as grain size [19,20] and total organic carbon content [19,20,21,22]. Fine sediments
typically contain higher concentrations of PCB s than coarser sediments because of more surface area [16].
Mobility of PCBs in sediment is generally quite low for the higher chlorinated biphenyls [18]. Therefore,
it is common for the lower chlorinated PCBs to have a greater dispersion from the original point source
[16]. Limited mobility and high rates of sedimentation could prevent some PCB congeners in the
sediment from reaching the overlying water via diffusion [18].
The persistence of PCB s in the environment is a result of their general resistance to degradation [17]. The
rate of degradation of PCB congeners by bacteria decreases with increasing degree of chlorination [23];
other structural characteristics of the individual PCBs can affect susceptibility to microbial degradation
572
-------
BIOACCUMULATION SUMMARY
PCB 105
to a lesser extent [17]. Photochemical degradation, via reductive dechlorination, is also known to occur
in aquatic environments; the higher chlorinated PCBs appear to be most susceptible to this process [22].
Toxicity of PCB congeners is dependent on the degree of chlorination as well as the position of chlorine
substitution. Lesser chlorinated congeners are more readily absorbed, but are metabolized more rapidly
than higher chlorinated congeners [24]. PCB congeners with no chlorine substituted in the ortho (2 and
2') positions but with four or more chlorine atoms at the meta (3 and 3') and para (4 and 4') positions can
assume a planar conformation that can interact with the same receptor as the highly toxic 2,3,7,8-
tetrachlorodibenzo-j?-dioxin (TCDD) [25]. Examples of these more toxic, coplanar congeners are
3,3',4,4'-tetrachlorobiphenyl (PCB 77), 3,3',4,4',5-pentachlorobiphenyl (PCB 126), and 3,3',4,4',5,5'-
hexachlorobiphenyl (PCB 169). A method that has been proposed to estimate the relative toxicity of
mixtures is to use toxic equivalency factors (TEFs) [26]. With this method, relative potencies for
individual congeners are calculated by expressing their potency in relation to 2,3,7,8-TCDD. The
following TEFs have been recommended [26,27]:
Congener Class
3,3',4,4',5-PentaCB
3,3',4,4',5,5'-HexaCB
3,3'4,4'-TetraCB
Monoortho coplanar PCBs
Diortho coplanar PCBs
Recommended TEF
0.1
0.05
0.01
0.001
0.00002
Due to the toxicity, high Kow values, and highly persistent nature of many PCBs, they possess a high
potential to bioaccumulate and exert reproductive effects in higher-trophic-level organisms. Aquatic
organisms have a strong tendency to accumulate PCBs from water and food sources. The log
bioconcentration factor for fish is approximately 4.70 [28]. This factor represents the ratio of
concentration in tissue to the ambient water concentration. Aquatic organisms living in association with
PCB-contaminated sediments generally have tissue concentrations equal to or greater than the
concentration of PCB in the sediment [28]. Once taken up by an organism, PCBs partition primarily into
lipid compartments [16]. Thus, differences in PCB concentration between species and between different
tissues within the same species may reflect differences in lipid content [16]. PCB concentrations in
polychaetes and fish have been strongly correlated to their lipid content [29]. Elimination of PCBs from
organisms is related to the characteristics of the specific PCB congeners present. It has been shown that
uptake and depuration rates in mussels are high for lower-chlorinated PCBs and much lower for higher-
chlorinated congeners [30,31]. In some species, tissue concentrations of PCBs in females can be reduced
during gametogenesis because of PCB transfer to the more lipophilic eggs. Therefore, the transferred
PCBs are eliminated from the female during spawning [32,33]. Fish and other aquatic organisms
biotransform PCBs more slowly than other species, and they appear less able to metabolize, or excrete,
the higher chlorinated PCB congeners [32]. Consequently, fish and other aquatic organisms may
accumulate more of the higher chlorinated PCB congeners than is found in the environment [17].
The acute toxicity of PCBs appears to be relatively low, but results from chronic toxicity tests indicate
that PCB toxicity is directly related to the duration of exposure [34]. Toxic responses have been noted
to occur at concentrations of 0.03 and 0.014 |ig/L in marine and freshwater environments, respectively
[34]. The LC50 for grass shrimp exposed to PCBs in marine waters for 4 days was 6.1 to 7.8 |ig/L [34].
573
-------
BIOACCUMULATION SUMMARY PCS 105
Chronic toxicity of PCBs presents a serious environmental concern because of their resistance to
degradation [35], although the acute toxicity of PCBs is relatively low compared to that of other
chlorinated hydrocarbons. Sediment contaminated with PCBs has been shown to elicit toxic responses
at relatively low concentrations. Sediment bioassays and benthic community studies suggest that chronic
effects generally occur in sediment at total PCB concentrations exceeding 370 |ig/kg [36].
A number of field and laboratory studies provide evidence of chronic sublethal effects on aquatic
organisms at low tissue concentrations [17]. Field and Dexter [17] suggest that a number of marine and
freshwater fish species have experienced chronic toxicity at PCB tissue concentrations of less than 1.0
mg/kg and as low as 0.1 mg/kg. Spies et al. [37] reported an inverse relationship between PCB
concentrations in starry flounder eggs in San Francisco Bay and reproductive success, with an effective
PCB concentration in the ovaries of less than 0.2 mg/kg. Monod [38] also reported a significant
correlation between PCB concentrations in eggs and total egg mortality in Lake Geneva char. PCBs have
also been shown to cause induction of the mixed function oxidase (MFO) system in aquatic animals, with
MFO induction by PCBs at tissue concentrations within the range of environmental exposures [17].
574
-------
Invertebrates
Summary of Biological Effects Tissue Concentrations for PCB 105
Species:
Taxa
Concentration, Units in1: Toxicity: Ability to Accumulate2: Source:
Log Log
Sediment Water Tissue (Sample Type) Effects BCF BAF BSAF Reference Comments3
Plankton,
Species not given
Surface
2.703 (mean) water: 0.003 0.666 (mean)
SD= 1.0659 (mean) SD = 0.1881
(n = 9) SD = 0.0020 (n = 5) fg/kg
fg/kg dw (n = 3)
ng/L
[39] F; collected in
western Lake Erie
(offshore Middle
Sister Island).
Sediment TOC =
7.4%(SD-1.78);
lipid= 1.2% (mean)
SD-0.24
Plankton (a mixture
of primarily
phytoplankton and
some zooplankton)
14 ±5.1 ng/g 10 ±8.4 0.8 ± 0.2 i
dw(0-3cm) pg/L (surface (n = 3)
(n = 38) water) (n =
7)
[13] F; Lake Ontario;
value is mean ± SD;
lipid content =
0.5%
Mainly Tiibifex
tubifex and
Limnodriliis
hoffmeisteri,
Oligochaete
14 ±5.1 ng/g 10 ±8.4 2.6 ± 1.4 i
dw (0-3 cm) pg/L (surface (n = 6)
(n = 38) water)
(n = 7)
[13] F; Lake Ontario;
value is mean ± SD;
lipid content = 1 %
Dreissena 2.703 (mean) 0.003 (mean) 1.627 (mean)
polymorpha, SD = 1.0659 SD = 0.0020 SD = 1.6470
Zebra mussel (n = 9) (n = 3) (n = 20) fg/kg
fg/kg dw ng/L
lipid = 1.3% (mean)
SD = 0.34
-------
-J
ON
Summary of Biological Effects Tissue Concentrations for PCB 105
Species:
Taxa
Macoma nasuta,
Bent-nose clam
Macoma nasuta,
Bent-nose clam
My sis relicta,
Mysid
Concentration, Units in1:
Sediment Water
52.6 ng/g dw
(grain size
< 1 mm)
43.2 ng/g dw
(grain size
< 0.25 mm)
48.8 ng/g dw
(grain size
< 0.125 mm)
ng/g dw:
1.51 ±0.032
1.26
8.6±0.37
20±3.7
70±7.6
89.97 ng/kg
dw (TOC =
22.8%)
Toxicity:
Tissue (Sample Type) Effects
1,046 ng/g dw
(n = 30)
575 ng/g dw
(n = 30)
297 ng/g dw
(n = 30)
ng/g dw:
6.6±0.83
1.8±0.67
8.2±0.75
11.9±0.84
20.3±2.83
Screened mysids:
1.46 |ig/kg
(whole body)
Ability to Accumulate2:
Log Log
BCF BAF BSAF
22.2 (dw) 1.63
14.5 (dw) 2.87
7.3 (dw) 3.85
0.68
0.22
0.64
0.56
0.39
Source:
Reference Comments3
[41] L; steady state
BAFs were
calculated with
average tissue
residues and
sediment concentra-
tions from exposure
days 42-1 19
[42] L; value given is
mean ± SE;
sediment TOC
ranged from 0.84%
to 7.4%
[40] L; mysids exposed
to field contam-
inated sediments
Unscreened mysids:
9.85 ng/kg
(whole body)
from Lake
Champlain, NY; 24
day exposure;
screened mysids
were screened from
direct contact with
sediments (% lipid
= 5.94±0.27);
unscreened mysids
were allowed to
burrow into
sediment.(% lipid =
5.80±0.18)
-------
Summary of Biological Effects Tissue Concentrations for PCB 105
Species:
Taxa
Mysis relicta,
Mysid
Concentration, Units in1:
Sediment
14 ± 5.1 ng/g
dw (0-3 cm)
(n = 38)
Water
10 ±8.4 pg/L
surface water
(n = 7)
Toxicity:
Tissue (Sample Type) Effects
8.5
(n =
± 3.5 ng/g
= 2)
Ability to Accumulate2: Source:
Log Log
BCF BAF BSAF Reference Comments3
[13] F; Lake Ontario;
value is mean ± SD;
lipid content = 3%
Gammarus fasciatus, 2.703 (mean) 0.003 (mean) 1.611 (mean)
Amphipod SD = 1.0659 SD = 0.0020 SD = 0.7505
(n = 9) (n = 3) (n = 4) fg/kg
fg/kg dw ng/L
lipid = 2.1% (mean)
SD=1.04
Pontoporeia affinis,
Amphipod
14 ±5.1 ng/g 10 ±8.4 12 ± 8 ng/g
dw (0-3 cm) pg/L (surface (n = 6)
(n = 38) water) (n =
7)
[13] F; Lake Ontario;
value is mean ± SD;
lipid content = 3%
Orconectes 2.703 (mean) 0.003 (mean) 0.606 (mean)
propinquus, SD = 1.0659 SD = 0.0020 0.1101
Crayfish (n = 9) (n = 3) (n = 5) fg/kg
fg/kg dw ng/L
lipid = 1.7% (mean)
SD = 0.11
Hydropsyche 2.703 (mean) 0.003 (mean) 1.109
alterans, SD = 1.0659 SD = 0.0020 (n = 1) fg/kg
Caddisfly larva (n = 9) (n = 3)
fg/kg dw ng/L
lipid = 1.7% (mean)
Fishes
Alosa
pseudoharengus,
Alewife
14 ±5.1 ng/g 10 ±8.4 pg/L 27 ng/g
dw (0-3 cm) surface water (one composite)
(n = 38) (n = 7)
[13] F; Lake Ontario;
value is mean ± SD;
lipid content = 7%
-------
<-f\
-J
oo
Summary of Biological
Species:
Taxa
Cottus cognatus,
Sculpin
Concentration, Units
Sediment Water
14 ± 5.1 ng/g
dw (0-3 cm)
(n = 38)
10 ±8.4
surface
(n = 7)
in1:
PS/L
water
Tissue (Sample
39 ng/g
(one composite)
Effects Tissue
Toxicity:
Type) Effects
Concentrations
for PCB
105
Ability to Accumulate2:
Log Log
BCF BAF BSAF
Source:
Reference
[13]
Comments3
F; Lake Ontario;
value is mean ± SD;
lipid content = 8%
Osmerus mordax,
Small rainbow smelt
14 ±5.1 ng/g 10±8.4pg/L 15 ±2.0 ng/g
dw (0-3 cm) surface water (n = 4)
(n = 38) (n = 7)
[13] F; Lake Ontario;
value is mean ± SD;
lipid content = 4%
Osmerus mordax,
Large rainbow smelt
Salmonids:
Oncorhynchus
kisiitch,
Coho salmon;
Oncorhynchus
mykiss (Salmo
gairdner),
Rainbow trout;
Salvelinus
namaycush,
Lake trout;
Salmo trutta,
Brown trout
14 ±5.1 ng/g 10 ±8.4 38 ng/g
dw (0-3 cm) pg/L (surface (one composite)
(n = 38) water) (n =
7)
10 ±8.4 ng/g 14 ±5.1 pg/L 110 ±82 ng/g
dw (0-3 cm) surface water (n = 60)
(n = 38) (n = 7)
4.49
[13]
[13]
[46]
F; Lake Ontario;
value is mean ± SD;
lipid content = 4%
F; Lake Ontario;
value is mean ± SD;
lipid content =
11%; wild fish.
Wildlife
Falco peregrinus,
Peregrine falcon
White leghorn
chicken
embryo
72 ng/g (eggs)(n = 6) 11.4% eggshell
thinning
2,200 |ig/kg (egg) LD50
[44] F; Kola Peninsula,
Russia
[43] L; PCBs were
injected into the air
cell of eggs
-------
Summary of Biological Effects Tissue Concentrations for PCB 105
Species: Concentration, Units in1: Toxicity:
Taxa Sediment Water Tissue (Sample Type) Effects
Mustela vison, Mink Diet:
510pg/g4 2,900 pg/g4 (liver) NOAEL
12,000 pg/g4 54,000 pg/g4 (liver) LOAEL;
reduced kit
body weights
followed
by reduced
survival
23,000 pg/g4 105,000 pg/g4 (liver) Reduced kit
body
weights
followed by
reduced survival
4 1 ,000 pg/g4 1 8 1 ,000 pg/g4 (liver) Significant
decrease in
number of live
kits
whelped per
female
Ability to Accumulate2: Source:
Log Log
BCF BAF BSAF Reference Comments3
[45] L;BMF= lipid-
Log normalized
BMP = concentration in the
0.58 liver divided by the
lipid-normalized
Log dietary concentra-
BMF = tion
0.68
Log
BMF =
0.66
Log
BMF =
0.83
1 Concentration units given in wet weight unless otherwise indicated.
2 BCF = bioconcentration factor, BAF = bioaccumulation factor, BSAF = biota-sediment accumulation factor.
3 L = laboratory study, spiked sediment, single chemical; F = field study, multiple chemical exposure; other unusual study conditions or observations noted.
4 Not clear whether units are in dry or wet weight.
-------
BIOACCUMULATION SUMMARY PCS 105
References
1. USEPA. 1996. Hazardous Substances Data Bank (HSDB). National Library of Medicine online
(TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental
Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. February.
2. MacKay, D.M., W.Y. Shiw, and K.C. Ma. 1992. Illustrated handbook of physical-chemical
properties and environmental fate for organic chemicals. Vol. I, Monoaromatic hydrocarbons,
chlorobenzenes and PCBs. Lewis Publishers, Boca Raton, FL.
3. USEPA. 1989. Chemical fate rate constants for SARA section 313 chemicals and Superfund
Health Evaluation Manual chemicals. Prepared by Chemical Hazard Assessment Division,
Syracuse Research Corporation, for U.S. Environmental Protection Agency, Office of Toxic
Substances, Exposure Evaluation Division, Washington, DC, and Environmental Criteria and
Assessment Office, Cincinnati, OH. August 11.
4. Karickhoff, S.W., and J.M. Long. 1995. Internal report on summary of measured, calculated and
recommended log Kow values. Draft. Prepared by U.S. Environmental Protection Agency, Office
of Research and Development, Environmental Research Laboratory-Athens, for E. Southerland,
Office of Water, Office of Science and Technology, Standards and Applied Science Division,
Washington, DC. April 10.
5. USEPA. 1996. Integrated Risk Information System (IRIS). National Library of Medicine online
(TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental
Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. September.
6. Jones, P.O., J.P. Giesy, T.J. Kubiak, D.A. Verbrugge, J.C. Newstead, J.P. Ludwig, D.E. Tillit, R.
Crawford, N. De Galan, and G.T. Ankley. 1993. Biomagnification of bioassay-derived 2, 3, 7, 8-
tetrachlorodibenzo-p-dioxin equivalents. Chemosphere 26:1203-1212.
7. Biddinger, G.R., and S.P. Gloss. 1984. The importance of trophic transfer in the bioaccumulation
of chemical contaminants in aquatic ecosystems. Residue Rev. 91:103-145.
8. Kay, S.H. 1984. Potential for biomagnification of contaminants within marine and freshwater
food webs. Technical Report D-84-7. U.S. Army Corps of Engineers, Waterways Experiment
Station, Vicksburg, MS.
9. USAGE. 1995. Trophic transfer and biomagnification potential of contaminants in aquatic
ecosystems. Environmental Effects of Dredging, Technical Notes EEDP-01-33. U.S. Army Corps
of Engineers, Waterways Experiment Station, Vicksburg, MS.
10. Thomann, R.V. 1989. Bioaccumulation model of organic chemical distribution in aquatic food
chains. Environ. Sci. Technol. 23:699.
11. Braune, B.M., and R.J. Norstrom. 1989. Dynamics of organochlorine compounds in herring gulls:
III. Tissue distribution and bioaccumulation in Lake Ontario Gulls. Environ. Toxicol. Chem.
8:957-968.
580
-------
BIOACCUMULATION SUMMARY PCS 105
12. Muir, D.C.G., RJ. Norstrom, and M. Simon. 1988. Organochlorine contaminants in arctic marine
food chains: Accumulation of specific polychlorinated biphenyls and chlordane-related compounds.
Environ. Sci. Technol. 22:1071-1079.
13. Oliver, E.G., and AJ. Niimi. 1988. Trophodynamic analysis of polychlorinated biphenyl
congeners and other chlorinated hydrocarbons in the Lake Ontario ecosystem. Environ. Sci.
Technol. 22:388-397.
14. Rasmussen, J.B., DJ. Rowan, D.R.S. Lean, and J.H. Carey. 1990. Food chain structure in Ontario
lakes determines PCB levels in lake trout (Salvelinus namaycush) and other pelagic fish. Can. J.
Fish. Aquat. Sci. 47:2030-2038.
15. Rand, G.M., P.O. WeUs, and L.S. McCarty. 1995. Chapter 1. Introduction to aquatic toxicology.
In Fundamentals of aquatic toxicology: Effects, environmental fate, and risk assessment, ed. G.M.
Rand, pp. 3-67. Taylor and Francis, Washington, DC.
16. Phillips, D.J.H. 1986. Use of organisms to quantify PCBs in marine and estuarine environments.
In PCBs and the environment, ed. J.S. Waid, pp. 127-182. CRC Press, Inc., Boca Raton, FL.
17. Field, L.J., and R.N. Dexter. 1998. A discussion of PCB target levels in aquatic sediments.
Unpublished document. January 11, 1988.
18. Fisher, J.B., R.L. Petty, and W. Lick. 1983. Release of polychlorinated biphenyls from
contaminated lake sediments: Flux and apparent diffusivities of four individual PCBs. Environ.
Pollut. 5B: 121-132.
19. Pavlou, S.P., and R.N. Dexter. 1979. Distribution of polychlorinated biphenyls (PCB) in estuarine
ecosystems: Testing the concept of equilibrium partitioning in the marine environment. Environ.
Sci. Technol. 13:65-71.
20. Lynch, T.R., and H.E. Johnson. 1982. Availability of hexachlorobiphenyl isomer to benthic
amphipods from experimentally contaminated sediments. In Aquatic Toxicology and Hazard
Assessment: Fifth Conference, ASTM STP 766, ed. J.G. Pearson, R.B. Foster, and W.E. Bishop
(eds.), pp. 273-287. American Society of Testing and Materials, Philadelphia, PA.
21. Chou, S.F.J., and R.A. Griffin. 1986. Solubility and soil mobility of polychlorinated biphenyls.
In PCBs and the environment, ed. J.S. Waid, Vol. 1, pp. 101-120. CRC Press, Inc. Boca Raton,
FL.
22. Sawhney, B.L. 1986. Chemistry and properties of PCBs in relation to environmental effects. In
PCBs and the environment, ed. J.S. Waid, pp. 47-65. CRC Press, Inc., Boca Raton, FL.
23. Furukawa, K. 1986. Modification of PCBs by bacteria and other microorganisms. In PCBs and
the environment, ed. J.S. Waid, Vol. 2, pp. 89-100. CRC Press, Inc., Boca Raton, FL.
24. Bolger, M. 1993. Overview of PCB toxicology. In Proceedings of the U.S. Environmental
Protection Agency's National Technical Workshop "PCBs in Fish Tissue," May 10-11, 1993, pp.
581
-------
BIOACCUMULATION SUMMARY PCS 105
37-53. EPA/823-R-93-003, U.S. Environmental Protection Agency, Office of Water, Washington,
DC.
25. Erickson, M.D. 1993. Introduction to PCBs and analytical methods. In Proceedings of the U.S.
Environmental Protection Agency's National Technical Workshop "PCBs in Fish Tissue," May
10-11, 1993, pp. 3-9. EPA/823-R-93-003, U.S. Environmental Protection Agency, Office of
Water, Washington, DC.
26. Safe, S. 1990. Polychlorinated biphenyls (PCBs), dibenzo-p-dioxins (PCDDs), dibenzofurans
(PCDFs), and related compounds: Environmental and mechanistic considerations which support
the development of toxic equivalency factors (TEFs). Crit. Rev.Toxicol 21(l):51-88.
27. USEPA. 1991. Workshop report on toxicity equivalency factors for polychlorinated biphenyl
congeners. EPA/625/3-91/020. U.S. Environmental Protection Agency. (Eastern Research Group,
Inc., Arlington, MA.)
28. Neff, J.M. 1984. Bioaccumulation of organic micropollutants from sediments and suspended
particulates by aquatic animals. Fres. Z. Anal. Chem. 319:132-136.
29. Shaw, G.R., and D.W. Connell. 1982. Factors influencing concentrations of polychlorinated
biphenyls in organisms from an estuarine ecosystem. Aust. J. Mar. Freshw. Res. 33:1057-1070.
30. Tanabe, S., R. Tatsukawa, and D.J.H. Phillips. 1987. Mussels as bioindicators of PCB pollution:
A case study on uptake and release of PCB isomers and congeners in green-lipped mussels (Perna
viridis) in Hong Kong waters. Environ. Pollut. 47:41-62.
31. Pruell, R.J., J.L. Lake, W.R. Davis, and J.G. Quinn. 1986. Uptake and depuration of organic
contaminants by blue mussels (Mytilus edulis) exposed to environmentally contaminated sediments.
Mar.Biol. 91:497-508.
32. Lech, J.J., and R.E. Peterson. 1983. Biotransformation and persistence of polychlorinated
biphenyls (PCBs) in fish. In PCBs: Human and environmental hazards, ed. P.M. D'ltri and M.A.
Kamrin, pp. 187-201. Ann Arbor Science Publishers, Inc., Ann Arbor, MI.
33. Stout, V.F. 1986. What is happening to PCBs? Elements of effective environmental monitoring
as illustrated by an analysis of PCB trends in terrestrial and aquatic organisms. In PCBs and the
Environment, ed. J.S. Waid. CRC Press, Inc., Boca Raton, FL.
34. USEPA. 1980. Ambient water quality criteria document: Poly'chlorinated biphenyls. EPA 440/5-
80-068. (Cited in USEPA. 1996. Hazardous Substances Data Bank (HSDB). National Library
of Medicine online (TOXNET). U.S. Environmental Protection Agency, Office of Health and
Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH.
February.)
35. Mearns, A.J., M. Malta, G. Shigenaka, D. MacDonald, M. Buchman, H. Harris, J. Golas, and G.
Lauenstein. 1991. Contaminant trends in the Southern California Bight: Inventory and
assessment. Technical Memorandum NOAA ORCA 62. National Oceanic and Atmospheric
Administration. Seattle, WA.
582
-------
BIOACCUMULATION SUMMARY PCS 105
36. 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. NOAA Tech. Memo. NOS OMA
52. National Oceanic and Atmospheric Administration, Seattle, WA.
37. Spies, R.B., D.W. Rice, Jr., P.A. Montagna, and R.R. Ireland. 1985. Reproductive success,
xenobiotic contaminants and hepatic mixed-function oxidase (MFO) activity in Platichthys stellatus
populations from San Francisco Bay. Mar. Environ. Res. 17:117-121.
38. Monod, G. 1985. Egg mortality of Lake Geneva char (Salvelinus alpinus) contaminated by PCB
and DDT derivatives. Bull. Environ. Contam. Toxicol. 35:531-536.
39. Morrison, H.A., F.A.P.C. Gobas, R. Lazar, and G.D. Haffner. 1996. Development and verification
of a bioaccumulation model for organic contaminants in benthic invertebrates. Environ. Sci.
Technol 30:3377-3384.
40. Lester, D.C., and A. Mclntosh. 1994. Accumulation of polychlorinated biphenyl congeners from
Lake Champlain sediments by Mysis relicta. Environ. Toxicol. Chem. 13:1825-1841.
41. Boese, B.L., M. Winsor, H. Leell, S. Echols, J. Pelletier, and R.Randal. 1995. PCB congeners
and hexachlorobenzene biota sediment accumulation factors for Macoma nasuta exposed to
sediments with different total organic carbon contents. Environ. Toxicol. Chem. 14(2): 303-310.
42. Ferraro, S.P., H. Lee H, L.M. Smith, RJ. Ozretich, and D.T. Sprecht. 1991. Accumulation factors
for eleven polychlorinated biphenyl congeners. Bull. Environ. Contam. Toxicol. 46:276-283.
43. Brunstrom, B. 1990. Mono-ortho-chlorinated chlorobiphenyls: Toxicity and induction of
7-ethoxyresorufin O-deethylase (EROD) activity in chick embryos. Arch. Toxicol. 64:188-192.
44. Henny, C.J., S.A. Ganusevich, P.P. Ward, and T.R. Schwartz. 1994. Organochlorine pesticides,
chlorinated dioxins and furans, and PCBs in peregrine falcon Falco peregrinus eggs from the Kola
Penninsula, Russia. In Raptor conservation today, ed. B.U. Meyburg and R.D. Chancellor, pp.
739-749. WWGPB/The Pica Press.
45. TiUitt, D.E., R.W. Gale, J.C. Meadows, J.L. Zajicek, P.M. Peterman, S.N. Heaton, P.O. Jones, S.J.
Bursian, T.J. Kubiak, J.P. Giesy, and R.J. Aulerich. 1996. Dietary exposure of mink to carp from
Saginaw Bay. 3. Characterization of dietary exposure to planar halogenated hydrocarbons, dioxin
equivalents, and biomagnification. Environ. Sci. Technol. 30:283-291.
46. USEPA. 1995. Great Lakes Water Quality Initiative technical support document for the procedure
to determine bioaccumulation factors. EPA-820-B-95-005. U.S. Environmental Protection Agency,
Office of Water, Washington, DC.
583
-------
584
-------
BIOACCUMULATION SUMMARY PCB 118
Chemical Category: POLYCHLORINATED BIPHENYLS
Chemical Name (Common Synonyms): CASRN: 31508-00-6
2,3 ',4,4',5-PENTACHLOROBIPHENYL
Chemical Characteristics
Solubility in Water: No data [1] Half-Life: No data [2,3]
Log Kow: — Log Koc: 5.51 - 6.39 L/kg organic carbon
Human Health
Oral RfD: No data [5] Confidence: —
Critical Effect: —
Oral Slope Factor: No data [5] Carcinogenic Classification: No data [5]
Wildlife
Partitioning Factors: In a laboratory study with mink, the lipid-normalized ratios of PCB 118 in liver
to food ranged from 3.4 to 5.9 (log BMF = 0.53 to 0.77) [49]. The ratio of PCB 118 in three species of
duck to sediment in the lower Detroit River ranged from 21 to 35 [40].
Food Chain Multipliers: For PCBs as a class, the most toxic congeners have been shown to be
selectively accumulated from organisms at one trophic level to the next [6]. At least three studies have
concluded that PCBs have the potential to biomagnify in food webs based on aquatic organisms and
predators that feed primarily on aquatic organisms [7,8,9]. The results from Biddinger and Gloss [7] and
USAGE [9] generally agreed that highly water-insoluble compounds (including PCBs) have the potential
to biomagnify in these types of food webs. Thomann's [10] model also indicated that highly water-
insoluble compounds (log Kow values 5 to 7) showed the greatest potential to biomagnify. The
biomagnification factor for PCB 118 from ale wife to herring gulls in Lake Ontario was 80 [11]. A study
of arctic marine food chains measured log biomagnification factors for pentachlorobiphenyls that ranged
from 0.71 to 1.05 for fish to seal, 0.28 to 0.49 for seal to bear, and 1.14 for fish to bear [12].
Aquatic Organisms
Partitioning Factors: Steady-state BSAFs for the bent-nose clam ranged from 0.59 to 4.7 in two
laboratory studies. The ratio of PCB 118 in carp tissue to sediment from the lower Detroit River was 25.
Food Chain Multipliers: Polychlorinated biphenyls as a class have been demonstrated to biomagnify
through the food web. Oliver and Niimi [13], studying accumulation of PCBs in various organisms in
the Lake Ontario food web, reported concentrations of total PCBs in phytoplankton, zooplankton, and
several species of fish. Their data indicated a progressive increase in tissue PCB concentrations moving
585
-------
BIOACCUMULATION SUMMARY PCB 118
from organisms lower in the food web to top aquatic predators. In a study of PCB accumulation in lake
trout (Salvelinus namaycush) of Lake Ontario, Rasmussen et al. [14] reported that each trophic level
contributed about a 3.5-fold biomagnification factor to the PCB concentrations in the trout. No specific
food chain multipliers were identified for PCB 118 or other pentachlorobiphenyls.
Toxicity/Bioaccumulation Assessment Profile
PCBs are a group (209 congeners/isomers) of organic chemicals, based on various substitutions of
chlorine atoms on a basic biphenyl molecule. These manufactured chemicals have been widely used in
various processes and products because of the extreme stability of many isomers, particularly those with
five or more chlorines [15]. A common use of PCBs was as dielectric fluids in capacitors and
transformers. In the United States, Aroclor is the most familiar registered trademark of commercial PCB
formulations. Generally, the first two digits in the Aroclor designation indicate that the mixture contains
biphenyls, and the last two digits give the weight percent of chlorine in the mixture.
As a result of their stability and their general hydrophobic nature, PCBs released to the environment have
dispersed widely throughout the ecosystem [15]. PCBs are among the most stable organic compounds
known, and chemical degradation rates in the environment are thought to be slow. As a result of their
highly lipophilic nature and low water solubility, PCBs are generally found at low concentrations in water
and at relatively high concentrations in sediment [16]. Individual PCB congeners have different physical
and chemical properties based on the degree of chlorination and position of chlorine substitution,
although differences with degree of chlorination are more significant [16]. Solubilities and octanol-water
partition coefficients for PCB congeners range over several orders of magnitude [17]. Octanol-water
partition coefficients, which are often used as estimators of the potential for bioconcentration, are highest
for the most chlorinated PCB congeners.
Dispersion of PCBs in the aquatic environment is a function of their solubility [16], whereas PCB
mobility within and sorption to sediment are a function of chlorine substitution pattern and degree of
chlorination [18]. The concentration of PCBs in sediments is a function of the physical characteristics
of the sediment, such as grain size [19,20] and total organic carbon content [19,20,21,22]. Fine sediments
typically contain higher concentrations of PCB s than coarser sediments because of more surface area [16].
Mobility of PCBs in sediment is generally quite low for the higher chlorinated biphenyls [18]. Therefore,
it is common for the lower chlorinated PCBs to have a greater dispersion from the original point source
[16]. Limited mobility and high rates of sedimentation could prevent some PCB congeners in the
sediment from reaching the overlying water via diffusion [18].
The persistence of PCB s in the environment is a result of their general resistance to degradation [17]. The
rate of degradation of PCB congeners by bacteria decreases with increasing degree of chlorination [23];
other structural characteristics of the individual PCBs can affect susceptibility to microbial degradation
to a lesser extent [17]. Photochemical degradation, via reductive dechlorination, is also known to occur
in aquatic environments; the higher chlorinated PCBs appear to be most susceptible to this process [22].
Toxicity of PCB congeners is dependent on the degree of chlorination as well as the position of chlorine
substitution. Lesser chlorinated congeners are more readily absorbed, but are metabolized more rapidly
than higher chlorinated congeners [24]. PCB congeners with no chlorine substituted in the ortho (2 and
2') positions but with four or more chlorine atoms at the meta (3 and 3') and para (4 and 4') positions can
assume a planar conformation that can interact with the same receptor as the highly toxic 2,3,7,8-
586
-------
BIOACCUMULATION SUMMARY
PCB 118
tetrachlorodibenzo-p-dioxin (TCDD) [25]. Examples of these more toxic, coplanar congeners are
3,3',4,4'-tetrachlorobiphenyl (PCB 77), 3,3',4,4',5-pentachlorobiphenyl (PCB 126), and 3,3',4,4',5,5'-
hexachlorobiphenyl (PCB 169). A method that has been proposed to estimate the relative toxicity of
mixtures is to use toxic equivalency factors (TEFs) [26]. With this method, relative potencies for
individual congeners are calculated by expressing their potency in relation to 2,3,7,8-TCDD. The
following TEFs have been recommended [26,27]:
Congener Class
3,3',4,4',5-PentaCB
3,3',4,4',5,5'-HexaCB
3,3'4,4'TetraCB
Monoortho coplanar PCBs
Diortho coplanar PCBs
Recommended TEF
0.1
0.05
0.01
0.001
0.00002
Due to the toxicity, high Kow values, and highly persistent nature of many PCBs, they possess a high
potential to bioaccumulate and exert reproductive effects in higher-trophic-level organisms. Aquatic
organisms have a strong tendency to accumulate PCBs from water and food sources. The log
bioconcentration factor for fish is approximately 4.70 [28]. This factor represents the ratio of
concentration in tissue to the ambient water concentration. Aquatic organisms living in association with
PCB-contaminated sediments generally have tissue concentrations equal to or greater than the
concentration of PCB in the sediment [28]. Once taken up by an organism, PCBs partition primarily into
lipid compartments [16]. Thus, differences in PCB concentration between species and between different
tissues within the same species may reflect differences in lipid content [16]. PCB concentrations in
polychaetes and fish have been strongly correlated to their lipid content [29]. Elimination of PCBs from
organisms is related to the characteristics of the specific PCB congeners present. It has been shown that
uptake and depuration rates in mussels are high for lower-chlorinated PCBs and much lower for higher-
chlorinated congeners [30,31]. In some species, tissue concentrations of PCBs in females can be reduced
during gametogenesis because of PCB transfer to the more lipophilic eggs. Therefore, the transferred
PCBs are eliminated from the female during spawning [32,33]. Fish and other aquatic organisms
biotransform PCBs more slowly than other species, and they appear less able to metabolize, or excrete,
the higher chlorinated PCB congeners [32]. Consequently, fish and other aquatic organisms may
accumulate more of the higher chlorinated PCB congeners than is found in the environment [17].
The acute toxicity of PCBs appears to be relatively low, but results from chronic toxicity tests indicate
that PCB toxicity is directly related to the duration of exposure [34]. Toxic responses have been noted
to occur at concentrations of 0.03 and 0.014 |ig/L in marine and freshwater environments, respectively
[34]. The LC50 for grass shrimp exposed to PCBs in marine waters for 4 days was 6.1 to 7.8 |ig/L [34].
Chronic toxicity of PCBs presents a serious environmental concern because of their resistance to
degradation [35], although the acute toxicity of PCBs is relatively low compared to that of other
chlorinated hydrocarbons. Sediment contaminated with PCBs has been shown to elicit toxic responses
at relatively low concentrations. Sediment bioassays and benthic community studies suggest that chronic
effects generally occur in sediment at total PCB concentrations exceeding 370 |ig/kg [36].
A number of field and laboratory studies provide evidence of chronic sublethal effects on aquatic
organisms at low tissue concentrations [17]. Field and Dexter [17] suggest that a number of marine and
587
-------
BIOACCUMULATION SUMMARY PCB 118
freshwater fish species have experienced chronic toxicity at PCB tissue concentrations of less than 1.0
mg/kg and as low as 0.1 mg/kg. Spies et al. [37] reported an inverse relationship between PCB
concentrations in starry flounder eggs in San Francisco Bay and reproductive success, with an effective
PCB concentration in the ovaries of less than 0.2 mg/kg. Monod [38] also reported a significant
correlation between PCB concentrations in eggs and total egg mortality in Lake Geneva char. PCBs have
also been shown to cause induction of the mixed function oxidase (MFO) system in aquatic animals, with
MFO induction by PCBs at tissue concentrations within the range of environmental exposures [17].
588
-------
Summary of Biological Effects Tissue Concentrations for PCB 118
: Species
Taxa
Concentration, Units in1:
Sediment Water
Toxicity:
Tissue (Sample Type) Effects
Ability to Accumulate2:
Log Log
BCF BAF BSAF
Source:
Reference Comments3
Invertebrates
Plankton
4.514 (mean) 0.007 (mean) 0.750 (mean)
SD= 1.8449 SD = 0.0044 SD = 0.4919
(n = 9) (n = 3) (n = 5) fg/kg
|ig/kg dw ng/L
[42] F; collected in
western Lake Erie
(offshore Middle
Sister Island);
sediment TOC =
7.4%; SD= 1.78
lipid= 1.2% (mean)
SD = 0.24
Tubifex sp.,
Oligochaetes
0.017 mg/kg
0.0069 mg/kg
[40]
F; lower Detroit
River
Macoma nasuta,
Bent-nose clam
ng/g dw:
2.93 ± 0.067
2.5
16.5 ± 1.42
45 ± 9.2
162 ± 16.5
ng/g dw:
20 ± 3.0
12.0 ±1.89
28.9 ±2.60
40.3 ± 2.64
66 ±8.9
1.08
0.73
1.17
0.82
0.54
[43] L; value given is
mean ± SE;
sediment TOC
ranged from 0.84%
to 7.4%
Macoma nasuta,
Bent-nose clam
44.2 ng/g dw
(grain size < 1 mm)
36.2 ng/g
(grain size < 0.25 mm)
41.6 ng/g dw
(grain size < 0.125 mm)
1,049 ng/g dw
(n = 30)
550 ng/g dw
(n = 30)
296 ng/g dw
(n = 30)
30.3 (dw) 2.02
18.5 (dw) 3.28
8.4 (dw) 4.74
[41] L; steady state
BAFs were
calculated with
average tissue
residues and
sediment concentra-
tions from exposure
days 42-119.
-------
Summary of Biological Effects Tissue Concentrations for PCB 118
: Species
Taxa
Dreissena
polymorpha,
Zebra mussel
Mytilus edulis,
Blue mussel
Daphnia magna,
Freshwater
cladoceran
Concentration, Units in1:
Sediment Water
4.514 (mean) 0.007 (mean)
SD= 1.8449 SD = 0.0044
(n = 9) (n = 3)
|ig/kg dw ng/L
Water column:
-16.0 ng/L
-4.0 ng/L
-0.8 ng/L
0.1 fg/L
l.Ofg/L
Tissue (Sample Type)
2.156 (mean)
SD = 0.8847
(n = 20) |ig/kg
Whole body:
~l,780ng/gdw
~l,000ng/gdw
-130 ng/g dw
-3.5 ng/mg dw
(n = 3)
-130 ng/mg dw
(n = 3)
Toxicity: Ability to Accumulate2:
Log Log
Effects BCF BAF BSAF
No significant
effect on
survival,
reproduction, or
biomass
No significant
effect on
survival,
reproduction, or
biomass
Source:
Reference Comments3
Lipid= 1.3%
(mean)
SD = 0.34
[45] F; New Bedford
Harbor, MA;
deployment study; -
-read all values off
figures
[39] L; 21 -day static
renewal tests; tissue
concentrations are
approximations (~),
as data were taken
from figures
Gammarus fasciatus, 4.514 (mean) 0.007 (mean) 3.113 (mean)
Amphipod SD= 1.8449 SD = 0.0044 SD = 1.7881
(n = 9) (n = 3) (n = 4) |ig/kg
|ig/kg dw ng/L
Lipid = 2.1
(mean)
SD= 1.04
-------
Summary of Biological Effects Tissue Concentrations for PCB 118
: Species
Taxa
Concentration, Units in1:
Sediment Water
Toxicity:
Tissue (Sample Type) Effects
Ability to Accumulate2:
Log Log
BCF BAF BSAF
Source:
Reference Comments3
Orconectes
propinqiius,
Crayfish
4.514 (mean) 0.007 (mean) 2.242 (mean)
SD= 1.8449 SD = 0.0044 SD = 0.3628
(n = 9) (n = 3) (n = 5)
|ig/kg dw ng/L l-ig/kg
Lipid = 1.7%
(mean)
SD = 0.11
Hydropsyche 4.514 (mean) 0.007 (mean) 4.780
alterans, SD = 1.8449 SD = 0.0044 (n=l)
Caddisfly larva (n = 9) (n = 3) |ig/kg
|ig/kg dw ng/L
Lipid= 1.7%
(mean)
Mysis relicta,
Mysid
135.73 |ig/kg
dw (TOC =
22.8%)
Screened mysids:
2.39 ng/kg
(whole body)
Unscreened mysids:
15.67 |ig/kg
(whole body)
[44] L; mysids exposed
to field
contaminated
sediments from
Lake Champlain,
NY; 24-day
exposure screened
mysids were
screened from
direct contact with
sedi-ments (% lipid
= 5.94 ± 0.27);
unscreened mysids
were allowed to
burrow into
sediment. (% lipid =
5.80 ±0.18)
-------
Summary of Biological Effects Tissue Concentrations for PCB 118
: Species
Taxa
Concentration, Units in1:
Sediment Water
Toxicity:
Tissue (Sample Type) Effects
Ability to Accumulate2:
Log Log
BCF BAF BSAF
Source:
Reference Comments3
Fishes
Salveliniis
namaycush
namayciish,
Lake trout
0.87 ng/
0.11
n = 4
'g ± 0.20 ng/L ± 290 ng/g lipid
0.29
n= 11
[46, 47] F; Siskiwit Lake,
Isle Royale, Lake
Superior; tissue
concentrations are
means of
concentrations
measured in several
size classes; organic
carbon content of
sediment was not
presented.
Coregonus
culpeaformis
neohantoniensus,
Whitefish
0.87 ng/g ±
0.11
n = 4
0.20 ng/L ±
0.29
n= 11
280 ng/g lipid
Salmonids
Cypriniis carpio,
Carp
8.15
4.09
1.72
0.017 mg/kg
(n=l)
0.42 ± 0.26 mg/kg
(n = 9)
[13]
[50]
[40]
F;%lipid= 11;
%sed OC = 2.7
F; lower Detroit
River
Wildlife
Bucephala clangula, 0.017 mg/kg
Goldeneye (n = 1)
0.36 ±0.041 mg/kg
(n = 3)
[40]
F; lower Detroit
River
-------
Summary of Biological Effects Tissue Concentrations for PCB 118
: Species
Taxa
Aythya affinis,
Lesser scaup
Aythya marila,
Greater scaup
Falco peregrinus,
Peregrine falcon
Mustela vison,
Mink
Concentration, Units in1: Toxicity: Ability to Accumulate2:
Log Log
Sediment Water Tissue (Sample Type) Effects BCF BAF BSAF
0.017 mg/kg 0.52 ± 0.26 mg/kg
(n=l) (n = 7)
0.017 mg/kg 0.59 ±0.10 mg/kg
(n =1) (n = 3)
450 ng/g (eggs) 1 1 .4% eggshell
(n = 6) thinning
Diet: 1,660 8,500 pg/g4 (liver) NOAEL log BMP
pg/g4 = 0.53
20,000 pg/g4 (liver) LOAEL;
35,000 pg/g4 reduced kit body log BMP
weights = 0.56
followed by
reduced survival
284,000 pg/g4 (liver) Reduced kit log BMP
68,000 pg/g4 body weights = 0.63
followed by
reduced survival
478,000 pg/g4 (liver) Significant log BMP
125,000 decrease in = 0.77
pg/g4 number of live
kits whelped per
female
Source:
Reference Comments3
[40] F; lower Detroit
River
[40] F; lower Detroit
River
[48] F; Kola Peninsula,
Russia
[49] L; BMP = lipid-
normalized
concentration in the
liver divided by the
lipid-normalized
dietary concentra-
tion
1 Concentration units expressed in wet weight unless otherwise noted.
2 BCF = bioconcentration factor, BAF = bioaccumulation factor, SAP = biota-sediment accumulation factor.
3 L = laboratory study, spiked sediment, single chemical; F = field study, multiple chemical exposure; other unusual study conditions or observations noted.
4 Not clear whether units are in dry or wet weight.
-------
BIOACCUMULATION SUMMARY PCS 118
References
1. USEPA. 1996. Hazardous Substances Data Bank (SDB). National Library of Medicine online
(TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental
Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. February.
2. MacKay, D.M., W.Y. Shiw, and K.C. Ma. 1992. Illustrated handbook of physical-chemical
properties and environmental fate for organic chemicals, Vol. I, Monoaromatic hydrocarbons,
chlorobenzenes and PCBs. Lewis Publishers, Boca Raton, FL.
3. USEPA. 1989. Chemical fate rate constants for SARA section 313 chemicals and Superfund
Health Evaluation Manual chemicals. Prepared by Chemical Hazard Assessment Division,
Syracuse Research Corporation, for U.S. Environmental Protection Agency, Office of Toxic
Substances, Exposure Evaluation Division, Washington, DC, and Environmental Criteria and
Assessment Office, Cincinnati, OH. August 11.
4. Karickhoff, S.W., and J.M. Long. 1995. Internal report on summary of measured, calculated
and recommended log Kow values. Draft. Prepared by U.S. Environmental Protection Agency,
Office of Research and Development, Environmental Research Laboratory-Athens, for E.
Southerland, Office of Water, Office of Science and Technology, Standards and Applied Science
Division, Washington, DC. April 10.
5. USEPA. 1996. Integrated Risk Information System (IRIS). National Library of Medicine online
(TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental
Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. September.
6. Jones, P.O., J.P. Giesy, T.J. Kubiak, D.A. Verbrugge, J.C. Newstead, J.P. Ludwig, D.E. Tillit,
R. Crawford, N. De Galan, and G.T. Ankley. 1993. Biomagnification of bioassay-derived 2, 3,
7, 8-tetrachlorodibenzo-j?-dioxin equivalents. Chemosphere 26:1203-1212.
7. Biddinger, G.R., and S.P. Gloss. 1984. The importance of trophic transfer in the
bioaccumulation of chemical contaminants in aquatic ecosystems. Residue Rev. 91:103-145.
8. Kay, S.H. 1984. Potential for biomagnification of contaminants within marine and freshwater
food webs. Technical Report D-84-7. U.S. Army Corps of Engineers, Waterways Experiment
Station, Vicksburg, MS.
9. USAGE. 1995. Trophic transfer and biomagnification potential of contaminants in aquatic
ecosystems. Environmental Effects of Dredging, Technical Notes EEDP-01-33. U.S. Army
Corps of Engineers, Waterways Experiment Station, Vicksburg, MS.
10. Thomann, R.V. 1989. Bioaccumulation model of organic chemical distribution in aquatic food
chains. Environ. Sci. Technol. 23:699.
11. Braune, B.M., and R.J. Norstrom. 1989. Dynamics of organochlorine compounds in herring
gulls: III. Tissue distribution and bioaccumulation in Lake Ontario Gulls. Environ. Toxicol.
Chem. 8:957-968.
594
-------
BIOACCUMULATION SUMMARY PCS 118
12. Muir, D.C.G., RJ. Norstrom, and M. Simon. 1988. Organochlorine contaminants in arctic
marine food chains: Accumulation of specific polychlorinated biphenyls and chlordane-related
compounds. Environ. Sci. Technol. 22:1071-1079.
13. Oliver, E.G., and AJ. Niimi. 1988. Trophodynamic analysis of polychlorinated biphenyl
congeners and other chlorinated hydrocarbons in the Lake Ontario ecosystem. Environ. Sci.
Technol. 22:388-397.
14. Rasmussen, J.B., DJ. Rowan, D.R.S. Lean, and J.H. Carey. 1990. Food chain structure in
Ontario lakes determines PCB levels in lake trout (Salvelinus namaycush) and other pelagic fish.
Can. J. Fish. Aquat. Sci. 47:2030-2038.
15. Rand, G.M., P.G. Wells, and L.S. McCarty. 1995. Chapter 1. Introduction to aquatic toxicology.
In Fundamentals of aquatic toxicology: Effects, environmental fate, and risk assessment, ed.
G.M. Rand, pp. 3-67. Taylor and Francis, Washington, DC.
16. Phillips, DJ.H. 1986. Use of organisms to quantify PCB s in marine and estuarine environments.
In PCBs and the environment, ed. J.S. Waid, pp.127-182. CRC Press, Inc., Boca Raton, FL.
17. Field, L.J., and R.N. Dexter. 1998. A discussion of PCB target levels in aquatic sediments.
Unpublished document. January 11.
18. Fisher, J.B., R.L. Petty, and W. Lick. 1983. Release of polychlorinated biphenyls from
contaminated lake sediments: Flux and apparent diffusivities of four individual PCBs. Environ.
Pollut. 5B: 121-132.
19. Pavlou, S.P., and R.N. Dexter. 1979. Distribution of polychlorinated biphenyls (PCB) in
estuarine ecosystems: Testing the concept of equilibrium partitioning in the marine environment.
Environ. Sci. Technol. 13:65-71.
20. Lynch, T.R., and H.E. Johnson. 1982. Availability of hexachlorobiphenyl isomer to benthic
amphipods from experimentally contaminated sediments. In Aquatic Toxicology and Hazard
Assessment: Fifth Conference, ASTM STP 766, ed. J.G. Pearson, R.B. Foster, and W.E. Bishop,
pp. 273-287. American Society of Testing and Materials, Philadelphia, PA.
21. Chou, S.F.J., and R.A. Griffin. 1986. Solubility and soil mobility of polychlorinated biphenyls.
In PCBs and the environment, ed. J.S. Waid, Vol. 1, pp. 101-120. CRC Press, Inc. Boca Raton,
FL.
22. Sawhney, B.L. 1986. Chemistry and properties of PCBs in relation to environmental effects.
In PCBs and the environment, ed. J.S. Waid, pp. 47-65. CRC Press, Inc., Boca Raton, FL.
23. Furukawa, K. 1986. Modification of PCBs by bacteria and other microorganisms. In PCBs and
the environment, ed. J. S. Waid, Vol. 2, pp. 89-100. CRC Press, Inc. Boca Raton, FL.
24. Bolger, M. 1993. Overview of PCB toxicology. In Proceedings of the U.S. Environmental
Protection Agency's National Technical Workshop "PCBs in Fish Tissue," May 10-11, 1993, pp.
595
-------
BIOACCUMULATION SUMMARY PCS 118
37-53. EPA/823-R-93-003, U.S. Environmental Protection Agency, Office of Water,
Washington, DC.
25. Erickson, M.D. 1993. Introduction to PCBs and analytical methods. In Proceedings of the U.S.
Environmental Protection Agency's National Technical Workshop "PCBs in Fish Tissue," May
10-11, 1993, pp. 3-9. EPA/823-R-93-003. U.S. Environmental Protection Agency, Office of
Water, Washington, DC.
26. Safe, S. 1990. Polychlorinated biphenyls (PCBs), dibenzo-/?-dioxins (PCDDs), dibenzofurans
(PCDFs), and related compounds: Environmental and mechanistic considerations which support
the development of toxic equivalency factors (TEFs). Crit. Rev. Toxicol. 21(l):51-88.
27. USEPA. 1991. Workshop report on toxicity equivalency factors for polychlorinated biphenyl
congeners. EPA/625/3-91/020. U.S. Environmental Protection Agency. (Eastern Research
Group, Inc., Arlington, MA.)
28. Neff, J.M. 1984. Bioaccumulation of organic micropollutants from sediments and suspended
particulates by aquatic animals. Fres. Z. Anal. Chem. 319:132-136.
29. Shaw, G.R., and D.W. Connell. 1982. Factors influencing concentrations of polychlorinated
biphenyls in organisms from an estuarine ecosystem. Aust. J. Mar. Freshw. Res. 33:1057-1070.
30. Tanabe, S., R. Tatsukawa, and DJ.H. Phillips. 1987. Mussels as bioindicators of PCB pollution:
A case study on uptake and release of PCB isomers and congeners in green-lipped mussels
(Perna viridis) in Hong Kong waters. Environ. Pollut. 47:41-62.
31. Pruell, R. J., J. L. Lake, W. R. Davis, and J. G. Quinn. 1986. Uptake and depuration of organic
contaminants by blue mussels (Mytilus edulis) exposed to environmentally contaminated
sediments. Mar. Biol. 91:497-508.
32. Lech, J.J., and R.E. Peterson. 1983. Biotransformation and persistence of polychlorinated
biphenyls (PCBs) in fish. In PCBs: Human and environmental hazards, ed. P.M. D'ltri and M.A.
Kamrin, pp. 187-201. Ann Arbor Science Publishers, Inc., Ann Arbor, MI.
33. Stout, V.F. 1986. What is happening to PCBs? Elements of effective environmental monitoring
as illustrated by an analysis of PCB trends in terrestrial and aquatic organisms. In PCBs and the
environment, ed. J.S. Waid. CRC Press, Inc., Boca Raton, FL.
34. USEPA. 1980. Ambient water quality criteria document: Polychlorinated biphenyls. EPA
440/5-80-068. (Cited in USEPA. 1996. Hazardous Substances Data Bank (HSDB). National
Library of Medicine online (TOXNET). U.S. Environmental Protection Agency, Office of Health
and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH.
February.)
35. Mearns, A.J., M. Malta, G. Shigenaka, D. MacDonald, M. Buchman, H. Harris, J. Golas, and G.
Lauenstein. 1991. Contaminant trends in the Southern California Bight: Inventory and
assessment. Technical Memorandum NOAA ORCA 62. National Oceanic and Atmospheric
Administration. Seattle, WA.
596
-------
BIOACCUMULATION SUMMARY PCS 118
36. 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. NOAA Technical
Memorandum NOS OMA 52. National Oceanic and Atmospheric Administration, Seattle, WA.
37. Spies, R. B., D. W. Rice, Jr., P. A. Montagna, and R. R. Ireland. 1985. Reproductive success,
xenobiotic contaminants and hepatic mixed-function oxidase (MFO) activity in Platichthys
stellatus populations from San Francisco Bay. Mar. Environ. Res. 17:117-121.
38. Monod, G. 1985. Egg mortality of Lake Geneva char (Salvelinus alpinus) contaminated by PCB
and DDT derivatives. Bull. Environ. Contam. Toxicol. 35:531-536.
39. DiUon, T.M., W.H. Benson, R.A. Stackhouse, and A.M. Crider. 1990. Effects of selected PCB
congeners on survival, growth, and reproduction in Daphnia magna. Environ. Toxicol. Chem.
9:1317-1326.
40. Smith., E.V., J.M. Spurr, J.C. Filkins, and JJ. Jones. 1985. Organochlorine contaminants of
wintering ducks foraging on Detroit River sediments. /. Great Lakes Res. 11(3):231-246.
41. Boese, B.L., M. Winsor, H. Lee H, S. Echols, J. PeUetier, and R. Randal. 1995. PCB congeners
and hexachlorobenzene biota sediment accumulation factors for Macoma nasuta exposed to
sediments with different total organic carbon contents. Environ. Toxicol. Chem. 14(2): 303-310.
42. Morrison, H.A., F.A.P.C. Gobas, R. Lazar, and G.D. Haffner. 1996. Development and
verification of a bioaccumulation model for organic contaminants in benthic invertebrates.
Environ. Sci. Technol 30:3377-3384.
43. Ferraro, S.P., H. Lee II, L.M. Smith, R.J. Ozretich, and D.T. Sprecht. 1991. Accumulation
factors for eleven polychlorinated biphenyl congeners. Bull. Environ. Contam. Toxicol. 46:276-
283.
44. Lester, D.C., and A. Mclntosh. 1994. Accumulation of polychlorinated biphenyl congeners from
Lake Champlain sediments by Mysis relicta. Environ. Toxicol. Chem. 13:1825-1841.
45. Bergen, B.J., W.G. Nelson, and R.J. Pruell. 1996. Bioaccumulation of PCB congeners by blue
mussels (Mytilus edulis) deployed in New Bedford Harbor, Massachusetts. Environ. Toxicol.
Chem. 12:1671-1681.
46. Swackhamer, D.L., B.D. McVeety, and R.A. Hites. 1988. Deposition and evaporation of
polychlorobiphenyl congeners to and from Siskiwit Lake, Isle Royale, Lake Superior. Environ.
Sci. Tech. 22:664-672.
47. Swackhamer, D.L., and R.A. Hites. 1988. Occurrence and bioaccumulation of organochlorine
compounds in fishes from Siskiwit Lake, Isle Royale, Lake Superior. Environ. Sci. Tech. 22:543-
548.
48. Henny, C.J., S.A. Ganusevich, F.P. Ward, and T.R. Schwartz. 1994. Organochlorine pesticides,
chlorinated dioxins and furans, and PCBs in peregrine falcon Falco peregrinus eggs from the
597
-------
BIOACCUMULATION SUMMARY PCS 118
Kola Peninsula, Russia. In Raptor conservation today, ed. B.U. Meyburg and R.D. Chancellor,
pp. 739-749. WWGPB/The Pica Press.
49. Tillitt, D.E., R.W. Gale, J.C. Meadows, J.L. Zajicek, P.M. Peterman, S.N. Heaton, P.O. Jones, SJ.
Bursian, TJ. Kubiak, J.P. Giesy, and RJ. Aulerich. 1996. Dietary exposure of mink to carp
from Saginaw Bay. 3. Characterization of dietary exposure to planar halogenated hydrocarbons,
dioxin equivalents, and biomagnification. Environ. Sci. Technol. 30:283-291.
50. USEPA. 1995. Great Lakes Water Quality Initiative technical support document for the
procedure to determine bio accumulation factors. EPA-820-B-95-005. U.S. Environmental
Protection Agency, Office of Water, Washington, DC.
598
-------
BIOACCUMULATION SUMMARY PCB 126
Chemical Category: POLYCHLORINATED BIPHENYLS
Chemical Name (Common Synonyms): CASRN: 57465-28-8
33 ',4,4',5-PENTACHLOROBIPHENYL
Chemical Characteristics
Solubility in Water: No data [1] Half-Life: No data [2,3]
0.004 - 0.099 mg/L [2]
Log Kow: 6.2 - 6.85 [2], No data [4] Log Koc: 6.09 - 6.73 L/kg organic carbon
Human Health
Oral RfD: No data [5] Confidence: No data [5]
Critical Effect: —
Oral Slope Factor: No data [5] Carcinogenic Classification: No data [5]
Wildlife
Partitioning Factors: Partitioning factors for PCB 126 in wildlife were not found.
Food Chain Multipliers: For PCBs as a class the most toxic congeners have been shown to be
selectively accumulated from organisms at one trophic level to the next [6]. At least three studies have
concluded that PCBs have the potential to biomagnify in food webs based on aquatic organisms and
predators that feed primarily on aquatic organisms [7,8,9]. The results from Biddinger and Gloss [7] and
USAGE [9] generally agreed that highly water-insoluble compounds (including PCBs) have the potential
to biomagnify in these types of food webs. Thomann's [10] model also indicated that highly water-
insoluble compounds (log Kow values 5 to 7) showed the greatest potential to biomagnify. The log
biomagnification factor for pentachlorobiphenyls from alewife to herring gulls in Lake Ontario ranged
from 1.18 to 2.00 [11]. A study of arctic marine food chains measured biomagnification factors for
pentachlorobiphenyls that ranged from 0.71 to 1.05 for fish to seal, 0.28 to 0.49 for seal to bear, and 1.14
for fish to bear [12]. No specific food chain multipliers were identified for PCB 126.
Aquatic Organisms
Partitioning Factors: In an 83-day laboratory study with three-spined stickleback, the lipid-normalized
ratio of PCB 126 in food to fish tissue ranged from 3.8 to 6.1. A log bioconcentration factor (BCF) for
deployed mussels in New Bedford Harbor, MA, was approximately 6.90, as reported in the attached table.
599
-------
BIOACCUMULATION SUMMARY PCS 126
Food Chain Multipliers: Polychlorinated biphenyls as a class have been demonstrated to biomagnify
through the food web. Oliver and Niimi [13], studying accumulation of PCBs in various organisms in
the Lake Ontario food web, reported concentrations of total PCBs in phytoplankton, zooplankton, and
several species of fish. Their data indicated a progressive increase in tissue PCB concentrations moving
from organisms lower in the food web to top aquatic predators. In a study of PCB accumulation in lake
trout (Salvelinus namaycush) of Lake Ontario, Rasmussen et al. [14] reported that each trophic level
contributed about a 3.5-fold biomagnification factor to the PCB concentrations in the trout. No specific
food chain multipliers were identified for PCB 126 or other pentachlorobiphenyls.
Toxicity/Bioaccumulation Assessment Profile
PCBs are a group (209 congeners/isomers) of organic chemicals, based on various substitutions of
chlorine atoms on a basic biphenyl molecule. These manufactured chemicals have been widely used in
various processes and products because of the extreme stability of many isomers, particularly those with
five or more chlorines [15]. A common use of PCBs was as dielectric fluids in capacitors and
transformers. In the United States, Aroclor is the most familiar registered trademark of commercial PCB
formulations. Generally, the first two digits in the Aroclor designation indicate that the mixture contains
biphenyls, and the last two digits give the weight percent of chlorine in the mixture.
As a result of their stability and their general hydrophobic nature, PCBs released to the environment have
dispersed widely throughout the ecosystem [15]. PCBs are among the most stable organic compounds
known, and chemical degradation rates in the environment are thought to be slow. As a result of their
highly lipophilic nature and low water solubility, PCBs are generally found at low concentrations in water
and at relatively high concentrations in sediment [16]. Individual PCB congeners have different physical
and chemical properties based on the degree of chlorination and position of chlorine substitution,
although differences with degree of chlorination are more significant [16]. Solubilities and octanol-water
partition coefficients for PCB congeners range over several orders of magnitude [17]. Octanol-water
partition coefficients, which are often used as estimators of the potential for bioconcentration, are highest
for the most chlorinated PCB congeners.
Dispersion of PCBs in the aquatic environment is a function of their solubility [16], whereas PCB
mobility within and sorption to sediment are a function of chlorine substitution pattern and degree of
chlorination [18]. The concentration of PCBs in sediments is a function of the physical characteristics
of the sediment, such as grain size [19,20] and total organic carbon content [19,20,21,22]. Fine sediments
typically contain higher concentrations of PCB s than coarser sediments because of more surface area [16].
Mobility of PCBs in sediment is generally quite low for the higher chlorinated biphenyls [18]. Therefore,
it is common for the lower chlorinated PCBs to have a greater dispersion from the original point source
[16]. Limited mobility and high rates of sedimentation could prevent some PCB congeners in the
sediment from reaching the overlying water via diffusion [18].
The persistence of PCB s in the environment is a result of their general resistance to degradation [17]. The
rate of degradation of PCB congeners by bacteria decreases with increasing degree of chlorination [23];
other structural characteristics of the individual PCBs can affect susceptibility to microbial degradation
to a lesser extent [17]. Photochemical degradation, via reductive dechlorination, is also known to occur
in aquatic environments; the higher chlorinated PCBs appear to be most susceptible to this process [22].
600
-------
BIOACCUMULATION SUMMARY
PCB 126
Toxicity of PCB congeners is dependent on the degree of chlorination as well as the position of chlorine
substitution. Lesser chlorinated congeners are more readily absorbed, but are metabolized more rapidly
than higher chlorinated congeners [24]. PCB congeners with no chlorine substituted in the ortho (2 and
2') positions but with four or more chlorine atoms at the meta (3 and 3') and para (4 and 4') positions can
assume a planar conformation that can interact with the same receptor as the highly toxic 2,3,7,8-
tetrachlorodibenzo-p-dioxin (TCDD) [25]. Examples of these more toxic, coplanar congeners are
3,3',4,4'-tetrachlorobiphenyl (PCB 77), 3,3',4,4',5-pentachlorobiphenyl (PCB 126), and 3,3',4,4',5,5'-
hexachlorobiphenyl (PCB 169). A method that has been proposed to estimate the relative toxicity of
mixtures is to use toxic equivalency factors (TEFs) [26]. With this method, relative potencies for
individual congeners are calculated by expressing their potency in relation to 2,3,7,8-TCDD. The
following TEFs have been recommended [26,27]:
Congener Class
3,3',4,4',5-PentaCB
3,3',4,4',5,5'-HexaCB
3,3'4,4'-TetraCB
Monoortho coplanar PCBs
Diortho coplanar PCBs
Recommended TEF
0.1
0.05
0.01
0.001
0.00002
Due to the toxicity, high Kow values, and highly persistent nature of many PCBs, they possess a high
potential to bioaccumulate and exert reproductive effects in higher-trophic-level organisms. Aquatic
organisms have a strong tendency to accumulate PCBs from water and food sources. The log
bioconcentration factor for fish is approximately 4.70 [28]. This factor represents the ratio of
concentration in tissue to the ambient water concentration. Aquatic organisms living in association with
PCB-contaminated sediments generally have tissue concentrations equal to or greater than the
concentration of PCB in the sediment [28]. Once taken up by an organism, PCBs partition primarily into
lipid compartments [16]. Thus, differences in PCB concentration between species and between different
tissues within the same species may reflect differences in lipid content [16]. PCB concentrations in
polychaetes and fish have been strongly correlated to their lipid content [29]. Elimination of PCBs from
organisms is related to the characteristics of the specific PCB congeners present. It has been shown that
uptake and depuration rates in mussels are high for lower-chlorinated PCBs and much lower for higher-
chlorinated congeners [30,31]. In some species, tissue concentrations of PCBs in females can be reduced
during gametogenesis because of PCB transfer to the more lipophilic eggs. Therefore, the transferred
PCBs are eliminated from the female during spawning [32,33]. Fish and other aquatic organisms
biotransform PCBs more slowly than other species, and they appear less able to metabolize, or excrete,
the higher chlorinated PCB congeners [32]. Consequently, fish and other aquatic organisms may
accumulate more of the higher chlorinated PCB congeners than is found in the environment [17].
The acute toxicity of PCBs appears to be relatively low, but results from chronic toxicity tests indicate
that PCB toxicity is directly related to the duration of exposure [34]. Toxic responses have been noted
to occur at concentrations of 0.03 and 0.014 |ig/L in marine and freshwater environments, respectively
[34]. The LC50 for grass shrimp exposed to PCBs in marine waters for 4 days was 6.1 to 7.8 |ig/L [34].
Chronic toxicity of PCBs presents a serious environmental concern because of their resistance to
degradation [35], although the acute toxicity of PCBs is relatively low compared to that of other
chlorinated hydrocarbons. Sediment contaminated with PCBs has been shown to elicit toxic responses
601
-------
BIOACCUMULATION SUMMARY PCS 126
at relatively low concentrations. Sediment bioassays and benthic community studies suggest that chronic
effects generally occur in sediment at total PCB concentrations exceeding 370 ug/kg [36].
A number of field and laboratory studies provide evidence of chronic sublethal effects on aquatic
organisms at low tissue concentrations [17]. Field and Dexter [17] suggest that a number of marine and
freshwater fish species have experienced chronic toxicity at PCB tissue concentrations of less than 1.0
mg/kg and as low as 0.1 mg/kg. Spies et al. [37] reported an inverse relationship between PCB
concentrations in starry flounder eggs in San Francisco Bay and reproductive success, with an effective
PCB concentration in the ovaries of less than 0.2 mg/kg. Monod [38] also reported a significant
correlation between PCB concentrations in eggs and total egg mortality in Lake Geneva char. PCBs have
also been shown to cause induction of the mixed function oxidase (MFO) system in aquatic animals, with
MFO induction by PCBs at tissue concentrations within the range of environmental exposures [17].
602
-------
Summary of Biological Effects Tissue Concentrations for PCB 126
Species:
Taxa
Concentration, Units in1:
Sediment Water
Toxicity:
Tissue (Sample Type) Effects
Ability to Accumulate2: Source:
Log Log
BAF BAF BSAF Reference Comments3
Invertebrates
Mytilus edulis,
Blue mussel
1993: particulate
0.2|ig/L±0.1
n = 9
dissolved
0.02 ng/L ±0.01
n = 9
1994: particulate -20 ng/g dw
0.2 |ig/L ±0.1 (whole body)
n = 3
6.90
[39] F; New Bedford
Harbor, MA;
deployment study;
tissue concentrations
were only presented
for 1994 samples;
BCF and tissue
concentrations read
from figures (~)
Fishes
dissolved
0.03 ng/L ±0.01
n = 3
Gasterosteus
aciileatiis,
Three-spined
stickleback
0.78 [41] L; 83-day dosing
(male) study; BAF = lipid-
0.58 normalized concent-
female) ration in fish divided
by the lipid-
normalized
concentration in food
Myoxocephalus 0.013
quadricornis, dw
Four-horn sculpin
0.035 ng/g (liver)
0.068 ng/g
(whole body)
[40] F; collected in or near
Hamlet in Cambridge
Bay, NW Territories,
Canada
Salmonids
3.21 [45]
ON
O
-------
ON
O
Summary of Biological Effects Tissue Concentrations for PCB 126
Species: Concentration, Units in1:
Taxa Sediment Water
Wildlife
Sterna hirundo,
Common tern
(embryo)
Falco peregrinus,
Peregrine falcon
Falco sparveriiis,
American kestrel
(embryo)
Falco sparveriiis,
American kestrel
(nestling)
Colinus
virginianus,
Bob white
(embryo)
White leghorn
chicken
(embryo)
White leghorn
chicken
(embryo)
Tissue (Sample Type)
45 ng/kg4
(egg)
1.3ng/g
(eggs) (n = 6)
65 ng/kg4
(egg)
156 ng/kg4
(liver)
24 ng/kg4
(egg)
0.4 |ig/kg
(egg)
3.1 |ig/kg
(egg)
Toxicity:
Effects
35% embryo
mortality
(through hatching)
11.4% eggshell
thinning
LD50 (through
hatching)
Histopathology of
liver, thyroid, and
spleen
LD50 (through
hatching)
LD50
LD50
Ability to Accumulate2: Source:
Log Log
BAF BAF BSAF Reference
[42]
[44]
[42]
[42]
[42]
[42]
[43]
Comments3
L; PCBs were injected
into the air cell of
eggs
F; Kola Peninsula,
Russia
L; PCBs were injected
into the air cell of
eggs
L
L; PCBs were injected
into the air cell of
eggs
L; PCBs were injected
into the air cell of
eggs from day 4 of
incubation through
hatching
L; PCBs were injected
into the air cell of
eggs from day 7
through day 10 of
incubation
1 Concentration units expressed in wet weight unless otherwise indicated.
2BCF = bioconcentration factor, BAF = bioaccumulation factor, BSAF = biota-sediment accumulation factor.
2 L = laboratory study, spiked sediment, single chemical; F = field study, multiple chemical exposure; other unusual study conditions or observations noted.
4 Not clear from reference if concentration is based on wet or dry weight.
-------
BIOACCUMULATION SUMMARY PCS 126
References
1. USEPA. 1996. Hazardous Substances Data Bank (HSDB). National Library of Medicine online
(TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental
Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. February.
2. Mac Kay, D.M., W.Y. Shiw, and K.C. Ma. 1992. Illustrated handbook of physical-chemical
properties and environmental fate for organic chemicals. Vol. I, Monoaromatic hydrocarbons,
chlorobenzenes and PCBs. Lewis Publishers, Boca Raton, FL.
3. USEPA. 1989. Chemical fate rate constants for SARA section 313 chemicals and Superfund
Health Evaluation Manual chemicals. Prepared by Chemical Hazard Assessment Division,
Syracuse Research Corporation, for U.S. Environmental Protection Agency, Office of Toxic
Substances, Exposure Evaluation Division, Washington, DC, and Environmental Criteria and
Assessment Office, Cincinnati, OH. August 11.
4. Karickhoff, S.W., and J.M. Long. 1995. Internal report on summary of measured, calculated and
recommended log Kow values. Draft. Prepared by U.S. Environmental Protection Agency, Office
of Research and Development, Environmental Research Laboratory-Athens, for E. Southerland,
Office of Water, Office of Science and Technology, Standards and Applied Science Division,
Washington, DC. April 10.
5. USEPA. 1996. Integrated Risk Information System (IRIS). National Library of Medicine online
(TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental
Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. September.
6. Jones, P.O., J.P. Giesy, T.J. Kubiak, D.A. Verbrugge, J.C. Newstead, J.P. Ludwig, D.E. Tillit, R.
Crawford, N. De Galan, and G.T. Ankley. 1993. Biomagnification of bioassay-derived 2, 3, 7, 8-
tetrachlorodibenzo-p-dioxin equivalents. Chemosphere 26:1203-1212.
7. Biddinger, G.R., and S.P. Gloss. 1984. The importance of trophic transfer in the bioaccumulation
of chemical contaminants in aquatic ecosystems. Residue Rev. 91:103-145.
8. Kay, S.H. 1984. Potential for biomagnification of contaminants within marine and freshwater
food webs. Technical Report D-84-7. U.S. Army Corps of Engineers, Waterways Experiment
Station, Vicksburg, MS.
9. USAGE. 1995. Trophic transfer and biomagnification potential of contaminants in aquatic
ecosystems. Environmental Effects of Dredging, Technical Notes EEDP-01-33. U.S. Army Corps
of Engineers, Waterways Experiment Station, Vicksburg, MS.
10. Thomann, R.V. 1989. Bioaccumulation model of organic chemical distribution in aquatic food
chains. Environ. Set Technol. 23:699.
11. Braune, B.M., and R.J. Norstrom. 1989. Dynamics of organochlorine compounds in herring gulls:
III. Tissue distribution and bioaccumulation in Lake Ontario gulls. Environ. Toxicol. Chem.
8:957-968.
605
-------
BIOACCUMULATION SUMMARY PCS 126
12. Muir, D.C.G., RJ. Norstrom, and M. Simon. 1988. Organochlorine contaminants in arctic marine
food chains: Accumulation of specific polychlorinated biphenyls and chlordane-related compounds.
Environ. Sci. Technol. 22:1071-1079.
13. Oliver, E.G., and AJ. Niimi. 1988. Trophodynamic analysis of polychlorinated biphenyl
congeners and other chlorinated hydrocarbons in the Lake Ontario ecosystem. Environ. Sci.
Technol. 22:388-397.
14. Rasmussen, J.B., DJ. Rowan, D.R.S. Lean, and J.H. Carey. 1990. Food chain structure in Ontario
lakes determines PCB levels in lake trout (Salvelinus namaycush) and other pelagic fish. Can. J.
Fish. Aquat. Sci. 47:2030-2038.
15. Rand, G.M., P.O. WeUs, and L.S. McCarty. 1995. Chapter 1. Introduction to aquatic toxicology.
In Fundamentals of aquatic toxicology: Effects, environmental fate, and risk assessment, ed. G.M.
Rand, pp. 3-67. Taylor and Francis, Washington, DC.
16. Phillips, D.J.H. 1986. Use of organisms to quantify PCBs in marine and estuarine environments.
In PCBs and the environment, ed. J.S. Waid, pp. 127-182. CRC Press, Inc., Boca Raton, FL.
17. Field, L.J., and R.N. Dexter. 1998. A discussion of PCB target levels in aquatic sediments.
Unpublished document. January 11, 1988.
18. Fisher, J.B., R.L. Petty, and W. Lick. 1983. Release of polychlorinated biphenyls from
contaminated lake sediments: Flux and apparent diffusivities of four individual PCBs. Environ.
Pollut. 5B: 121-132.
19. Pavlou, S.P., and R.N. Dexter. 1979. Distribution of polychlorinated biphenyls (PCB) in estuarine
ecosystems: Testing the concept of equilibrium partitioning in the marine environment. Environ.
Sci. Technol. 13:65-71.
20. Lynch, T.R., and H.E. Johnson. 1982. Availability of hexachlorobiphenyl isomer to benthic
amphipods from experimentally contaminated sediments. In Aquatic Toxicology and Hazard
Assessment: Fifth Conference, ASTM STP 766, ed. J.G. Pearson, R.B. Foster, and W.E. Bishop,
pp. 273-287. American Society of Testing and Materials, Philadelphia, PA.
21. Chou, S.F.J., and R.A. Griffin. 1986. Solubility and soil mobility of polychlorinated biphenyls.
In PCBs and the environment, ed. J. S. Waid, Vol. 1, pp. 101-120. CRC Press, Inc. Boca Raton,
FL.
22. Sawhney, B.L. 1986. Chemistry and properties of PCBs in relation to environmental effects. In
PCBs and the environment, ed. J. S. Waid, pp. 47-65. CRC Press, Inc., Boca Raton, FL.
23. Furukawa, K. 1986. Modification of PCBs by bacteria and other microorganisms. In PCBs and
the environment, ed. J. S. Waid, Vol. 2, pp. 89-100. CRC Press, Inc. Boca Raton, FL.
24. Bolger, M. 1993. Overview of PCB toxicology. In Proceedings of the U.S. Environmental
Protection Agency's National Technical Workshop "PCBs in Fish Tissue", May 10-11, 1993, pp.
606
-------
BIOACCUMULATION SUMMARY PCS 126
37-53. EPA/823-R-93-003, U.S. Environmnetal Protection Agency, Office of Water, Washington,
DC.
25. Erickson, M.D. 1993. Introduction to PCBs and analytical methods. Proceedings of the U.S.
Environmental Protection Agency's National Technical Workshop "PCBs in Fish Tissue", May
10-11,1993, pp. 3-9. EPA/823-R-93-003, U.S. Environmnetal Protection Agency, Office of Water,
Washington, DC.
26. Safe, S. 1990. Polychlorinated biphenyls (PCBs), dibenzo-j?-dioxins (PCDDs), dibenzofurans
(PCDFs), and related compounds: Environmental and mechanistic considerations which support
the development of toxic equivalency factors (TEFs). Crit. Rev. Toxicol. 21(l):51-88.
27. USEPA. 1991. Workshop report on toxicity equivalency factors for polychlorinated biphenyl
congeners. EPA/625/3-91/020. U.S. Environmental Protection Agency. (Eastern Research Group,
Inc., Arlington, MA.)
28. Neff, J.M. 1984. Bioaccumulation of organic micropollutants from sediments and suspended
particulates by aquatic animals. Fres. Z. Anal. Chem. 319:132-136.
29. Shaw, G.R., and D.W. Connell. 1982. Factors influencing concentrations of polychlorinated
biphenyls in organisms from an estuarine ecosystem. Aust. J. Mar. Freshw. Res. 33:1057-1070.
30. Tanabe, S., R. Tatsukawa, and D.J.H. Phillips. 1987. Mussels as bioindicators of PCB pollution:
A case study on uptake and release of PCB isomers and congeners in green-lipped mussels (Perna
viridis) in Hong Kong waters. Environ. Pollut. 47:41-62.
31. Pruell, R. J., J. L. Lake, W. R. Davis, and J. G. Quinn. 1986. Uptake and depuration of organic
contaminants by blue mussels (Mytilus edulis) exposed to environmentally contaminated sediments.
Mar.Biol. 91:497-508.
32. Lech, J.J., and R.E. Peterson. 1983. Biotransformation and persistence of polychlorinated
biphenyls (PCBs) in fish. In PCBs: Human and environmental hazards, ed. P.M. D'ltri and M.A.
Kamrin, pp. 187-201. Ann Arbor Science Publishers, Inc., Ann Arbor, MI.
33. Stout, V.F. 1986. What is happening to PCBs? Elements of effective environmental monitoring
as illustrated by an analysis of PCB trends in terrestrial and aquatic organisms. In PCBs and the
Environment, ed. J.S. Waid. CRC Press, Inc., Boca Raton, FL.
34. USEPA. 1980. Ambient water quality criteria document: Polychlorinated biphenyls. EPA 440/5-
80-068. (Cited in USEPA. 1996. Hazardous Substances Data Bank (HSDB). National Library
of Medicine online (TOXNET). U.S. Environmental Protection Agency, Office of Health and
Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH.
February.)
35. Mearns, A.J., M. Malta, G. Shigenaka, D. MacDonald, M. Buchman, H. Harris, J. Golas, and G.
Lauenstein. 1991. Contaminant trends in the Southern California Bight: Inventory and
607
-------
BIOACCUMULATION SUMMARY PCS 126
assessment. Technical Memorandum NOAA ORCA 62. National Oceanic and Atmospheric
Administration. Seattle, WA.
36. 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. NOAA Technical Memorandum
NOS OMA 52. National Oceanic and Atmospheric Administration, Seattle, WA.
37. Spies, R. B., D. W. Rice, Jr., P. A. Montagna, and R. R. Ireland. 1985. Reproductive success,
xenobiotic contaminants and hepatic mixed-function oxidase (MFO) activity in Platichthys stellatus
populations from San Francisco Bay. Mar. Environ. Res. 17:117-121.
38. Monod, G. 1985. Egg mortality of Lake Geneva char (Salvelinus alpinus) contaminated by PCB
and DDT derivatives. Bull. Environ. Contam. Toxicol. 35:531-536.
39. Bergen, B.J., W.G. Nelson, and RJ.Pruell. 1996. Comparison of nonplanar and coplanar PCB
congener partitioning in seawater and bioaccumulation in blue mussels (Mytilus edulis). Environ.
Toxicol. Chem. 15:1517-1523.
40. Bright, D.A., S.L. Grundy, and K.J. Reimer. 1995. Differential bioaccumulation of non-ortho
substituted and other PCB congeners in coastal arctic invertebrates and fish. Environ. Sci. Technol.
29:2504-2512.
41. Van Bavel, B., P. Andersson, H. Wingfors, J. Ahgren, P. Bergqvist, L. Norrgren, C. Rappe, and M.
Tysklind. 1996. Multivariate modeling of PCB bioaccumulation in three-spined stickleback
(Gasterosteus aculeatus). Environ. Toxicol. Chem. 6:947-954.
42. Hoffman, D.J., MJ. Melancon, J.D. Eisemann, and P.N. Klein. 1995. Comparative toxicity of
planar PCB congeners by egg injection. Abstract, 16th Annual Meeting, Society of Environmental
Toxicology and Chemistry, Washington, DC, November 17-21, 1995.
43. Brunstrom, B., and L. Andersson. 1988. Toxicity and 7-ethoxyresorufin O-deethylase-inducing
potency of coplanar polychlorinated biphenyls (PCBs) in chick embryos. Arch. Toxicol. 62:263-
266.
44. Henny, C.J., S.A. Ganusevich, P.P. Ward, and T.R. Schwartz. 1994. Organochlorine pesticides,
chlorinated dioxins and furans, and PCBs in peregrine falcon Falco peregrinus eggs from the Kola
Penninsula, Russia. In Raptor conservation today, ed. B.U. Meyburg and R.D. Chancellor, pp.
739-749. WWGPB/The Pica Press.
45. USEPA. 1995. Great Lakes Water Quality Initiative technical support document for the procedure
to determine bioaccumulation factors. EPA-820-B-95-005. U.S. Environmental Protection
Agency, Office of Water, Washington, DC.
608
-------
BIOACCUMULATION SUMMARY
PCB 156
Chemical Category: POLYCHLORINATED BIPHENYLS
Chemical Name (Common Synonyms):
2,3,3',4,4',5-HEXACHLOROBIPHENYL
CASRN: 38380-08-4
Chemical Characteristics
Solubility in Water: No data [1], 0.004 - 0.038 mg/L [2] Half-Life: No data [2,3]
Log Kow: 6.7 - 7.3 [2] Log Koc: 6.59 - 7.18 L/kg organic carbon
Human Health
Oral RfD: No data [5]
Critical Effect: —
Oral Slope Factor: No data [5]
Confidence: —
Carcinogenic Classification: No data [5]
Wildlife
Partitioning Factors: In a laboratory study with mink, the lipid-normalized ratios of PCB 156 in liver
to food ranged from 5.5 to 11.6. The ratio of PCB 156 in tissues of three species of duck to sediment in
the lower Detroit River ranged from 27 to 41.
Food Chain Multipliers: For PCBs as a class the most toxic congeners have been shown to be
selectively accumulated from organisms at one trophic level to the next [6]. At least three studies have
concluded that PCBs have the potential to biomagnify in food webs based on aquatic organisms and
predators that feed primarily on aquatic organisms [7,8,9]. The results from Biddinger and Gloss [7] and
USAGE [9] generally agreed that highly water-insoluble compounds (including PCBs) have the potential
to biomagnify in these types of food webs. Thomann's [10] model also indicated that highly water-
insoluble compounds (log Kow values 5 to 7) showed the greatest potential to biomagnify. The log
biomagnification factors for hexachlorobiphenyls from alewife to herring gulls in Lake Ontario ranged
from 1.30 to 2.14 [11]. A study of arctic marine food chains measured log biomagnification factors for
hexachlorobiphenyls that ranged from 0.99 to 1.36 for fish to seal, 0.97 to 1.26 for seal to bear, and 2.23
for fish to bear [12]. No specific food chain multipliers were identified for PCB 156.
Aquatic Organisms
Partitioning Factors: In Lake Ontario, ratios of PCB-156 in tissue (wet weight) to sediment (dry weight)
for plankton, oligochaetes, mysids, and amphipods were 0.10, 0.14, 0.57, and 1.9 respectively; ratios in
sculpin, alewife, rainbow smelt, and salmonids were 6.7, 3.0, 2.9, and 16, respectively. In carp from the
lower Detroit River the tissue to sediment ratio (wet weight) was 25. BSAFs for clam in a laboratory
study ranged from 0.16 to 0.67.
609
-------
BIOACCUMULATION SUMMARY PCS 156
Food Chain Multipliers: Polychlorinated biphenyls as a class have been demonstrated to biomagnify
through the food web. Oliver and Niimi [13], studying accumulation of PCBs in various organisms in
the Lake Ontario food web, reported concentrations of total PCBs in phytoplankton, zooplankton, and
several species of fish. Their data indicated a progressive increase in tissue PCB concentrations moving
from organisms lower in the food web to top aquatic predators. In a study of PCB accumulation in lake
trout (Salvelinus namaycush) of Lake Ontario, Rasmussen et al. [14] reported that each trophic level
contributed about a 3.5-fold biomagnification factor to the PCB concentrations in the trout. No specific
food chain multipliers were identified for PCB 156 or other hexachlorobiphenyls.
Toxicity/Bioaccumulation Assessment Profile
PCBs are a group (209 congeners/isomers) of organic chemicals, based on various substitutions of
chlorine atoms on a basic biphenyl molecule. These manufactured chemicals have been widely used in
various processes and products because of the extreme stability of many isomers, particularly those with
five or more chlorines [15]. A common use of PCBs was as dielectric fluids in capacitors and
transformers. In the United States, Aroclor is the most familiar registered trademark of commercial PCB
formulations. Generally, the first two digits in the Aroclor designation indicate that the mixture contains
biphenyls, and the last two digits give the weight percent of chlorine in the mixture.
As a result of their stability and their general hydrophobic nature, PCBs released to the environment have
dispersed widely throughout the ecosystem [15]. PCBs are among the most stable organic compounds
known, and chemical degradation rates in the environment are thought to be slow. As a result of their
highly lipophilic nature and low water solubility, PCBs are generally found at low concentrations in water
and at relatively high concentrations in sediment [16]. Individual PCB congeners have different physical
and chemical properties based on the degree of chlorination and position of chlorine substitution,
although differences with degree of chlorination are more significant [16]. Solubilities and octanol-water
partition coefficients for PCB congeners range over several orders of magnitude [17]. Octanol-water
partition coefficients, which are often used as estimators of the potential for bioconcentration, are highest
for the most chlorinated PCB congeners.
Dispersion of PCBs in the aquatic environment is a function of their solubility [16], whereas PCB
mobility within and sorption to sediment are a function of chlorine substitution pattern and degree of
chlorination [18]. The concentration of PCBs in sediments is a function of the physical characteristics
of the sediment, such as grain size [19,20] and total organic carbon content [19,21,22]. Fine sediments
typically contain higher concentrations of PCB s than coarser sediments because of more surface area [16].
Mobility of PCBs in sediment is generally quite low for the higher chlorinated biphenyls [18]. Therefore,
it is common for the lower chlorinated PCBs to have a greater dispersion from the original point source
[16]. Limited mobility and high rates of sedimentation could prevent some PCB congeners in the
sediment from reaching the overlying water via diffusion [18].
The persistence of PCB s in the environment is a result of their general resistance to degradation [17]. The
rate of degradation of PCB congeners by bacteria decreases with increasing degree of chlorination [23];
other structural characteristics of the individual PCBs can affect susceptibility to microbial degradation
to a lesser extent [17]. Photochemical degradation, via reductive dechlorination, is also known to occur
in aquatic environments; the higher chlorinated PCBs appear to be most susceptible to this process [22].
610
-------
BIOACCUMULATION SUMMARY
PCB 156
Toxicity of PCB congeners is dependent on the degree of chlorination as well as the position of chlorine
substitution. Lesser chlorinated congeners are more readily absorbed, but are metabolized more rapidly
than higher chlorinated congeners [24]. PCB congeners with no chlorine substituted in the ortho (2 and
2') positions but with four or more chlorine atoms at the meta (3 and 3') and para (4 and 4') positions can
assume a planar conformation that can interact with the same receptor as the highly toxic 2,3,7,8-
tetrachlorodibenzo-p-dioxin (TCDD) [25]. Examples of these more toxic, coplanar congeners are
3,3',4,4'-tetrachlorobiphenyl (PCB 77), 3,3',4,4',5-pentachlorobiphenyl (PCB 126), and 3,3',4,4',5,5'-
hexachlorobiphenyl (PCB 169). A method that has been proposed to estimate the relative toxicity of
mixtures is to use toxic equivalency factors (TEFs) [26]. With this method, relative potencies for
individual congeners are calculated by expressing their potency in relation to 2,3,7,8-TCDD. The
following TEFs have been recommended [26,27]:
Congener Class
3,3',4,4',5-PentaCB
3,3',4,4',5,5'-HexaCB
3,3'4,4'-TetraCB
Monoortho coplanar PCBs
Diortho coplanar PCBs
Recommended TEF
0.1
0.05
0.01
0.001
0.00002
Due to the toxicity, high Kow values, and highly persistent nature of many PCBs, they possess a high
potential to bioaccumulate and exert reproductive effects in higher-trophic-level organisms. Aquatic
organisms have a strong tendency to accumulate PCBs from water and food sources. The log
bioconcentration factor for fish is approximately 4.70 [28]. This factor represents the ratio of
concentration in tissue to the ambient water concentration. Aquatic organisms living in association with
PCB-contaminated sediments generally have tissue concentrations equal to or greater than the
concentration of PCB in the sediment [28]. Once taken up by an organism, PCBs partition primarily into
lipid compartments [16]. Thus, differences in PCB concentration between species and between different
tissues within the same species may reflect differences in lipid content [16]. PCB concentrations in
polychaetes and fish have been strongly correlated to their lipid content [29]. Elimination of PCBs from
organisms is related to the characteristics of the specific PCB congeners present. It has been shown that
uptake and depuration rates in mussels are high for lower-chlorinated PCBs and much lower for higher-
chlorinated congeners [30,31]. In some species, tissue concentrations of PCBs in females can be reduced
during gametogenesis because of PCB transfer to the more lipophilic eggs. Therefore, the transferred
PCBs are eliminated from the female during spawning [32,33]. Fish and other aquatic organisms
biotransform PCBs more slowly than other species, and they appear less able to metabolize, or excrete,
the higher chlorinated PCB congeners [32]. Consequently, fish and other aquatic organisms may
accumulate more of the higher chlorinated PCB congeners than is found in the environment [17].
The acute toxicity of PCBs appears to be relatively low, but results from chronic toxicity tests indicate
that PCB toxicity is directly related to the duration of exposure [34]. Toxic responses have been noted
to occur at concentrations of 0.03 and 0.014 |ig/L in marine and freshwater environments, respectively
[34]. The LC50 for grass shrimp exposed to PCBs in marine waters for 4 days was 6.1 to 7.8 |ig/L [34].
Chronic toxicity of PCBs presents a serious environmental concern because of their resistance to
degradation [35], although the acute toxicity of PCBs is relatively low compared to that of other
chlorinated hydrocarbons. Sediment contaminated with PCBs has been shown to elicit toxic responses
611
-------
BIOACCUMULATION SUMMARY PCS 156
at relatively low concentrations. Sediment bioassays and benthic community studies suggest that chronic
effects generally occur in sediment at total PCB concentrations exceeding 370 ug/kg [36].
A number of field and laboratory studies provide evidence of chronic sublethal effects on aquatic
organisms at low tissue concentrations [17]. Field and Dexter [17] suggest that a number of marine and
freshwater fish species have experienced chronic toxicity at PCB tissue concentrations of less than 1.0
mg/kg and as low as 0.1 mg/kg. Spies et al. [37] reported an inverse relationship between PCB
concentrations in starry flounder eggs in San Francisco Bay and reproductive success, with an effective
PCB concentration in the ovaries of less than 0.2 mg/kg. Monod [38] also reported a significant
correlation between PCB concentrations in eggs and total egg mortality in Lake Geneva char. PCBs have
also been shown to cause induction of the mixed function oxidase (MFO) system in aquatic animals, with
MFO induction by PCBs at tissue concentrations within the range of environmental exposures [17].
612
-------
Summary of Biological Effects Tissue Concentrations for PCS 156
Species:
Taxa
Invertebrates
Plankton (a mixture
of primarily
phytoplankton and
some zooplankton)
Mainly Tubifex
tubifex and
Limnodrilus
hoffmeisteri,
Oligochaete
Tubifex sp,
Oligochaetes
Macoma nasuta,
Bent-nose clam
Concentration, Units in1:
Sediment Water
2.1 ± 1.4 ng/g Not detected in
dw (0-3 cm) surface water
(n = 38) (n = 7)
2.1 ± 1.4 ng/g Not detected in
dw (0-3 cm) surface water
(n = 38) (n = 7)
0.0024 mg/kg
(n=l)
ng/g dw:
0.60 ±0.019
0.48
NA
11.6 ±2.29
34 ± 5.3
Toxicity:
Tissue (Sample Type) Effects
0.2 ±0.1 ng/g
(n = 3)
0.3 ± 0.4 ng/g
(n = 6)
0.00 16 mg/kg
(n=l)
ng/g dw:
2.6 ±0.59
1.93 ±0.284
2.61 ±0.192
2.89 ±0.215
4.1 ±0.77
Ability to Accumulate2: Source:
Log Log
BCF BAF BSAF Reference Comments3
[13] F; Lake Ontario;
value is mean ± SD;
lipid content = 0.5%
[13] F; Lake Ontario;
value is mean ± SD;
lipid content = 1 %
[39] F; lower Detroit
River
[40] L; values given are
mean ± SE;
0.67 sediment TOC
0.61 ranged from 0.84%
Q 51 to 7.4%. Macoma
Q 23 were exposed to 5
Q ,,- sediments
containing different
PCB concentra-
tions; NA means
number was not
legible.
Pontoporeia affinis, 2.1 ±1.4 ng/g Not detected in 3.9 ±2.3 ng/g
Amphipods dw (0-3 cm) surface water (n = 6)
(n = 38) (n = 7)
[13] F; Lake Ontario;
value is mean ± SD;
lipid content = 3%
-------
Summary of Biological Effects Tissue Concentrations for PCS 156
Species:
Taxa
Mysis relicta,
Mysids
Concentration
Sediment
2.1 ± 1.4 ng/g
dw (0-3 cm)
(n = 38)
, Units
Water
in1:
Not detected in
surface water
(n = 7)
Toxicity:
Tissue (Sample Type) Effects
1.
(n
2 ±0.1 ng/g
= 2)
Ability to Accumulate2:
Log Log
BCF BAF BSAF
Source:
Reference
[13]
Comments3
F; Lake Ontario;
value is mean ± SD;
lipid content = 3%
Fishes
Salmonids:
Oncorhynchiis
velinus namaycush,
Coho salmon;
Oncorhynchus
mykiss (Salmo
gairdneri),
Rainbow trout;
Salvelinus
namaycush,
Lake trout;
Salmo trutta,
Brown trout
2.1 ± 1.4 ng/g Not detected in 34 ± 27 ng/g
dw (0-3 cm) surface water (n = 60)
(n = 38) (n = 7)
3.97 [13]
F; Lake Ontario;
value is mean ± SD;
lipid content = 11 %
Cypriniis carpio,
Carp
0.0024 mg/kg
(n=l)
0.061±0.024 mg/kg
(n = 9)
[39]
F; lower Detroit
River
Cottits cognatus,
Sculpin
2.1 ± 1.4 ng/g Not detected in 14 ng/g
dw (0-3 cm) surface water (one composite)
(n = 38) (n = 7)
[13] F; Lake Ontario;
value is mean ± SD;
lipid content = 8%
Alewife
2.1 ± 1.4 ng/g Not detected in 6.3 ng/g
dw (0-3 cm) surface water (one composite)
(n = 38) (n = 7)
[13] F; Lake Ontario;
value is mean ± SD;
lipid content = 7%
Osmerus mordax,
Small rainbow
smelt
2.1 ± 1.4 ng/g Not detected in 2.7 ± 1.9 ng/g
dw (0-3 cm) surface water (n = 4)
(n = 38) (n = 7)
[13] F; Lake Ontario;
value is mean ± SD;
lipid content = 4%
-------
Summary of Biological Effects Tissue Concentrations for PCS 156
Species:
Taxa
Concentration, Units in1:
Sediment
Water
Toxicity:
Tissue (Sample Type) Effects
Ability to Accumulate2: Source:
Log Log
BCF BAF BSAF Reference Comments3
Osmerus mordax,
Large rainbow
smelt
2.1 ± 1.4 ng/g Not detected in 6.1 ng/g
dw (0-3 cm) surface water (one composite)
(n = 38) (n = 7)
[13] F; Lake Ontario;
value is mean ± SD;
lipid content = 4%
Wildlife
Bucephala
clangiila,
Goldeneye
0.0024 mg/kg
(n=l)
0.064±0.018 mg/kg
(n = 3)
[39]
F; lower Detroit
River
Aythya affinis,
Lesser scaup
0.0024 mg/kg
(n=l)
0.090±0.044 mg/kg
(n = 7)
[39]
F; lower Detroit
River
Aythya marila,
Greater scaup
0.0024 mg/kg
(n=l)
0.098±0.0091 mg/kg
(n = 3)
[39]
F; lower Detroit
River
Falco peregrinus,
Peregrine falcon
82 ng/g (eggs)
(n = 6)
11.4% eggshell
thinning
[41] F; Kola Peninsula,
Russia
-------
2: Summary of Biological Effects Tissue Concentrations for PCB 156
01 Species: Concentration, Units in1: Toxicity:
Taxa Sediment Water Tissue (Sample Type) Effects
Miistela vison, Diet:
Mink 110 pg/g4 920 pg/g4 (liver) NOAEL
1,300 pg/g4 12,000 pg/g4 (liver) LOAEL; reduced kit
body weights
followed by reduced
survival
2,800 pg/g4 23,000 pg/g4 (liver) reduced kit body
weights followed by
reduced survival
5,000 pg/g4 37, 100 pg/g4 (liver) Significant decrease
in number of live kits
whelped per female
Ability to Accumulate2: Source:
Log Log
BCF BAF BSAF Reference
[42]
Log
BMF =
0.74
Log
BMF =
0.96
Log
BMF =
0.91
Log
BMF =
1.06
Comments3
L;BMF= lipid-
normalized
concentration in the
liver divided by the
lipid-normalized
dietary concentra-
tion
1 Concentration units expressed in wet weight unless otherwise noted.
2 BCF = bioconcentration factor, BAF = bioaccumulation factor, BSAF = biota-sediment accumulation factor.
3 L = laboratory study, spiked sediment, single chemical; F = field study, multiple chemical exposure; other unusual study conditions or observations noted.
4 Not clear whether units are in dry or wet weight.
-------
BIOACCUMULATION SUMMARY PCB 156
References
1. USEPA. 1996. Hazardous Substances Data Bank (HSDB). National Library of Medicine online
(TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental
Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. February.
2. Mac Kay, D.M., W.Y. Shiw, and K.C. Ma. 1992. Illustrated handbook of physical-chemical
properties and environmental fate for organic chemicals. Vol. I, Monoaromatic hydrocarbons,
chlorobenzenes and PCBs. Lewis Publishers, Boca Raton, FL.
3. USEPA. 1989. Chemical fate rate constants for SARA section 313 chemicals and Superfund
Health Evaluation Manual chemicals. Prepared by Chemical Hazard Assessment Division,
Syracuse Research Corporation, for U.S. Environmental Protection Agency, Office of Toxic
Substances, Exposure Evaluation Division, Washington, DC, and Environmental Criteria and
Assessment Office, Cincinnati, OH. August 11.
4. Karickhoff, S.W., and J.M. Long. 1995. Internal report on summary of measured, calculated and
recommended log Kow values. Draft. Prepared by U.S. Environmental Protection Agency, Office
of Research and Development, Environmental Research Laboratory-Athens, for E. Southerland,
Office of Water, Office of Science and Technology, Standards and Applied Science Division,
Washington, DC. April 10.
5. USEPA. 1996. Integrated Risk Information System (IRIS). National Library of Medicine online
(TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental
Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. September.
6. Jones, P.O., J.P. Giesy, T.J. Kubiak, D.A. Verbrugge, J.C. Newstead, J.P. Ludwig, D.E. Tillit, R.
Crawford, N. De Galan, and G.T. Ankley. 1993. Biomagnification of bioassay-derived 2, 3, 7, 8-
tetrachlorodibenzo-j?-dioxin equivalents. Chemosphere 26:1203-1212.
7. Biddinger, G.R., and S.P. Gloss. 1984. The importance of trophic transfer in the bioaccumulation
of chemical contaminants in aquatic ecosystems. Residue Rev. 91:103-145.
8. Kay, S.H. 1984. Potential for biomagnification ofcontaminants within marine and freshwater
food webs. Technical Report D-84-7. U.S. Army Corps of Engineers, Waterways Experiment
Station, Vicksburg, MS.
9. USAGE. 1995. Trophic transfer and biomagnification potential of contaminants in aquatic
ecosystems. Environmental Effects of Dredging, Technical Notes EEDP-01-33. U.S. Army Corps
of Engineers, Waterways Experiment Station, Vicksburg, MS.
10. Thomann, R.V. 1989. Bioaccumulation model of organic chemical distribution in aquatic food
chains. Environ. Sci. Technol. 23:699.
617
-------
BIOACCUMULATION SUMMARY PCS 156
11 Braune, B.M., and RJ. Norstrom. 1989. Dynamics of organochlorine compounds in herring gulls:
HI. Tissue distribution and bioaccumulation in Lake Ontario Gulls. Environ. Toxicol Chem.
8:957-968.
12. Muir, D.C.G., RJ. Norstrom, and M. Simon. 1988. Organochlorine contaminants in arctic marine
food chains: Accumulation of specific polychlorinated biphenyls and chlordane-related compounds.
Environ. Sci. Technol. 22:1071-1079.
13. Oliver, E.G., and AJ. Niimi. 1988. Trophodynamic analysis of polychlorinated biphenyl
congeners and other chlorinated hydrocarbons in the Lake Ontario ecosystem. Environ. Sci.
Technol. 22:388-397.
14. Rasmussen, J.B., DJ. Rowan, D.R.S. Lean, and J.H. Carey. 1990. Food chain structure in Ontario
lakes determines PCB levels in lake trout (Salvelinus namaycush) and other pelagic fish. Can. J.
Fish. Aquat. Sci. 47:2030-2038.
15. Rand, G.M., P.O. WeUs, and L.S. McCarty. 1995. Chapter 1. Introduction to aquatic toxicology.
In Fundamentals of aquatic toxicology: Effects, environmental fate, and risk assessment, ed. G.M.
Rand, pp. 3-67. Taylor and Francis,Washington, DC.
16. Phillips, D.J.H. 1986. Use of organisms to quantify PCBs in marine and estuarine environments.
In PCBs and the environment, ed. J.S. Waid, pp. 127-182. CRC Press, Inc., Boca Raton, FL.
17. Field, L.J., and R.N. Dexter. 1998. A discussion of PCB target levels in aquatic sediments.
Unpublished document. January 11, 1988.
18. Fisher, J.B., R.L. Petty, and W. Lick. 1983. Release of polychlorinated biphenyls from
contaminated lake sediments: Flux and apparent diffusivities of four individual PCBs. Environ.
Pollut. 5B: 121-132.
19. Pavlou, S.P., and R.N. Dexter. 1979. Distribution of polychlorinated biphenyls (PCB) in estuarine
ecosystems: Testing the concept of equilibrium partitioning in the marine environment. Environ.
Sci. Technol. 13:65-71.
20. Lynch, T.R., and H.E. Johnson. 1982. Availability of hexachlorobiphenyl isomer to benthic
amphipods from experimentally contaminated sediments. In Aquatic Toxicology and Hazard
Assessment: Fifth Conference, ASTM STP 766, ed. J.G. Pearson, R.B. Foster, and W.E. Bishop,
pp. 273-287. American Society of Testing and Materials, Philadelphia, PA.
21. Chou, S.F.J., and R.A. Griffin. 1986. Solubility and soil mobility of polychlorinated biphenyls.
In PCBs and the environment, ed. J.S. Waid, Vol. 1, pp. 101-120. CRC Press, Inc. Boca Raton,
FL.
22. Sawhney, B.L. 1986. Chemistry and properties of PCBs in relation to environmental effects. In
PCBs and the environment, ed. J.S. Waid, pp. 47-65. CRC Press, Inc., Boca Raton, FL.
618
-------
BIOACCUMULATION SUMMARY PCS 156
23. Furukawa, K. 1986. Modification of PCBs by bacteria and other microorganisms. In PCBs and
the environment, ed. J.S. Waid, Vol. 2, pp. 89-100. CRC Press, Inc. Boca Raton, FL.
24. Bolger, M. 1993. Overview of PCB toxicology. In Proceedings of the U.S. Environmental
Protection Agency's National Technical Workshop "PCBs in Fish Tissue," May 10-11, 1993, pp.
37-53. EPA/823-R-93-003, U.S. Environmental Protection Agency, Office of Water, Washington,
DC.
25. Erickson, M.D. 1993. Introduction to PCBs and analytical methods. In Proceedings of the U.S.
Environmental Protection Agency's National Technical Workshop "PCBs in Fish Tissue," May
10-11,1993, pp. 3-9. EPA/823-R-93-003, U.S. Environmental Protection Agency, Office of Water,
Washington, DC.
26. Safe, S. 1990. Polychlorinated biphenyls (PCBs), dibenzo-j?-dioxins (PCDDs), dibenzofurans
(PCDFs), and related compounds: Environmental and mechanistic considerations which support
the development of toxic equivalency factors (TEFs). Crit. Rev. Toxicol. 21(l):51-88.
27. USEPA. 1991. Workshop report on toxicity equivalency factors for poly chlorinate d biphenyl
congeners. EPA/625/3-91/020. U.S. Environmental Protection Agency. (Eastern Research Group,
Inc., Arlington, MA.)
28. Neff, J.M. 1984. Bioaccumulation of organic micropollutants from sediments and suspended
particulates by aquatic animals. Fres. Z. Anal. Chem. 319:132-136.
29. Shaw, G.R., and D.W. Connell. 1982. Factors influencing concentrations of polychlorinated
biphenyls in organisms from an estuarine ecosystem. Aust. J. Mar. Freshw. Res. 33:1057-1070.
30. Tanabe, S., R. Tatsukawa, and D.J.H. Phillips. 1987. Mussels as bioindicators of PCB pollution:
A case study on uptake and release of PCB isomers and congeners in green-lipped mussels (Perna
viridis) in Hong Kong waters. Environ. Pollut. 47:41-62.
31. Pruell, R. J., J. L. Lake, W. R. Davis, and J. G. Quinn. 1986. Uptake and depuration of organic
contaminants by blue mussels (Mytilus edulis) exposed to environmentally contaminated sediments.
Mar.Biol. 91:497-508.
32. Lech, J.J., and R.E. Peterson. 1983. Biotransformation and persistence of polychlorinated
biphenyls (PCBs) in fish. In PCBs: Human and environmental hazards, ed. P.M. D'ltri and M.A.
Kamrin, pp. 187-201. Ann Arbor Science Publishers, Inc., Ann Arbor, MI.
33. Stout, V.F. 1986. What is happening to PCBs? Elements of effective environmental monitoring
as illustrated by an analysis of PCB trends in terrestrial and aquatic organisms. In PCBs and the
environment, ed. J.S. Waid. CRC Press, Inc., Boca Raton, FL.
34. USEPA. 1980. Ambient water quality criteria document: Polychlorinated biphenyls. EPA 440/5-
80-068. (Cited in USEPA. 1996. Hazardous Substances Data Bank (HSDB). National Library
of Medicine online (TOXNET). U.S. Environmental Protection Agency, Office of Health and
619
-------
BIOACCUMULATION SUMMARY PCS 156
Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH.
February.)
35. Mearns, A.J., M. Malta, G. Shigenaka, D. MacDonald, M. Buchman, H. Harris, J. Golas, and G.
Lauenstein. 1991. Contaminant trends in the Southern California Bight: Inventory and
assessment. Technical Memorandum NOAA ORCA 62. National Oceanic and Atmospheric
Administration. Seattle, WA.
36. 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. NOAA Technical Memorandum
NOS OMA 52. National Oceanic and Atmospheric Administration, Seattle, WA.
37. Spies, R. B., D. W. Rice, Jr., P. A. Montagna, and R. R. Ireland. 1985. Reproductive success,
xenobiotic contaminants and hepatic mixed-function oxidase (MFO) activity in Platichthys stellatus
populations from San Francisco Bay. Mar. Environ. Res. 17:117-121.
38. Monod, G. 1985. Egg mortality of Lake Geneva char (Salvelinus alpinus) contaminated by PCB
and DDT derivatives. Bull. Environ. Contain. Toxicol. 35:531-536.
39. Smith, E.V., J.M. Spurr, J.C. Filkins, and JJ. Jones. 1985. Organochlorine contaminants of
wintering ducks foraging on Detroit River sediments. /. Great Lakes Res. 11(3):231-246.
40. Ferraro, S.P., H. Lee H, L.M. Smith, R.J. Ozretich, and D.T. Sprecht. 1991. Accumulation factors
for eleven polychlorinated biphenyl congeners. Bull. Environ. Contain. Toxicol. 46:276-283.
41. Henny, C.J., S.A. Ganusevich, P.P. Ward, and T.R. Schwartz. 1994. Organochlorine pesticides,
chlorinated dioxins and furans, and PCBs in peregrine falcon Falco peregrinus eggs from the Kola
Penninsula, Russia. In Raptor conservation today., ed. B.U. Meyburg and R.D. Chancellor, pp.
739-749. WWGPB/The Pica Press.
42. TiUitt, D.E., R.W. Gale, J.C. Meadows, J.L. Zajicek, P.H. Peterman, S.N. Heaton, P.O. Jones, S.J.
Bursian, T.J. Kubiak, J.P. Giesy, and R.J. Aulerich. 1996. Dietary exposure of mink to carp from
Saginaw Bay. 3. Characterization of dietary exposure to planar halogenated hydrocarbons, dioxin
equivalents, and biomagnification. Environ. Sci. Technol. 30:283-291.
620
-------
BIOACCUMULATION SUMMARY
PCB 169
Chemical Category: POLYCHLORINATED BIPHENYLS
Chemical Name (Common Synonyms):
3,3',4,4',5,5'-HEXACHLOROBIPHENYL
CASRN: 32774-16-6
Chemical Characteristics
Solubility in Water: No data [1], 0.5 mg/L [2]
Log Kow: 7.4 [5]
Half-Life: No data [2,3]
Log Koc: 7.27 L/kg organic carbon
Human Health
Oral RfD: No data [5]
Confidence: —
Critical Effect: —
Oral Slope Factor: No data [5]
Carcinogenic Classification: No data [5]
Wildlife
Partitioning Factors: In a laboratory study with mink, the lipid-normalized ratios of PCB 169 in liver
to food ranged from 12.4 to 21.4.
Food Chain Multipliers: For PCBs as a class the most toxic congeners have been shown to be
selectively accumulated from organisms at one trophic level to the next [6]. At least three studies have
concluded that PCBs have the potential to biomagnify in food webs based on aquatic organisms and
predators that feed primarily on aquatic organisms [7,8,9]. The results from Biddinger and Gloss [7] and
USAGE [9] generally agreed that highly water-insoluble compounds (including PCBs) have the potential
to biomagnify in these types of food webs. Thomann's [10] model also indicated that highly water-
insoluble compounds (log Kow values 5 to 7) showed the greatest potential to biomagnify. The log
biomagnification factors for hexachlorobiphenyls from alewife to herring gulls in Lake Ontario ranged
from 1.30 to 2.14 [11]. A study of arctic marine food chains measured log biomagnification factors for
hexachlorobiphenyls that ranged from 0.99 to 1.36 for fish to seal, 0.99 to 1.26 for seal to bear, and 2.23
for fish to bear [12]. Log BMFs ranged from 1.09 to 1.33 for mink fed PCB 169 in the diet [40].
Aquatic Organisms
Partitioning Factors: In an 83-day laboratory study with three-spined stickleback, the lipid-normalized
ratio of PCB 169 in food to fish tissue (log BAF) ranged from 0.50 to 0.79.
621
-------
BIOACCUMULATION SUMMARY PCB 169
Food Chain Multipliers: Polychlorinated biphenyls as a class have been demonstrated to biomagnify
through the food web. Oliver and Niimi [13], studying accumulation of PCBs in various organisms in
the Lake Ontario food web, reported concentrations of total PCBs in phytoplankton, zooplankton, and
several species of fish. Their data indicated a progressive increase in tissue PCB concentrations moving
from organisms lower in the food web to top aquatic predators. In a study of PCB accumulation in lake
trout (Salvelinus namaycusK) of Lake Ontario, Rasmussen et al. [14] reported that each trophic level
contributed about a 3.5-fold biomagnification factor to the PCB concentrations in the trout. No specific
food chain multipliers were identified for PCB 169 or other hexachlorobiphenyls.
Toxicity/Bioaccumulation Assessment Profile
PCBs are a group (209 congeners/isomers) of organic chemicals, based on various substitutions of
chlorine atoms on a basic biphenyl molecule. These manufactured chemicals have been widely used in
various processes and products because of the extreme stability of many isomers, particularly those with
five or more chlorines [15]. A common use of PCBs was as dielectric fluids in capacitors and
transformers. In the United States, Aroclor is the most familiar registered trademark of commercial PCB
formulations. Generally, the first two digits in the Aroclor designation indicate that the mixture contains
biphenyls, and the last two digits give the weight percent of chlorine in the mixture.
As a result of their stability and their general hydrophobic nature, PCBs released to the environment have
dispersed widely throughout the ecosystem [15]. PCBs are among the most stable organic compounds
known, and chemical degradation rates in the environment are thought to be slow. As a result of their
highly lipophilic nature and low water solubility, PCBs are generally found at low concentrations in water
and at relatively high concentrations in sediment [16]. Individual PCB congeners have different physical
and chemical properties based on the degree of chlorination and position of chlorine substitution,
although differences with degree of chlorination are more significant [16]. Solubilities and octanol-water
partition coefficients for PCB congeners range over several orders of magnitude [17]. Octanol-water
partition coefficients, which are often used as estimators of the potential for bioconcentration, are highest
for the most chlorinated PCB congeners.
Dispersion of PCBs in the aquatic environment is a function of their solubility [18], whereas PCB
mobility within and sorption to sediment are a function of chlorine substitution pattern and degree of
chlorination [18]. The concentration of PCBs in sediments is a function of the physical characteristics
of the sediment, such as grain size [19,20] and total organic carbon content [19,20,21,22]. Fine sediments
typically contain higher concentrations of PCB s than coarser sediments because of more surface area [16].
Mobility of PCBs in sediment is generally quite low for the higher chlorinated biphenyls [18]. Therefore,
it is common for the lower chlorinated PCBs to have a greater dispersion from the original point source
[16]. Limited mobility and high rates of sedimentation could prevent some PCB congeners in the
sediment from reaching the overlying water via diffusion [18].
The persistence of PCB s in the environment is a result of their general resistance to degradation [19]. The
rate of degradation of PCB congeners by bacteria decreases with increasing degree of chlorination [23];
other structural characteristics of the individual PCBs can affect susceptibility to microbial degradation
to a lesser extent [17]. Photochemical degradation, via reductive dechlorination, is also known to occur
in aquatic environments; the higher chlorinated PCBs appear to be most susceptible to this process [22].
622
-------
BIOACCUMULATION SUMMARY
PCB 169
Toxicity of PCB congeners is dependent on the degree of chlorination as well as the position of chlorine
substitution. Lesser chlorinated congeners are more readily absorbed, but are metabolized more rapidly
than higher chlorinated congeners [24]. PCB congeners with no chlorine substituted in the ortho (2 and
2') positions but with four or more chlorine atoms at the meta (3 and 3') and para (4 and 4') positions can
assume a planar conformation that can interact with the same receptor as the highly toxic 2,3,7,8-
tetrachlorodibenzo-p-dioxin (TCDD) [25]. Examples of these more toxic, coplanar congeners are
3,3',4,4'-tetrachlorobiphenyl (PCB 77), 3,3',4,4',5-pentachlorobiphenyl (PCB 126), and 3,3',4,4',5,5'-
hexachlorobiphenyl (PCB 169). A method that has been proposed to estimate the relative toxicity of
mixtures is to use toxic equivalency factors (TEFs) [26]. With this method, relative potencies for
individual congeners are calculated by expressing their potency in relation to 2,3,7,8-TCDD. The
following TEFs have been recommended [26,27]:
Congener Class
3,3',4,4',5-PentaCB
3,3',4,4',5,5'-HexaCB
3,3'4,4'-TetraCB
Monoortho coplanar PCBs
Diortho coplanar PCBs
Recommended TEF
0.1
0.05
0.01
0.001
0.00002
Due to the toxicity, high Kow values, and highly persistent nature of many PCBs, they possess a high
potential to bioaccumulate and exert reproductive effects in higher-trophic-level organisms. Aquatic
organisms have a strong tendency to accumulate PCBs from water and food sources. The log
bioconcentration factor for fish is approximately 4.70 [28]. This factor represents the ratio of
concentration in tissue to the ambient water concentration. Aquatic organisms living in association with
PCB-contaminated sediments generally have tissue concentrations equal to or greater than the
concentration of PCB in the sediment [28]. Once taken up by an organism, PCBs partition primarily into
lipid compartments [16]. Thus, differences in PCB concentration between species and between different
tissues within the same species may reflect differences in lipid content [16]. PCB concentrations in
polychaetes and fish have been strongly correlated to their lipid content [29]. Elimination of PCBs from
organisms is related to the characteristics of the specific PCB congeners present. It has been shown that
uptake and depuration rates in mussels are high for lower-chlorinated PCBs and much lower for higher-
chlorinated congeners [30,31]. In some species, tissue concentrations of PCBs in females can be reduced
during gametogenesis because of PCB transfer to the more lipophilic eggs. Therefore, the transferred
PCBs are eliminated from the female during spawning [32,33]. Fish and other aquatic organisms
biotransform PCBs more slowly than other species, and they appear less able to metabolize, or excrete,
the higher chlorinated PCB congeners [32]. Consequently, fish and other aquatic organisms may
accumulate more of the higher chlorinated PCB congeners than is found in the environment [17].
The acute toxicity of PCBs appears to be relatively low, but results from chronic toxicity tests indicate
that PCB toxicity is directly related to the duration of exposure [34]. Toxic responses have been noted
to occur at concentrations of 0.03 and 0.014 |ig/L in marine and freshwater environments, respectively
[34]. The LC50 for grass shrimp exposed to PCBs in marine waters for 4 days was 6.1 to 7.8 |ig/L [34].
Chronic toxicity of PCBs presents a serious environmental concern because of their resistance to
degradation [35], although the acute toxicity of PCBs is relatively low compared to that of other
623
-------
BIOACCUMULATION SUMMARY PCB 169
chlorinated hydrocarbons. Sediment contaminated with PCBs has been shown to elicit toxic responses
at relatively low concentrations. Sediment bioassays and benthic community studies suggest that chronic
effects generally occur in sediment at total PCB concentrations exceeding 370 |ig/kg [36].
A number of field and laboratory studies provide evidence of chronic sublethal effects on aquatic
organisms at low tissue concentrations [17]. Field and Dexter [17] suggest that a number of marine and
freshwater fish species have experienced chronic toxicity at PCB tissue concentrations of less than 1.0
mg/kg and as low as 0.1 mg/kg. Spies et al. [37] reported an inverse relationship between PCB
concentrations in starry flounder eggs in San Francisco Bay and reproductive success, with an effective
PCB concentration in the ovaries of less than 0.2 mg/kg. Monod [38] also reported a significant
correlation between PCB concentrations in eggs and total egg mortality in Lake Geneva char. PCBs have
also been shown to cause induction of the mixed function oxidase (MFO) system in aquatic animals, with
MFO induction by PCBs at tissue concentrations within the range of environmental exposures [17].
624
-------
Summary of Biological Effects Tissue Concentrations for PCB 169
Species: Concentration, Units in1: Toxicity:
Taxa Sediment Water Tissue (Sample Type) Effects
Fishes
Gasterosteus
aculeatus, Three-
spined stickleback
Ability to Accumulate2:
Log Log
BCF BAF BSAF
0.79
(male)
0.50
(female)
Source:
Reference
[39]
Comments3
L; 83-day dosing
study; BAF =
lipid-normalized
concentration in
fish divided by the
lipid-normalized
concentration in
food
Wildlife
Mustela vison,
Diet:
Mink 2pg/g4 65pg/g4 (liver) NOAEL
5pg/g4 65pg/g4 (liver) LOAEL;
reduced kit body
weights
followed by
reduced survival
10pg/g4 120pg/g4 (liver) Reduced kit
body weights
followed by
reduced survival
™ / 4 ™r / 4 /i- N Significant
20pg/g4 205pg/g4(hver) degcreasein
number of live
kits whelped per
female
ON
K>
CJl
Log
BMF =
1.33
Log
BMF =
1.10
Log
BMF =
1.09
Log
BMF =
1.20
[40] L;BMF= lipid-
normalized
concentration in
the liver divided
by the lipid-
normalized dietary
concentration
-------
ON
K>
ON
1 Concentration units expressed as wet weight unless otherwise noted.
2BCF = bioconcentration factor, BAF = bioaccumulation factor, BSAF = biota-sediment accumulation factor.
3 L = laboratory study, spiked sediment, single chemical; F = field study, multiple chemical exposure; other unusual study conditions or observations noted.
4 Not clear from reference if concentration is based on wet or dry weight.
-------
BIOACCUMULATION SUMMARY PCS 169
References
1. USEPA. 1996. Hazardous Substances Data Bank (HSDB). National Library of Medicine online
(TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental
Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. February.
2. MacKay, D.M., W.Y. Shiw, and K.C. Ma. 1992. Illustrated handbook of physical-chemical
properties and environmental fate for organic chemicals. Vol. I, Monoaromatic hydrocarbons,
chlorobenzenes and PCBs. Lewis Publishers, Boca Raton, FL.
3. USEPA. 1989. Chemical fate rate constants for SARA section 313 chemicals and Superfund
Health Evaluation Manual chemicals. Prepared by Chemical Hazard Assessment Division,
Syracuse Research Corporation, for U.S. Environmental Protection Agency, Office of Toxic
Substances, Exposure Evaluation Division, Washington, DC, and Environmental Criteria and
Assessment Office, Cincinnati, OH. August 11.
4. Karickhoff, S.W., and J.M. Long. 1995. Internal report on summary of measured, calculated and
recommended log Kow values. Draft. Prepared by U.S. Environmental Protection Agency, Office
of Research and Development, Environmental Research Laboratory-Athens, for E. Southerland,
Office of Water, Office of Science and Technology, Standards and Applied Science Division,
Washington, DC. April 10.
5. Debruyn, J.F. Busser, W. Seinen, and J. Hermens. 1989. Determinination of octanol/water
partition coefficients for hydrophobic organic chemicals with the Aslow stirring method. Environ.
Toxicol. Chem. 8: 499-512.
6. Jones, P.O., J.P. Giesy, T.J. Kubiak, D.A. Verbrugge, J.C. Newstead, J.P. Ludwig, D.E. Tillit, R.
Crawford, N. De Galan, and G.T. Ankley. 1993. Biomagnification of bioassay-derived 2, 3, 7,
8-tetrachlorodibenzo-/?-dioxin equivalents. Chemosphere 26:1203-1212.
7. Biddinger, G.R., and S.P. Gloss. 1984. The importance of trophic transfer in the bioaccumulation
of chemical contaminants in aquatic ecosystems. Residue Rev. 91:103-145.
8. Kay, S.H. 1984. Potential for biomagnification ofcontaminants within marine and freshwater
food webs. Technical Report D-84-7. U.S. Army Corps of Engineers, Waterways Experiment
Station, Vicksburg, MS.
9. USAGE. 1995. Trophic transfer and biomagnification potential of contaminants in aquatic
ecosystems. Environmental Effects of Dredging, Technical Notes EEDP-01-33. U.S. Army Corps
of Engineers, Waterways Experiment Station, Vicksburg, MS.
10. Thomann, R.V. 1989. Bioaccumulation model of organic chemical distribution in aquatic food
chains. Environ. Set Technol. 23:699.
627
-------
BIOACCUMULATION SUMMARY PCB 169
11. Braune, B.M., and RJ. Norstrom. 1989. Dynamics of organochlorine compounds in herring
gulls: III. Tissue distribution and bioaccumulation in Lake Ontario Gulls. Environ. Toxicol
Chem. 8:957-968.
12. Muir, D.C.G., RJ. Norstrom, and M. Simon. 1988. Organochlorine contaminants in arctic marine
food chains: Accumulation of specific polychlorinated biphenyls and chlordane-related
compounds. Environ. Sci. Technol. 22:1071-1079.
13. Oliver, E.G., and A.J. Niimi. 1988. Trophodynamic analysis of polychlorinated biphenyl
congeners and other chlorinated hydrocarbons in the Lake Ontario ecosystem. Environ. Sci.
Technol. 22:388-397.
14. Rasmussen, J.B., DJ. Rowan, D.R.S. Lean, and J.H. Carey. 1990. Food chain structure in
Ontario lakes determines PCB levels in lake trout (Salvelinus namaycush) and other pelagic fish.
Can. J. Fish. Aquat. Sci. 47:2030-2038.
15. Rand, G.M., P.O. Wells, and L.S. McCarty. 1995. Chapter 1. Introduction to aquatic toxicology.
In Fundamentals of aquatic toxicology: Effects, environmental fate, and risk assessment, ed. G.M.
Rand, pp. 3-67. Taylor and Francis, Washington, DC.
16. Phillips, D.J.H. 1986. Use of organisms to quantify PCBs in marine and estuarine environments.
In PCBs and the environment, ed. J.S. Waid, pp. 127-182. CRC Press, Inc., Boca Raton, FL.
17. Field, LJ. and R.N. Dexter. 1998. A discussion of PCB target levels in aquatic sediments.
Unpublished document. January 11, 1988.
18. Fisher, J.B., R.L. Petty, and W. Lick. 1983. Release of polychlorinated biphenyls from
contaminated lake sediments: Flux and apparent diffusivities of four individual PCBs. Environ.
Pollut. 5B: 121-132.
19. Pavlou, S.P., and R.N. Dexter. 1979. Distribution of polychlorinated biphenyls (PCB) in
estuarine ecosystems: Testing the concept of equilibrium partitioning in the marine environment.
Environ. Sci. Technol. 13:65-71.
20. Lynch, T.R., and H.E. Johnson. 1982. Availability of hexachlorobiphenyl isomer to benthic
amphipods from experimentally contaminated sediments. In Aquatic Toxicology and Hazard
Assessment: Fifth Conference, ASTM STP 766, ed. J.G. Pearson, R.B. Foster, and W.E. Bishop,
pp. 273-287. American Society of Testing and Materials, Philadelphia, PA.
21. Chou, S.F.J., and R.A. Griffin. 1986. Solubility and soil mobility of polychlorinated biphenyls.
In PCBs and the environment, Vol. 1, pp. 101-120. CRC Press, Inc., Boca Raton, FL.
628
-------
BIOACCUMULATION SUMMARY PCS 169
22. Sawhney, B.L. 1986. Chemistry and properties of PCBs in relation to environmental effects. In
PCBs and the environment, ed. J.S. Waid, pp. 47-65. CRC Press, Inc., Boca Raton, FL.
23. Furukawa, K. 1986. Modification of PCBs by bacteria and other microorganisms. In PCBs and
the environment, ed. J.S. Waid, Vol. 2, pp. 89-100. CRC Press, Inc. Boca Raton, FL.
24. Bolger, M. 1993. Overview of PCB toxicology. In Proceedings of the U.S. Environmental
Protection Agency's National Technical Workshop "PCBs in Fish Tissue" May 10-11, 1993, pp.
37-53. EPA/823-R-93-003, U.S. Environmental Protection Agency, Office of Water, Washington,
DC.
25. Erickson, M.D. 1993. Introduction to PCBs and analytical methods. In Proceedings of the U.S.
Environmental Protection Agency's National Technical Workshop "PCBs in Fish Tissue" May
10-11, 1993, pp. 3-9. EPA/823-R-93-003, U.S. Environmental Protection Agency, Office of
Water, Washington, DC.
26. Safe, S. 1990. Polychlorinated biphenyls (PCBs), dibenzo-/?-dioxins (PCDDs), dibenzofurans
(PCDFs), and related compounds: Environmental and mechanistic considerations which support
the development of toxic equivalency factors (TEFs). Crit. Rev. Toxicol. 21(l):51-88.
27. USEPA. 1991. Workshop report on toxicity equivalency factors for poly chlorinated biphenyl
congeners. EPA/625/3-91/020. U.S. Environmental Protection Agency. (Eastern Research
Group, Inc., Arlington, MA.)
28. Neff, J.M. 1984. Bioaccumulation of organic micropollutants from sediments and suspended
particulates by aquatic animals. Fres. Z. Anal. Chem. 319:132-136.
29. Shaw, G.R., and D.W. Connell. 1982. Factors influencing concentrations of polychlorinated
biphenyls in organisms from an estuarine ecosystem. Aust. J. Mar. Freshw. Res. 33:1057-1070.
30. Tanabe, S., R. Tatsukawa, and DJ.H. Phillips. 1987. Mussels as bioindicators of PCB pollution:
A case study on uptake and release of PCB isomers and congeners in green-lipped mussels (Perna
viridis) in Hong Kong waters. Environ. Pollut. 47:41-62.
31. Pruell, R. J., J. L. Lake, W. R. Davis, and J. G. Quinn. 1986. Uptake and depuration of organic
contaminants by blue mussels (Mytilus edulis) exposed to environmentally contaminated
sediments. Mar. Biol. 91:497-508.
32. Lech, J.J., and R.E. Peterson. 1983. Biotransformation and persistence of polychlorinated
biphenyls (PCBs) in fish. In PCBs: Human and environmental hazards, ed. F.M. D'ltri and M.A.
Kamrin, pp. 187-201. Ann Arbor Science Publishers, Inc., Ann Arbor, MI.
629
-------
BIOACCUMULATION SUMMARY PCS 169
33. Stout, V.F. 1986. What is happening to PCBs? Elements of effective environmental monitoring
as illustrated by an analysis of PCB trends in terrestrial and aquatic organisms. In PCBs and the
Environment, ed. J.S. Waid. CRC Press, Inc., Boca Raton, FL.
34. USEPA. 1980. Ambient water quality criteria document: Poly chlorinated biphenyls. EPA 440/5-
80-068. (Cited in USEPA. 1996. Hazardous Substances Data Bank (HSDB). National Library
of Medicine online (TOXNET). U.S. Environmental Protection Agency, Office of Health and
Environmental Assessment, Environmental Criteria and Assessment Office, Cinncinati, OH.
February.)
35. Mearns, A.J., M. Malta, G. Shigenaka, D. MacDonald, M. Buchman, H. Harris, J. Golas, and G.
Lauenstein. 1991. Contaminant trends in the Southern California Bight: Inventory and
assessment. Technical Memorandum NOAA ORCA 62. National Oceanic and Atmospheric
Administration. Seattle, WA.
36. 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. NOAA Technical Memorandum
NOS OMA 52. National Oceanic and Atmospheric Administration, Seattle, WA.
37. Spies, R. B., D. W. Rice, Jr., P. A. Montagna, and R. R. Ireland. 1985. Reproductive success,
xenobiotic contaminants and hepatic mixed-function oxidase (MFO) activity in Platichthys
stellatus populations from San Francisco Bay. Mar. Environ. Res. 17:117-121.
38. Monod, G. 1985. Egg mortality of Lake Geneva char (Salvelinus alpinus) contaminated by PCB
and DDT derivatives. Bull. Environ. Contam. Toxicol. 35:531-536.
39. Van Bavel, B., P. Andersson, H. Wingfors, J. Ahgren, P. Bergqvist, L. Norrgren, C. Rappe, and
M. Tysklind. 1996. Multivariate modeling of PCB bioaccumulation in three-spined stickleback
(Gasterosteus aculeatus). Environ. Toxicol. Chem. 6:947-954.
40. TiUitt, D.E., R.W. Gale, J.C. Meadows, J.L. Zajicek, P.H. Peterman, S.N. Heaton, P.O. Jones, S.J.
Bursian, T.J. Kubiak, J.P. Giesy, and R.J. Aulerich. 1996. Dietary exposure of mink to carp from
Saginaw Bay. 3. Characterization of dietary exposure to planar halogenated hydrocarbons, dioxin
equivalents, and biomagnification. Environ. Sci. Technol. 30:283-291.
630
-------
BIOACCUMULATION SUMMARY
PENTACHLOROPHENOL
Chemical Category: SUBSTITUTED PHENOLS
Chemical Name (Common Synonyms): PENTACHLOROPHENOL (PCP) CASRN: 87-86-5
Chemical Characteristics
Solubility in Water: 14 mg/L at 20°C [1]
Half-Life: 23 - 178 days, sediment grab sample,
estimated unacclimated aqueous
aerobic biodegradation [2]
Log Kow: 5.09 [3]
Log Koc: 5.00 L/kg organic carbon
Human Health
Oral RfD: 3 x 10'2 mg/kg/day [4]
Confidence: Medium, uncertainty factor =100
Critical Effect: Liver and kidney pathology
Oral Slope Factor: 1.2 x 10"1 per (mg/kg)/day [4] Carcinogenic Classification: B2 [4]
Wildlife
Partitioning Factors: Partitioning factors for pentachlorophenol in wildlife were not found in the
literature.
Food Chain Multipliers: Food chain multipliers for pentachlorophenol in wildlife were not found in
the literature.
Aquatic Organisms
Partitioning Factors: Partitioning factors for pentachlorophenol in aquatic organisms were not found
in the literature.
Food Chain Multipliers: Food chain multipliers for pentachlorophenol in aquatic organims were not
found in the literature.
631
-------
BIOACCUMULATION SUMMARY PENTACHLOROPHENOL
Toxicity/Bioaccumulation Assessment Profile
Technical PCP has been reported to contain chlorodiphenylethers, chlorodibenzo-p-dioxins,
chlorodibezofurans, and hydroxychlorodiphenylethers, whereas commercial PCP contains significant
quantities of tetrachlorophenol [5]. These impurities contribute to PCP toxicity, especially sublethal
effects at low concentrations of PCP. PCP undergoes rapid degradation (by chemical, microbiological,
or photochemical processes) in the environment.
PCP affects energy metabolism by increasing oxygen consumption and altering the activities of several
glycolytic and citric acid cycle enzymes and by increasing the consumption rate of stored lipid [6]. PCP
toxicity ranged from 3 to 100 |ig/L for invertebrates and 1 to 68 |ig/L for fish. In oral doses PCP was
fatal to birds at 380 to 580 mg/kg. Adverse sublethal effects in birds were observed in a diet containing
1 mg/kg of PCP [5].
Residues above 11 mg/kg in bird tissues were associated with acute toxicity. Studies with birds showed
that PCP killed various species at single oral doses of 380 to 504 mg/kg at dietary concentration of 3,850
mg/kg, fed over a 5-day period. Residues of PCP in dead birds were 11 mg/kg in brain, 20 mg/kg in
kidney, and 46 mg/kg in liver [7]. Chickens fed 1 mg/kg PCP over an 8-week period accumulated
substantial amounts of PCP: 2 mg/kg in muscle, 80 mg/kg in kidney, 25 mg/kg in liver [8]. Residues of
PCP in dead organisms after treatment in rice fields were 8.1 mg/kg in frogs and 36.8 mg/kg in snails,
and the residues ranged from 31.2 to 59.5 mg/kg in three fish species [7].
Accumulation of PCP is pH-dependent; at pH 4, PCP is completely protonated and therefore highly
lipophilic. At this pH, PCP has the greatest accumulation potential. Conversely, PCP is completely
ionized at pH 9. Early studies estimated the lethal body burden or critical body residue for goldfish was
0.36 mmol PCP/kg [12] and 0.75 mmol PCP/kg for brown trout [13] (these were prior to 1985 and are
not included in the following table). Experiments with rainbow trout [9] showed that neither the twofold
difference in body weight nor the 3-percent difference in body lipid content gave fish resistance to the
toxicity of PCP. Mean lethal body residues (= critical body residue) ranged from 0.08 to 0.15 mmol/kg.
The PCP accumulation by medaka (Oryzias latipes) acclimated in freshwater and saltwater decreased with
increased salinity [10]. However, the amount of PCP accumulated by killifish acclimated to freshwater
was greater than that accumulated by killifish acclimated to saltwater. The growth rate of bluegill was
reduced by 75 percent during the 22-day subchronic exposure to 173 |ig/L of PCP [11]. The critical body
residue for chlorophenols for fathead minnows ranged from 1.1 to 1.7 mmol/kg [14].
PCP is rapidly accumulated and rapidly excreted, and it has no tendency to persist in living organisms.
However, PCP tends to accumulate in mammalian tissues unless it is efficiently conjugated into a readily
excretable form [15]. Humans eliminate 75 percent of all PCP in the urine. Rats (Rattus sp.) and mice
can eliminate PCP in the urine very efficiently; however, rhesus monkeys (Macaca mulatto) are unable
to excrete PCP efficiently.
632
-------
Summary of Biological Effects Tissue Concentrations for Pentachlorophenol
Species:
Taxa
Invertebrates
Glycera
dibranchiata,
Polychaete
Neanthes virens,
Polychaete -
sand worm
Concentration, Units in1:
Sediment Water Tissue (Sample Type)
6.64 mg/kg
(whole body)4
1 .55 mg/kg
(whole body)4
28 mg/kg
(whole body)4
112 mg/kg
(whole body)4
13.8 mg/kg
(whole body)4
469 mg/kg
Toxicity: Ability to Accumulate2:
Log Log
Effects BCF BAF BSAF
Cellular, LOED
Physiological,
LOED
Physiological,
LOED
Physiological,
LOED
Mortality,
ED 100
Mortality, ED50
Source:
Reference
[20]
[20]
[23]
[23]
[32]
[9]
Comments3
L; reduced ability of
amebocytes to
recognize foreign
material
L; reduced antibacterial
activity
L; significant reduction
in coelomic fluid
glucose level, number
of replicates is 8 to 10
L; decrease in tissue
glycogen
L; lethal body burden
L; median survival time
(extractable lipid)4
471 mg/kg
(extractable lipid)4
Mortality, ED50
with fish fed low fat
diet for 11 weeks then
PCP exposure
[9] L; median survival time
with fish fed high fat
diet for 11 weeks then
PCP exposure
-------
Summary of Biological Effects Tissue Concentrations for Pentachlorophenol
Species:
Taxa
Concentration, Units in1:
Sediment Water Tissue (Sample Type)
29.8 mg/kg
(whole body'4
39.4 mg/kg
(whole body)4
Toxicity: Ability to Accumulate2:
Log Log
Effects BCF BAF BSAF
Mortality, ED50
Mortality, ED50
Source:
Reference Comments3
[9] L; median survival time
with fish fed low fat
diet for 1 1 weeks then
PCP exposure
[9] L; median survival time
with fish fed high fat
diet for 1 1 weeks then
PCP exposure
-------
Summary of Biological Effects Tissue Concentrations for Pentachlorophenol
Species:
Taxa
Eisenia fetida,
Earthworm,
Physa sp., Snail
Concentration, Units in1:
Sediment Water
6.75
mmol/kg
3.75
mmol/kg
2.10
mmol/kg
1.20
mmol/kg
0.68
mmol/kg
0.38
mmol/kg
0.21
mmol/kg
0.12
mmol/kg
0.068
mmol/kg
0.038
mmol/kg
Toxicity: Ability to Accumulate2: Source:
Log Log
Tissue (Sample Type) Effects BCF BAF BSAF Reference Comments3
1.39-2.65 [19] L
mmol/kg
0.74-1.19
mmol/kg
0.62-1.35
mmol/kg
0.56-1.16
mmol/kg
0.59-1.58
mmol/kg
0.51-0.80
mmol/kg
0.33-0.84
mmol/kg
0.79-1.16
mmol/kg
0.44-1.29
mmol/kg
0.21
mmol/kg
0.33 mg/kg Mortality, [28] L; no effect on
(whole body)4 NOED survivorship in 24
hours
-------
ON
U>
ON
Summary of Biological Effects Tissue Concentrations for Pentachlorophenol
Species:
Taxa
Anodonta anatina,
Duck mussel
Mytiliis edulis,
Blue mussel
Mytilus edulis,
Mussel
Concentration, Units in1:
Sediment Water Tissue (Sample Type)
3.1 mg/kg
(whole body)4
1.5 mg/kg
(whole body)4
3.1 mg/kg
(whole body)4
5 |ig/kg 32-244 |ig/kg
2.34 mg/kg
(whole body)4
2.34 mg/kg
(whole body)4
9.9 mg/kg
(whole body)4
29.4 mg/kg
(whole body)4
Toxicity: Ability to Accumulate2:
Log Log
Effects BCF BAF BSAF
Behavior, LOED
Behavior,
NOED
Mortality,
NOED
Physiological,
LOED
Physiological,
NA
Physiological,
NA
Physiological,
NA
Source:
Reference
[30]
[30]
[30]
[16]
[34]
[34]
[34]
[34]
Comments3
L; behavioral changes,
distended foot could
not be retracted
L; no effect on
behavior
L; no effect on
mortality
F
L; significant increase
in anoxic heat
dissipation (j/h/g)at test
concentration
L; 10% reduction in
anoxia tolerance as
percent of controls
L; 36% reduction in
anoxia tolerance as
percent of controls
L; 54% reduction in
anoxia tolerance as
percent of controls
-------
Summary of Biological Effects Tissue Concentrations for Pentachlorophenol
ON
U>
-J
Species: Concentration, Units in1:
Taxa Sediment Water
Mercenaria
mercenaria, Quahog
clam
Daphnia magna,
Cladoceran
Pontoporeia hoyi,
Amphipod
200 mmol/L
300 mmol/L
430 mmol/L
Chironomus
riparius, Midge
Tissue (Sample Type)
0.498 mg/kg
(whole body)4
0.498 mg/kg
(whole body)4
0.45 mg/kg
(whole body)4
48.6 mg/kg
(whole body)4
3.8 mmol/kg
5.6 mmol/kg
7.6 mmol/kg
CBR = 0.33tol.l
mmol/kg
1.1 mg/kg
(whole body)4
0.87 mg/kg
(whole body)4
0.38 mg/kg
(whole body)4
Toxicity: Ability to Accumulate2:
Log Log
Effects BCF BAF BSAF
Physiological,
LOED
Mortality,
NOED
Mortality,
NOED
Survival, ED50
lethal
lethal
lethal
Behavior,
NOED
Behavior,
NOED
Behavior,
NOED
Source:
Reference
[21]
[21]
[28]
[27]
[17]
[29]
[29]
[29]
Comments3
L; impaired ability to
clear flavobacterium
L; no effect on
mortality
L; no effect on
survivorship in 24
hours
L
L
L; no effect on
swimming behavior
L; no effect on
swimming behavior
L; no effect on
swimming behavior
-------
ON
oo
Summary of Biological Effects Tissue Concentrations for Pentachlorophenol
Species:
Taxa
Strongylocentrotus
purpuratus, Purple
sea urchin
Concentration, Units in1:
Sediment Water Tissue (Sample Type)
95 mg/kg
(whole body)4
927 mg/kg
(whole body)4
662 mg/kg
(whole body)4
Toxicity: Ability to Accumulate2:
Log Log
Effects BCF BAF BSAF
Development,
LOED
Development,
LOED
Reproduction,
LOED
Source:
Reference
[22]
[22]
[22]
Comments3
L; increase in number
of abnormal embryos
L; genotoxicity,
anaphase aberrations
L; reduced fertilization
of embryos
Fishes
Oncorhynchus
kisutch,
Coho salmon
1.3|ig/L 21|ig/kg
[17]
Oncorhynchus
mykiss, Rainbow
trout
1.3|ig/L 24|ig/kg
-------
Summary of Biological Effects Tissue Concentrations for Pentachlorophenol
Species:
Taxa
Salmo trittta, Brown
trout
Salveliniis
namaycush,
Lake trout
Carassiiis auratus,
Goldfish
Concentration, Units in1:
Sediment Water Tissue (Sample Type)
1100 mmol/L 3.8 mmol/kg
1 150 mmol/L 4.0 mmol/kg
1300 mmol/L 4.3 mmol/kg
1400 mmol/L 4.4 mmol/kg
1600 mmol/L 5.2 mmol/kg
1700 mmol/L 6.0 mmol/kg
2300 mmol/L 8.0 mmol/kg
CBR = 0.08 to 0.15
mmol/kg
0.2 mg/1 200 mg/kg
(whole body)4
1.3|ig/L ling/kg
82 mg/kg
(whole body)4
97 mg/kg
(whole body)4
89 mg/kg
(whole body)4
Toxicity: Ability to Accumulate2:
Log Log
Effects BCF BAF BSAF
lethal
lethal
lethal
lethal
lethal
lethal
lethal
Mortality, ED50
Mortality,
ED 100
Mortality,
ED 100
Mortality,
ED 100
Source:
Reference Comments3
[17] L
[13] L; lethal body burden
[17] L
[25] L; lethal body burden
[25] L; lethal body burden
[25] L; lethal body burden
-------
Summary of Biological Effects Tissue Concentrations for Pentachlorophenol
Species: Concentration, Units in1:
Taxa Sediment Water Tissue (Sample Type)
88 mg/kg
(whole body)4
97 mg/kg
(whole body)4
99 mg/kg
(whole body)4
87 mg/kg
(whole body)4
86 mg/kg
(whole body)4
82 mg/kg
(whole body)4
107 mg/kg
(whole body)4
92 mg/kg
(whole body)4
89 mg/kg
(whole body)4
100 mg/kg
(whole body)4
82 mg/kg
(whole body)4
Toxicity:
Effects
Mortality,
ED 100
Mortality,
ED 100
Mortality,
ED 100
Mortality,
ED 100
Mortality,
ED 100
Mortality,
ED 100
Mortality,
ED 100
Mortality,
ED 100
Mortality,
ED 100
Mortality,
ED 100
Mortality,
ED 100
Ability to Accumulate2: Source:
Log Log
BCF BAF BSAF Reference
[25]
[25]
[25]
[25]
[25]
[25]
[25]
[25]
[25]
[25]
[25]
Comments3
L; lethal body burden
L; lethal body burden
L; lethal body burden
L; lethal body burden
L; lethal body burden
L; lethal body burden
L; lethal body burden
L; lethal body burden
L; lethal body burden
L; lethal body burden
L; lethal body burden
-------
Summary of Biological Effects Tissue Concentrations for Pentachlorophenol
Species:
Taxa
Pimephales
promelas,
Fathead minnow
Pimephales
promelas, Fathead
minnow
Concentration, Units in1:
Sediment Water Tissue (Sample Type)
99 mg/kg
(whole body)4
86 mg/kg
(whole body)4
95 mg/kg
(whole body)4
CBR= 1.1-1.7
mmol/kg
69 mg/kg
(whole body)4
22.1 mg/kg
(whole body)4
25.1 mg/kg
(whole body)4
43.8 mg/kg
(whole body)4
69 mg/kg
(whole body)4
Toxicity: Ability to Accumulate2:
Log Log
Effects BCF BAF BSAF
Mortality,
ED 100
Mortality,
ED 100
Mortality, ED50
50% mortality
Growth, LOED
Growth, LOED
Growth, LOED
Morphology,
LOED
Morphology,
LOED
Source:
Reference Comments3
[25] L; lethal body burden
[25] L; lethal body burden
[26] L; mortality
[14] L
[33] L; pH was 8.5
[33] L; pH was 8.0
[33] L; pH was 7.5
[33] L; pH was 8.0
[33] L; pH was 8.5
-------
Summary of Biological Effects Tissue Concentrations for Pentachlorophenol
Species: Concentration, Units in1:
Taxa Sediment Water Tissue (Sample Type)
35.1 mg/kg
(whole body)4
45.9 mg/kg
(whole body)4
45.9 mg/kg
(whole body)4
43.8 mg/kg
(whole body)4
12.6 mg/kg
(whole body)4
12.3 mg/kg
(whole body)4
45.9 mg/kg
(whole body)4
35.1 mg/kg
(whole body)4
35.1 mg/kg
(whole body)4
22.1 mg/kg
(whole body)4
2 1.5 mg/kg
(whole body)4
Toxicity: Ability to Accumulate2:
Log Log
Effects BCF BAF BSAF
Mortality,
LOED
Mortality,
LOED
Mortality,
LOED
Mortality,
LOED
Growth, NOED
Growth, NOED
Growth, NOED
Growth, NOED
Morphology,
NOED
Morphology,
NOED
Morphology,
NOED
Source:
Reference
[33]
[33]
[33]
[33]
[33]
[33]
[33]
[33]
[33]
[33]
[33]
Comments3
L; pH was 8,
L; pH was 6,
L; pH was 6,
L; pH was 8
L; pH was 8,
L; pH was 7,
L; pH was 6,
L; pH was 8,
L; pH was 8,
L; pH was 8,
L; pH was 6,
.5
.5
.5
.0
.0
.5
.5
.5
.5
.0
.5
-------
Summary of Biological Effects Tissue Concentrations for Pentachlorophenol
Species: Concentration, Units in1:
Taxa Sediment Water Tissue (Sample Type)
25.1 mg/kg
(whole body)4
17.8 mg/kg
(whole body)4
22.1 mg/kg
(whole body)4
25.1 mg/kg
(whole body)4
2 1.5 mg/kg
(whole body)4
25.1 mg/kg
(whole body)4
45.9 mg/kg
(whole body)4
69 mg/kg
(whole body)4
43.8 mg/kg
(whole body)4
Toxicity: Ability to Accumulate2:
Log Log
Effects BCF BAF BSAF
Morphology,
NOED
Mortality,
NOED
Mortality,
NOED
Mortality,
NOED
Mortality,
NOED
Reproduction,
NOED
Reproduction,
NOED
Reproduction,
NOED
Reproduction,
NOED
Source:
Reference
[33]
[33]
[33]
[33]
[33]
[33]
[33]
[33]
[33]
Comments3
L; pH was 7.
L; pH was 8,
L; pH was 8,
L; pH was 7
L; pH was 6
L; pH was 7
L; pH was 6
L; pH was 8,
L; pH was 8
,5
.5
.0
.5
.5
.5
.5
.5
.0
Ictalurus nebulosus,
Brown bullhead
5.7
260 |ig/kg
[18]
-------
Summary of Biological Effects Tissue Concentrations for Pentachlorophenol
Species:
Taxa
Oryzias latipes,
Medaka
Gambiisia affinis,
Mosquito fish
Osmerus mordax,
Rainbow smelt
Leiicisciis idus,
Golden ide
Micropterus
salmoides,
Largemouth bass
Concentration, Units in1:
Sediment Water Tissue (Sample Type)
100|ig/L 41.02|ig/g
38.02 |ig/g
37.50 ng/g
0.8 mg/kg
(whole body)4
1.3|jg/L 6|ig/kg
13 mg/kg
(whole body)4
9.6 mg/kg
(whole body)4
9.6 mg/kg
(whole body)4
9.6 mg/kg
(whole body)4
10.8 mg/kg
(whole body)4
Toxicity: Ability to Accumulate2:
Log Log
Effects BCF BAF BSAF
Mortality,
NOED
Mortality,
NOED
Behavior, LOED
Growth, LOED
Physiological,
LOED
Mortality,
NOED
Source:
Reference
[10]
[28]
[17]
[24]
[31]
[31]
[31]
[31]
Comments3
L
L; no effect on
survivorship in 24
hours
L
L; no effect on
survivorship in 3 days
L; reduced success rate
of prey capture
L; reduction in growth
L; reduced food
conversion efficiency,
condition factor
L; no effect on
mortality
-------
Summary of Biological Effects Tissue Concentrations for Pentachlorophenol
Species:
Taxa
Percaflavescens,
Yellow perch
Concentration, Units in1:
Sediment Water
5.7 ng/L
Toxicity:
Tissue (Sample Type) Effects
260 |ig/kg
Ability to Accumulate2:
Log Log
BCF BAF BSAF
Source:
Reference Comments3
[18] F
1 Concentration units based on wet weight unless otherwise noted.
2 BCF = bioconcentration factor, BAF = bioaccumulation factor, BSAF = biota-sediment accumulation factor.
3 L = laboratory study, spiked sediment, single chemical; F = field study, multiple chemical exposure; other unusual study conditions or observations noted.
4 This entry was excerpted directly from the Environmental Residue-Effects Database (ERED, www.wes.army.mil/el/ered, U.S. Army Corps of Engineers and U.S.
Environmental Protection Agency). The original publication was not reviewed, and the reader is strongly urged to consult the publication to confirm the information
presented here.
-------
BIOACCUMULATION SUMMARY PENTACHLOROPHENOL
References
1. Iverschueren handbook of environmental data for organic chemicals, 1983, p. 953. (Cited in:
USEPA. 1995. Hazardous Substances Data Bank (HSDB). National Library of Medicine online
(TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental
Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. September.)
2. USEPA. 1989. Chemical fate rate constants for SARA section 313 chemicals and Superfund Health
Evaluation Manual chemicals. Prepared by Chemical Hazard Assessment Division, Syracuse
Research Corporation, for U.S. Environmental Protection Agency, Office of Toxic Substances,
Exposure Evaluation Division, Washington, DC, and Environmental Criteria and Assessment Office,
Cincinnati, OH. August 11.
3. Karickhoff, S.W., and J.M. Long. 1995. Internal report on summary of measured, calculated and
recommended log Kow values. Draft. Prepared by U.S. Environmental Protection Agency, Office
of Research and Development, Environmental Research Laboratory-Athens, for E. Southerland,
Office of Water, Office of Science and Technology, Standards and Applied Science Division,
Washington, DC. April 10.
4. USEPA. 1995. Integrated Risk Information System (IRIS). National Library of Medicine online
(TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental
Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. September.
5. Eisler, R. 1989. Pentachlorophenol hazards to fish, wildlife, and invertebrates: A synoptic review.
Fish and Wildlife Service, Biological Report 85(1.17).
6. Brown, J.A., P.H. Johansen, P.W. Colgan, and R.A. Mathers. 1987. Impairment of early feeding
behavior of largemouth bass by pentachlorophenol exposure: A preliminary assessment. Trans. Am.
Fish. Soc. 116:71-78.
7. Vermeer, K., R.W. Risebrough, A.L. Spaans, and L.M. Reynolds. 1974. Pesticide effects on fishes
and birds in rice fields of Surinam, South America. Environ. Pollut. 7:217-236.
8. Prescott, C.A., B.N. Wilke, B. Hunter, and R.J. Julian. 1982. Influence of a purified grade of
pentachlorophenol on the immune response of chickens. Amer. J. Vet. Res. 43:481-487.
9. Van den Heuvel, M.R., L.S. McCarty, R.P.Lanno, B.E. Hickie, and D.G. Dixon. 1991. Effect of
total body lipid on the toxicity and toxicokinetics of pentachlorophenol in rainbow trout
(Oncorhynchus mykiss). Aquatic Toxicol. 20:235-252.
10. Tachikawa, M., and R. Sawamura. 1994. The effects of salinity on pentachlorophenol accumulation
and elimination by killifish (Oryzias latipes). Arch. Environ. Contam. Toxicol. 26:304-308.
646
-------
BIOACCUMULATION SUMMARY PENTACHLOROPHENOL
11. Samis, A.J.W., P.W. Colgan, and P.M. Johansen. 1993. Pentachlorophenol and reduced food intake
of bluegiU. Trans. Am. Fish. Soc. 122:1156-1160.
12. Kobayashi, K., H. Akitake, and K. Manabe. 1979. Relation between toxicity and accumulation of
various chlorophenols in goldfish. Bull. Japan Soc. Sci. Fish. 45:173-175.
13. Hattula, M.L., V.M. Wasenius, H. Reunanen, and A.U. Arstila. 1981. Acute toxicity of some
chlorinates, phenols, catechols and cresols to trout. Bull. Environ. Contain. Toxicol. 26:295-298.
14. van Wezel, A.P., S.S. Punte, and A. Opperhuizen. 1995. Lethal body burdens of polar narcotics:
Chlorophenols. Environ. Toxicol. Chem. 14:1579-1585.
15. Kinzell, J.H., R.M. McKenzie, B.A. Olson, D.K.Kirsch, and L.R. Shull. 1985. Metabolic fate of
(U-14C) pentachlorophenol in a lactating dairy cow. /. Agri. Food Chem. 33:827-833.
16. Folke, J., and J. Birklund. 1986. Danish coastal water levels of 2,3,4,6-tetrachlorophenol,
pentachlorophenol, and total organohalogens in blue mussels (Mytilus edulis). Chemosphere
15:895-900.
17. Windle, W.M., and L.S. McCarty. 1995. Advocating the routine measurement of critical body
burdens in standard toxicity protocols for use in regulatory programs. Presented at the Aquatic
Toxicology Workshop, St. Andrews, New Brunswick.
18. Niimi, A.J., and C.Y. Cho. 1983. Laboratory and field analysis of pentachlorophenol (PCP)
accumulation by salmonids. Water Res. 17:1791-1795.
19. Fitzgerald, D.G., K.A. Warner, R.P.Lanno, and D.G. Dixon. 1996. Assessing the effects of
modifying factors on pentachlorophenol toxicity to earthworms: Applications of body residues.
Environ. Toxicol. Chem. 15:2299-2304.
20. Anderson, R.S., C.S. Giam, and L.E. Ray. 1984. Effects of hexachlorobenzene and
pentachlorophenol on cellular and humoral immune parameters in Glycera dibranchiata. Mar.
Environ. Res. 14:317-326.
21. Anderson, R.S., C.S. Giam, L.E. Ray, and M.R. Tripp. 1981. Effects of environmental pollutants
on immunological competency of the clam Mercenaria mercenaria: Impaired bacterial clearance.
Aquat. Toxicol. 1:187-195.
22. Anderson, S.L., J.E. Hose, and J.P. Knezovich. 1994. Genotoxic and developmental effects in Sea
urchins are sensitive indicators of effects on genotoxic chemicals. Environ. Toxicol. Chem. 13:1033-
1041.
647
-------
BIOACCUMULATION SUMMARY PENTACHLOROPHENOL
23. Carr, R.S., and J.M.Neff. 1981. Biochemical indices of stress in the sandworm Neanthes virens
(Sars). I. Responses to pentachlorophenol. Aquat. Toxicol 1:313-327.
24. Freitag, D., L. Ballhorn, H. Geyer, and F. Korte. 1985. Environmental hazard profile of organic
chemicals: An experimental method for the assessment of the behaviour of organic chemicals in the
ecosphere by means of laboratory tests with 14C labelled chemicals. Chemosphere 14:1589-1616.
25. Kobayashi, K., and T. Kishino. 1980. Effect of pH on the toxicity and accumulation of
pentachlorophenol in goldfish. Bull Japan. Soc. Set Fish. 46:167-170.
26. Kobayashi, K., H. Akitake, and K. Manabe. 1979. Relation between toxicity and accumulation of
various chlorophenols in goldfish. Bull. Japan. Soc. Sci. Fish. 45:173-175.
27. Landrum P.P., and W.S. Dupuis. 1990. Toxicity and toxicokinetics of pentachlorophenol and
carbaryl to Pontoporeia hoyi and My sis relicta. In Aquatic Toxicology and Risk Assessment, Vol.
13, ed. W.G. Landisetal.
28. Lu, P.Y., and Metcalf. 1975. Environmental fate and biodegradability of benzene derivatives as
studied in a model aquatic ecosystem. Environ. Health Perspect. 10:269-284.
29. Lydy, M.J., K.A. Bruner, D.M.Fry, and S.W. Fisher. 1990. Effects of sediment and the route of
exposure on the toxicity and accumulation of neutral lipophilic and moderately water soluble
metabolizable compounds in the midge, Chironomus riparius. In Aquatic toxicology and risk
assessment, ed. W.G. Landis et al., Vol 13, pp. 140-164.
30. Makela, P., and A.O.J. Oikari. 1990. Uptake and body distribution of chlorinated phenolics in the
freshwater mussel, Anodonta anatina L. Ecotoxicol. Environ. Saf. 20:354-362.
31. Mathers, R.A., J.A. Brown, and P.M. Johansen. 1985. The growth and feeding behaviour responses
of largemouth bass (Micropterus salmoides) exposed to PCP. Aquat. Toxicol. 6:157-164.
32. Mckim, J.M., and P.K. Schmieder. 1991. Bioaccumulation: Does it reflect toxicity?. In
Proceeedings, Bioaccumulation in Aquatic Systems: Contributions to Assessment, ed. R. Nagel
etal., pp. 161-188.
33. 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. Environ. Toxicol. Chem. 4:389-397.
34. Wang, W.X., J. Widdows, and D.S. Page. 1992. Effects of organic toxicants on the anoxic energy
metabolism of the mussel Mytilus edulis. Mar. Environ. Res. 34: 327-331.
648
-------
BIOACCUMULATION SUMMARY
PHENANTHRENE
Chemical Category: POLYNUCLEAR AROMATIC HYDROCARBON (low molecular weight)
Chemical Name (Common Synonyms): PHENANTHRENE CASRN: 85-01-8
Chemical Characteristics
Solubility in Water: 0.6 ± 0.1 mg/L, 22°C [1] Half-Life: 16-200 days, aerobic soil
die-away test [2]
Log Kow: 4.55 [3]
Log Koc: 4.47 L/kg organic carbon
Human Health
OralRfD: No data [4]
Critical Effect:
Oral Slope Factor: No data [4]
Confidence:
Carcinogenic Classification: D [4]
Wildlife
Partitioning Factors: Partitioning factors for phenanthrene in wildlife were not found in the literature.
Food Chain Multipliers: Food chain multipliers for phenanthrene in wildlife were not found in the
literature.
Aquatic Organisms
Partitioning Factors: The water quality criterion tissue level (WQCTL) for phenanthrene, which is
calculated by multiplying the water quality chronic value (4.6 |ig/L) by the BCF (1380.38), is 6,350 ug/kg
[5]. The partitioning between interstitial water and sediment particles increases with sediment aging [6].
The increasing partitioning suggests that phenanthrene becomes more tightly bound with increased
contact time. A log BCF of 2.51 was reported for Daphnia magna [16].
Food Chain Multipliers: Food chain multipliers for phenanthrene in aquatic organisms were not found
in the literature.
Toxicity/Bioaccumulation Assessment Profile
PAHs are readily metabolized and excreted by fish and invertebrates [11], affecting bioaccumulation
kinetics and equilibrium tissue residues. The bioconcentration of phenanthrene by Hexagenia was related
649
-------
BIOACCUMULATION SUMMARY PHENANTHRENE
to the weight of the mayflies [12]. The bioaccumulation of phenanthrene by three amphipod species was
much higher (up to 24 times) for the water-only exposure than for uptake from the sediment [13].
According to Landrum et al. [7], accumulation of sediment-associated PAHs (including phenanthrene)
by the amphipod Diporeia spp. was limited by both the desorption rate to the interstitial water and the
rate of accumulation through ingestion. Because of these limitations the concentration required to
produce biological effects (mortality) was approximately 20 times greater than would be predicted using
an equilibrium-partitioning approach. Amphipods exposed to 0.08, 0.18, 0.45, and 0.62 |imol/g of
phenanthrene accumulated up to 5.8 |imol/g. The highest concentration (0.62 |imol/g of phenanthrene)
was slightly toxic to the amphipods (12% mortality in highest concentration). According to the authors
the amphipods never reached 6.1 |imol/g in their tissues, the concentration that was required (according
to equilibrium-partitioning) to produce toxicity. The results reported by Swartz et al. [8] suggest that
phenanthrene at a concentration more than two orders of magnitude higher than the acute concentration
measured in the laboratory was not toxic to amphipods. The toxic level of phenanthrene established in
the laboratory for the amphipod Rhepoxynius abronius was 3.68 mg/kg [9] (10-day LC50 value), while
exposure of amphipods to 2,000 mg/kg of phenanthrene in sediment from Eagle Harbor did not produce
acute responses. According to McCarty et al. [10], the toxic (critical) body residue of individual PAHs
in tissues ranged from 513 to 4,248 mg/kg.
650
-------
Summary of Biological Effects Tissue Concentrations for Phenanthrene
Species:
Taxa
Invertebrates
Nereis succinea,
Polychaete worm,
Crassostrea
virginica,
Eastern oyster
Concentration, Units in1:
Sediment Water
umol/g umol/L
0.001
0.004
0.006
0.023
0.023
0.028
0.042
0.051
0.00001
0.00001
0.00001
0.00002
0.00002
0.00004
0.00004
0.00005
0.00005
0.00005
0.00007
0.00007
0.00007
0.00007
Toxicity: Ability to Accumulate2: Source:
Tissue (Sample Type) Log Log
umol/g Effects BCF BAF BSAF Reference Comments3
0.094 [14] F
0.035
0.007
0.029
0.063
0.046
0.340
0.039
0.00003 [15] F
0.00013
0.00017
0.00015
0.00010
0.00020
0.00018
0.00029
0.00022
0.00025
0.00022
0.00009
0.00022
0.00018
-------
Summary of Biological Effects Tissue Concentrations for Phenanthrene
Species:
Taxa
Crassostrea
virginica,
Eastern oyster
Concentration, Units in1:
Sediment Water
umol/g umol/L
0.00008
0.00008
0.00008
0.00008
0.00010
0.00010
0.00010
0.00010
0.00010
0.00010
0.00010
0.00010
0.0002
0.0002
0.0003
0.0005
0.0009
Toxicity: Ability to Accumulate2: Source:
Tissue (Sample Type) Log Log
umol/g Effects BCF BAF BSAF Reference Comments3
0.0001
0.0002
0.0001
DDL4
0.0003
0.0006
0.0002
0.0001
0.0001
0.0001
0.0002
0.0001
0.0002
0.0002
0.0004
0.0001
0.0001
Mytilus edulis,
Mussel
30.7 mg/kg (whole
body)5
Physiological,
ED50
[22] L; 50% reduction
in feeding rate
Macoma batihica,
Baltic macoma
Daphnia magna,
Cladoceran
0.001
0.004
0.006
0.023
0.023
0.028
0.042
0.051
0.225
0.216
0.062
0.026
0.027
0.110
0.396
73 nM/G
1.51
[16]
L
-------
Summary of Biological Effects Tissue Concentrations for Phenanthrene
Species:
Taxa
Diporeia sp.,
Amphipod
Concentration, Units in1: Toxicity: Ability to Accumulate2: Source:
Sediment Water Tissue (Sample Type) Log Log
umol/g umol/L umol/g Effects BCF BAF BSAF Reference Comments3
0.08 Day 1: 0.2 [7] L
Day 3: 0.4
Day 8: 0.2
Day 16: 0.1
Day 32: 0.1
0.18 Day 1: 0.2
Day 3: 0.4
Day 8: 0.2
Day 16:0.1
Day 32: 0.1
0.45 Day 1: 3.2
Day 3: 3.8
Day 8: 1.4
Day 16: 0.6
Day 32: 0.4
Diporeia sp.,
Amphipod
0.62
Day 1: 2.2
Day 3: 5.8
Day 8: 2.8
Day 16: 1.2
Day 32: 0.4
[7]
L
Diporeia spp.
Amphipod
71 mg/kg
(whole body)5
Mortality,
LOED
[21]
L; 12% mortality
-------
Summary of Biological Effects Tissue Concentrations for Phenanthrene
Species:
Taxa
Eohaustorius
estuarius,
Amphipod
Grandidierella
japonica,
Amphipod
Leptocheirus
plumulosus,
Amphipod
Pontoporeia hoyi,
Amphipod
Concentration, Units in1:
Sediment Water
umol/g umol/L
0.208 0.014
overlying
water
0.14
overlying
water
0.208 0.0140
overlying
water
0.140
overlying
water
0.208 0.0140
overlying
water
0.140
overlying
water
0.0004 0.006
0.004 0.008
Toxicity: Ability to Accumulate2: Source:
Tissue (Sample Type) Log Log
umol/g Effects BCF BAF BSAF Reference Comments3
[13] L
0.225, lipid
5.899, total
0.719, lipid
17.191, total
[13] L
0.096, lipid
1.0 11, total
0.938, lipid
10.169, total
0.073, lipid [13] L
0.899, total
0.360, lipid
3.427, total
0.004 [18] L
0.007
Fishes
-------
Summary of Biological Effects Tissue Concentrations for Phenanthrene
Species:
Taxa
Oncorhynchus
mykiss,
Rainbow trout
Concentration
Sediment
umol/g
, Units in1:
Water
umol/L
Tissue (Sample Type)
umol/g
30 mg/kg
(whole body)5
Toxicity:
Effects
Physiological,
LOED
Ability
Log
BCF
to Accumulate2:
Log
BAF BSAF
Source:
Reference
[24]
Comments3
L; induction of
hepatic mixed
function oxidases
Brachydanio rerio, 0.013
Zebrafish
0.004 0.013-24 hours
0.0007 - 240 hours
[20]
L
Leuciscus idus,
Golden ide
88 mg/kg
(whole body)5
Mortality,
NOED
[23] L; no effect on
survivorship In 3
days
Pleuronectesvetulus, 0.0009-1.07
English sole
0.0005 (liver)
<0.00001 (muscle)
[19]
Concentration units based on wet weight unless otherwise noted.
BCF = bioconcentration factor, BAF = bioaccumulation factor, BSAF = biota-sediment accumulation factor.
L = laboratory study, spiked sediment, single chemical; F = field study, multiple chemical exposure; other unusual study conditions or observations noted.
BDL = below detection limit.
This entry was excerpted directly from the Environmental Residue-Effects Database (ERED, www.wes.army.mil/el/ered, U.S. Army Corps of Engineers and U.S.
Environmental Protection Agency). The original publication was not reviewed, and the reader is strongly urged to consult the publication to confirm the information
presented here.
-------
BIOACCUMULATION SUMMARY PHENANTHRENE
References
1. Iverschueren handbook of environmental data for organic chemicals, 1983, p. 970. (Cited in:
USEPA. 1995. Hazardous Substances Data Bank (HSDB). National Library of Medicine online
(TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental
Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. September.)
2. USEPA. 1989. Chemical fate rate constants for SARA section 313 chemicals and Superfund Health
Evaluation Manual chemicals. Prepared by Chemical Hazard Assessment Division, Syracuse
Research Corporation, for U.S. Environmental Protection Agency, Office of Toxic Substances,
Exposure Evaluation Division, Washington, DC, and Environmental Criteria and Assessment Office,
Cincinnati, Ohio. August 11.
3. Karickhoff, S.W., and J.M. Long. 1995. Internal report on summary of measured, calculated and
recommended log Kow values. Draft. Prepared by U.S. Environmental Protection Agency, Office of
Research and Development, Environmental Research Laboratory-Athens, for E. Southerland, Office
of Water, Office of Science and Technology, Standards and Applied Science Division, Washington,
DC. April 10.
4. USEPA. 1995. Integrated Risk Information System (IRIS). National Library of Medicine online
(TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental
Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. September.
5. Neff, J.M. 1995. Water quality criterion tissue level approach for establishing tissue residue criteria
for chemicals. Report to U.S. Environmental Protection Agency.
6. Landrum, P.F., BJ. Eadie, and W.R. Faust. 1992. Variation in the bioavailability of polycyclic
aromatic hydrocarbons to the amphipod Diporeia spp. Environ. Toxicol. Chem. 11:1197-1208.
7. Landrum, P.F., W.S. Dupuis, and J. Kukkonen. 1994. Toxicokinetics and toxicity of sediment-
associated pyrene and phenanthrene in Diporeia spp.: Examination of equilibrium-partitioning
theory and residue-based effects for assessing hazards. Environ. Toxicol. Chem. 13:1769-1780.
8. Swartz, R.C., P.P. Kemp, D.W. Schults, G.R. Ditsworth, and RJ. Ozretich. 1989. Acute toxicity
of sediment from Eagle Harbor, Washington, to the infaunal amphipod Rhepoxynius abronius.
Environ. Toxicol. Chem. 8:215-222.
9. Swartz, R.C. Schults D.W., G.R. Ditsworth, and W.A. DeBen. 1984. Effects of mixtures of
sediment contaminants on the marine infuanal amphipod Rhepoxynius abronius. Arch. Environ.
Contam. Toxicol. 13:207-215.
10. McCarty, L.S., D. Mackay, A.D. Smith, G.W. Ozburn, and D.G. Dixon. 1992. Residue-based
interpretation of toxicity and bioconcentration QSARs from aquatic bioassays: Neutral narcotic
organics. Environ. Toxicol. Chem. 11:917-930.
11. Stegeman, J.J., and P.J. Kloepper-Sams. 1987. Cytochrome P-450 isozymes and monooxygenase
activity in aquatic animals. Environ. Health Persp. 71:87-95.
656
-------
BIOACCUMULATION SUMMARY PHENANTHRENE
12. Stehly, G.R., P.P. Landrum, M.G. Henry, and C. Klemm. 1990. Toxicokinetics of PAHs in
Hexagenia. Environ. Toxicol. Chem. 12:155-165.
13. Fuji, T., and LJ. Weber. 1995. A comparison of the accumulation of phenanthrene by marine
amphipods in waters versus sediment. Abstract, 16th Annual Meeting, Society of Environmental
Toxicology and Chemistry, Vancouver, British Columbia, November 5-9, 1995.
14. Foster, G.D., and D.A. Wright. 1988. Unsubstituted polynuclear aromatic hydrocarbons in
sediments, clams, and clam worms from Chesapeake Bay. Mar. Pollut. Bull. 19:459-465.
15. Sanders, M. 1994. Distribution of polycyclic aromatic hydrocarbons in oyster (Crassostrea
virginicd) and surface sediment from two estuaries in South Carolina. Arch. Environ. Contain.
Toxicol. 28:397-405.
16. Newsted, J.L., and J.P. Giesy. 1987. Predictive models for photoinduced acute toxicity of
polycyclic aromatic hydrocarbons to Daphnia magna Strauss (Cladocera, Crustacea). Environ.
Toxicol. Chem. 6:445-461.
17. Landrum, P.P., BJ. Eadie, and W.R. Faust. 1991. Toxicokinetics and toxicity of a mixture of
sediment-associated polycyclic aromatic hydrocarbons to the amphipod Diporeia spp. Environ.
Toxicol. Chem. 10:35-46.
18. Eadie, B.J., P.P. Landrum, and W. Faust. 1982. Polycyclic aromatic hydrocarbons in sediments,
pore water, and the amphipod Pontoporeia hoyi from Lake Michigan. Chemosphere 11: 847-857.
19. Malins, D.C., M.M. Krahn M.S., M.S. Myers, L.D. Rhodes, D.W. Brown, C.A. Krone, B.N.
McCain, and S.L. Chan. 1985. Toxic chemicals in sediments and biota from a creosote-polluted
harbor: Relationships with hepatic neoplasms and other hepatic lesions in English sole (Parophrys
vetulus). Carcinogenesis 6:1463-1469.
20. Djomo, J.E., P.Garrigues, and J.F. Narbonne. 1996. Uptake and depuration of polycyclic aromatic
hydrocarbons from sediment by the zebrafish (Brachydanio rerio). Environ. Toxicol. Chem.
15:1177-1181.
21. Landrum, P.P., W.S. Dupuis, and J. Kukkonen. 1994. Toxicokinetics and toxicity of sediment-
associated pyrene and phenanthrene in Diporeia spp.: Examination of equilibrium partitioning
theory and residue-based effects for assessing hazard. Environ. Toxicol Chem. 13:1769-1780.
22. Donkin, P., J. Widdows, S.V. Evans, C.M. Worrall, and M. Carr. 1989. Quantitative structure-
activity relationships for the effect of hydrophobic organic chemicals on rate of feeding by mussels
(Mytilus edulis). Aquat. Toxicol. 14:277-294.
23. Freitag, D., L. Ballhorn, H. Geyer, and F. Korte. 1985. Environmental hazard profile of organic
chemicals: An experimental method for the assessment of the behaviour of organic chemicals in the
ecosphere by means of laboratory tests with 14C labelled chemicals. Chemosphere 14:1589-1616.
24. Gerhart, E.H. and R.H. Carlson. 1978. Hepatic mixed-function oxidase activity in rainbow trout
exposed to several polycyclic aromatic hydrocarbons. Environ. Res. 17:284-295.
657
-------
658
-------
BIOACCUMULATION SUMMARY PYRENE
Chemical Category: POLYNUCLEAR AROMATIC HYDROCARBON (high molecular weight)
Chemical Name (Common Synonyms): PYRENE CASRN: 129-00-0
Chemical Characteristics
Solubility in Water: 0.135 mg/L at 25°C [1] Half-Life: 210 days - 5.2 yrs based on aerobic
soil die-away test data at
10-30°C [2]
Log Kow: 5.11 [3] Log Koc: 5.02 L/kg organic carbon
Human Health
Oral RfD: 3 x 10"2 mg/kg/day [4] Confidence: Low, uncertainty factor = 3000
Critical Effect: Kidney effects (renal tubular pathology, decreased kidney weights)
Oral Slope Factor (Reference): No data [4] Carcinogenic Classification: No data [4]
Wildlife
Partitioning Factors: Partitioning factors for pyrene in wildlife were not found in the literature.
Food Chain Multipliers: Food chain multipliers for pyrene in wildlife were not found in the literature.
Aquatic Organisms
Partitioning Factors: Log BCFs for pyrene ranged from 2.85 for midges [6] to 4.05 for guppies [17].
Log BAFs ranged from -0.43 for clams to 4.65 for amphipods [16].
Food Chain Multipliers: Food chain multipliers for pyrene in aquatic organisms were not found in the
literature.
Toxicity/Bioaccumulation Assessment Profile
The acute toxicity of hydrocarbons, including pyrene, to both fresh and saltwater crustaceans is largely
nonselective, i.e., it is not primarily influenced by molecular structure, but is rather controlled by
organism-water partitioning which, for nonpolar organic chemicals, is in turn a reflection of aqueous
solubility. The toxic effect is believed to occur at a relatively constant concentration within the organism
[5]. Bioconcentration and depuration of pyrene and its biotransformation products display a clear pH-
dependency both in rate and bioconcentration [6]. Decreasing ambient pH leads to decreasing
659
-------
BIOACCUMULATION SUMMARY PYRENE
bioconcentration rates, depuration rates, bioconcentration factors. The accumulation kinetics of pyrene
suggest that uptake occurs largely via the sediment interstitial water and is controlled by desorption from
sediment particles and dissolved organic matter [7].
Bioavailability of sediment-associated PAHs has been observed to decline with increased contact time
[8]. The concentration of pyrene declined significantly over the course of the exposures for all aging
durations. Increases in the length of contact between the sediment and pyrene reduced its bioavailability
compared to 3 days of aging, but after 60 days, the bioavailability appeared to stabilize. Pyrene exhibited
increased partitioning between interstitial water and sediment particles as aging increased [8]. The
increasing partitioning suggests that the compounds are becoming more tightly bound with increased
contact time.
The results from the laboratory experiments performed by Harkey et al. [9] indicated that accumulation
of pyrene from pore-water exposures was lower than accumulation from whole sediment. The
concentrations of pyrene in whole sediment and pore water were 0.14-0.87 ng/g and 0.001-0.016 mg/mL,
respectively. Harkey et al. [9] concluded that aqueous extracts of whole sediment did not accurately
represent the exposure observed in whole sediment. The aqueous extracts of whole sediment
underexposed organisms compared to whole sediment, even after adjusting accumulation to the fraction
of organic carbon contained in the test media. While the total pyrene concentration in the sediment stayed
constant, total concentration decreased appreciably in pore water and elutriate over the course of the
exposure, and it is likely that the bioavailability concentrations in these media also decreased. The
dissolved organic material in the interstitial waters interfered with the direct uptake of PAHs, e.g., pyrene,
in a manner similar to that observed with humic material [10]. Unlike the Aldrich humics that showed
a very close relationship between log Kow and log Kb, sorption by dissolved organic carbon from
interstitial waters would not necessarily be predicted from Kow. Pyrene was quickly accumulated by
Lumbriculus variegatus and achieved apparent steady state within 48 to 168 hours [11].
The relative pyrene distribution among sediment particle size revealed 44 percent of pyrene within 43-63
|im particle size [12]. In general, most of pyrene was found in the smallest-sized particles. The narcotic
effect for Diporeia exposed to pyrene depends on attaining a certain molar concentration in the organism
[12]. Using equilibrium-partitioning theory, the BCF value, and critical body residue (LD50), Landrum
et al. [12] calculated the sediment concentration that would produce 50 percent amphipod mortality.
Based on these assumptions, the pyrene concentration of 14.2 |ig/g in sediment should produce 50 percent
mortality. The LC50 based on laboratory exposure was estimated to be between 147 and 223 |ig/g
pyrene. The comparison of the calculated values with the estimated LC50 value (147 to 223 |ig/g) from
the laboratory experiments suggested that the equilibrium-partitioning approach overestimated the toxicity
of sediment-associated pyrene by a factor of 10 at minimum.
660
-------
Summary of Biological Effects Tissue Concentrations for Pyrene
Species:
Taxa
Invertebrates
Nereis virens,
Polychaete
Lumbriculus
variegatus,
Oligochate
Dreissena polymorpha,
Zebra mussel
Concentration, Units in1:
Sediment Water
umol/g umol/L
0.006 0.008
0.003 17.327
0.000001
0.0003
0.0007
0.001
0.0013
Toxicity:
Tissue (Sample Type)
umol/g Effects
0.023-0.031 in 4 days
0.004
0.0002 in 2 days,
0.0003 in 25 days,
0.0004 in 58 days,
0.00 15 in 96 h,
0.0014 in 168 h,
0.00 19 in 96 h,
0.0020 in 168 h,
0.00 19 in 96 h,
0.0020 in 168 h,
0.0023 in 96 h,
0.0016 in 168 h,
Ability to Accumulate2: Source:
Log Log
BCF BAF BSAF Reference Comments3
3.33 [14] L
[16] L
[11] L
[11] L
[11] L
[11] L
[11] L
4.65 [13] L;notlipid
normalized
Mytilus editlis,
Mussel
0.006
0.008
0.022-0.031 in 4 days
3.70
[14]
ON
ON
-------
ON
ON
Summary of Biological Effects Tissue Concentrations for Pyrene
Species:
Taxa
Concentration, Units in1: Toxicity:
Sediment Water Tissue (Sample Type)
umol/g umol/L umol/g Effects
Ability to Accumulate2: Source:
Log Log
BCF BAF BSAF Reference
Comments
Mytilus edulis, Mussel
189mg/kg
(whole body)4
Physiological,
ED50
[20]
L;50%
reduction in
feeding rate,
exp_conc =
>0.04
Macoma nasuta,
Clam
0.00006
0.00006
0.0005
0.0006
0.0018
0.0025
0.0002
0.0002
0.0003
0.0004
0.0009
0.0008
-0.28
[15]
0.36
0.43
0.30
0.33
0.37
[15]
[15]
[15]
[15]
[15]
F
F
F
F
F
Diporeia spp.,
Amphipod
1270 mg/kg
(whole body)4
Mortality,
ED50
[12]
L; 50%
mortality
Diporeia spp..
Amphipod
0.52
0.86
1.11
6.8 in 28d,
2.8 in 14d,
7.4 in 28d,
4.6 in 14d,
6.6 in 28d,
4.6 in 14d,
LD50 (critical body
residue) was 6.3 and 9.4
|imol/g
LC50 was between 147
and 223 |ig/g (0.72-1.1
|imol/g)
[12]
[12]
[12]
-------
Summary of Biological Effects Tissue Concentrations for Pyrene
Species: Concentration, Units in1: Toxicity:
Sediment Water Tissue (Sample Type)
Taxa umol/g umol/L umol/g Effects
Pontoporeia hoyi, 0.0006 0.005
Amphipod
0.0002 0.02 0.007
Pontoporeia hoyi, 0.0014 0.014 0.015
Amphipod
Chironomus riparius
Crangon separenaria, 0.006 0.008 0.010-0.011 in 4 days
Shrimp
Fishes
Oncorhynchus mykiss, 30 mg/kg Physiological,
Rainbow trout (whole body)4 LOED
Ability to Accumulate2: Source:
Log Log
BCF BAF BSAF Reference
[7]
4.65 [16]
[16]
2.85 [6]
[6]
[6]
2.95 [14]
[21]
Comments3
L
L
L
L;atpHof4
L; at pH of 6
L; at pH of 8
L
L; increased
hepatic
concentration
of cytochrome
P450
ON
ON
-------
ON
ON
Summary of Biological Effects Tissue Concentrations for Pyrene
Species:
Taxa
Cyprinus carpio,
Common carp
Concentration, Units in1: Toxicity:
Sediment Water Tissue (Sample Type)
umol/g umol/L umol/g Effects
28.7 mg/kg (liver)4 Physiological, NA
Ability to Accumulate2: Source:
Log Log
BCF BAF BSAF Reference Comments3
[19] L; significant
increrase in
EROD
enzyme and
P450 la
protein
content
Brachydanio rerio,
Zebrafish
0.011 0.088 0.008-24 hours
0.001 -240 hours
[18]
L
Poecilia reticulata,
Guppy
0.6
0.742
4.05
[17]
L
1 Concentration units based on wet weight unless otherwise noted.
2 BCF = bioconcentration factor, BAF = bioaccumulation factor, BSAF = biota-sediment accumulation factor.
3 L = laboratory study, spiked sediment, single chemical; F = field study, multiple chemical exposure; other unusual study conditions or observations noted.
4 This entry was excerpted directly from the Environmental Residue-Effects Database (ERED, www.wes.army.mil/el/ered, U.S. Army Corps of Engineers and U.S.
Environmental Protection Agency). The original publication was not reviewed, and the reader is strongly urged to consult the publication to confirm the information
presented here.
-------
BIOACCUMULATION SUMMARY PYRENE
References
1. MacKay, D., and Shin Wy; /. Chem Eng Data 22:399 (1977). (Cited in: USEPA. 1995.
Hazardous Substances Data Bank (HSDB). National Library of Medicine online (TOXNET). U.S.
Environmental Protection Agency, Office of Health and Environmental Assessment, Environmental
Criteria and Assessment Office, Cincinnati, OH. September.)
2. USEPA. 1989. Chemical fate rate constants for SARA section 313 chemicals and Superfund Health
Manual chemicals. Prepared by Chemical Hazard Assessment Division, Syracuse Research
Corporation, for U.S. Environmental Protection Agency, Office of Toxic Substances, Exposure
Evaluation Division, Washington, DC, and Environmental Criteria and Assessment Office,
Cincinnati, OH. August 11.
3. Karickhoff, S.W., and J.M. Long. 1995. Internal report on summary of measured, calculated, and
recommended log Kow values. Draft. Prepared by U.S. Environmental Protection Agency, Office
of Research and Development, Environmental Research Laboratory-Athens, for E. Southerland,
Office of Water, Office of Science and Technology, Standards and Applied Science Division,
Washington, DC. April 10.
4. USEPA. 1997. Integrated Risk Information System (IRIS). National Library of Medicine online
(TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental
Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. January.
5. Abernethy, S., A.M. Bobra, W.Y. Shiu, P.G.Weils, and D. MacKay. 1986. Acute lethal toxicity
of hydrocarbons and chlorinated hydrocarbons to two planktonic crustaceans: The key role of
organism-water partitioning. Aquatic Tox. 8:163-174.
6. Wild, E., R. Nagel, and C.E.W. Steinberg. 1994. Effects of pH on the bioconcentration of pyrene
in the larval midge, Chironomus riparius. Water Res. 28:2553-2559.
7. Landrum, P.F. 1989. Bioavailability and toxicokinetics of polycyclic aromatic hydrocarbons sorbed
to sediments for the amphipod Pontoporeia hoyi. Environ. Sci. Technol. 23:588-595.
8. Landrum, P.F., B.J. Eadie, and W.R. Faust. 1992. Variation in the bioavailability of polycyclic
aromatic hydrocarbons to the amphipod Diporeia (spp.) with sediment aging. Environ. Toxicol.
Chem. 11:1197-1208.
9. Harkey, G.A., P.F. Landrum, and SJ. Klaine. 1994. Comparison of whole-sediment, elutriate and
pore-water exposures for use in assessing sediment-associated organic contaminants in bioassays.
Environ. Toxicol. Chem. 13:1315-1329.
10. Landrum, P.P., S.R. Nihart, BJ. Eadie, and L.R. Herche. 1987. Reduction in bioavailability of
organic contaminants to the amphipod Pontoporeia hoyi by dissolved organic matter of sediment
interstitial waters. Environ. Toxicol. Chem. 6:11-20.
11. Kukkonene, J., and P.F. Landrum. 1994. Toxicokinetics and toxicity of sediment-associated pyrene
to Lumbriculus variegatus (Oligochaeta). Environ. Toxicol. Chem. 13:1457-1468.
665
-------
BIOACCUMULATION SUMMARY PYRENE
12. Landrum, P.P., W.S. Dupuis, and J. Kukkonen. 1994. Toxicokinetics and toxicity of sediment
associated pyrene and phenanthrene in Diporeia spp.: Pxamination of equilibrium-partitioning
theory and residue-based effects for assessing hazard. Environ. Toxicol.Chem, 13:1769-1780.
13. Fisher, S.W., D.C. Gossiaux, K.A. Bruner, and P.P. Landrum. 1993. Investigations of the
toxicokinetics of hydrophobic contaminants in the zebra mussel (Dreissena polymorpha). In Zebra
mussels, biology, impacts and control, ed. T. Nalepa and D.W. Schloesser, pp. 465-490. CRC
Press, Boca Raton, PL.
14. McLeese, D.W., and P.P. Burridge. 1987. Comparative accumulation of PAHs in four marine
invertebrates. In Oceanic progress in marine pollution, ed. J.M. Capuzzo and D.R. Kester. Krieger
Publishing Company, Malatar, PP.
15. Ferraro, S.P., H. Pee n, RJ. Ozretich, and D.T. Specht. 1990. Predicting bioaccumulation potential:
A test of a fugacity-based model. Arch. Environ. Contain. Toxicol 19:386-394.
16. Padie, B.J., P.P. Pandrum, and W. Faust. 1982. Polycyclic aromatic hydrocarbons in sediments,
pore water and the amphipod Pontoporeia hoyi from Pake Michigan. Chemosphere 11:847-858.
17. de Voogt, P., B. van Hattum, P. Peonards, J.C. Klamer, and H. Covers. 1991. Bioconcentration
of polycyclic heteroaromatic hydrocarbons in the guppy (Poecilia reticulatd). Aquat. Tox. 20:169-
194.
18. Djomo, J.P., P.Garrigues, and J.F. Narbonne. 1996. Uptake and depuration of polycyclic aromatic
hydrocarbons from sediment by the zebrafish (Brachydanio rerio). Environ. Toxicol. Chem.
15:1177-1181.
19. Van Der Weidern, M.E.J., Hanegraaf, F.H.M, Pggens, M.P., Celander, M., Seinen, W., Ven Den
Berg, M. 1994. Temporal induction of cytochrome P450 la in the mirror carp (Cyprinus carpio)
after administration of several polycyclic aromatic hydrocarbons. Environ. Toxicol. Chem. 13:797-
802.
20. Donkin, P., J. Widdows, S.V. Pvans, C.M. Worrall and M. Carr. 1989. Quantitative structure-
activity relationships for the effect of hydrophobic organic chemicals on rate of feeding by mussels
(Mytilus edulis). Aquat. Toxicol. 14:277-294.
21. Gerhart, E.H., and R.H. Carlson. 1978. Hepatic mixed-function oxidase activity in rainbow trout
exposed to several polycyclic aromatic hydrocarbons. Environ. Res. 17:284-295.
666
-------
BIOACCUMULATION SUMMARY SELENIUM
Chemical Category: METAL
Chemical Name (Common Synonyms): SELENIUM CASRN: 7782-49-2
Chemical Characteristics
Solubility in Water: Insoluble [1] Half-Life: Not applicable, stable [1]
LogKow: - LogKoc: -
Human Health
Oral RfD: 5 x 10"3 mg/kg/day [2] Confidence: High, uncertainty factor = 3
Critical Effect: Clinical selenosis (hair or nail loss, morphological changes of the nails, skin lesions,
central nervous system abnormalities including peripheral anesthesia, acroparesthesia, and pain in the
extremities, and liver dysfunction indicated by prolongation of blood clotting time and reduced serum
glutathione liter)
Oral Slope Factor: Inadequate data [2] Carcinogenic Classification: D, selenium
sulfide B2 [2]
Wildlife
Partitioning Factors: Partitioning factors for selenium in wildlife were not found in the literature.
Food Chain Multipliers: Food chain multipliers for selenium in wildlife were not found in the literature.
Aquatic Organisms
Partitioning Factors: Most of the selenium in sediments is bound to humic and fulvic acids.
Microorganisms are closely involved with the selenium cycle and are capable of oxidizing elemental
selenium to selenite [6].
Food Chain Multipliers: The results of several studies showed that selenium can biomagnify within the
aquatic system [7,8].
Toxicity/Bioaccumulation Assessment Profile
Selenium is an element normally found at low levels in aquatic ecosystems. Although the literature values
for acute (600 to 35,000 ug/L) or chronic (30 to 60 ug/L) toxicity via water exposure for fish are a few
orders of magnitude higher than its concentration in surface waters, a dietary uptake at relatively low
667
-------
BIOACCUMULATION SUMMARY SELENIUM
levels (5 to 10 |ig/L) can be toxic to fish. The dietary toxicity was confirmed by Schultz and Hermanutz
[1] and Woock et al. [2]. They demonstrated that fish fed with invertebrates containing high levels of
selenium developed signs of selenosis and some of them died. Female fish transferred selenium to their
progeny, and embryos showed an increased incidence of edema and lordosis. Monitoring concentrations
of selenium in sediment and benthic fauna is essential since selenium can biomagnify sufficiently to cause
acute toxicity to fishes.
Three species, Chlorella vulgaris, Brachionus calyciflorus, and Pimephales promelas were exposed to
selenate for 25 days in a three-trophic level system [10]. Selenium as selenate reduced larval fathead
minnow biomass and impared both the algal and rotifer population growth rates at 108.1 |ig/L. The
results of Dobbs et. al [10] supported the work of earlier researchers [7,8] who found that selenium had
a negative impact on aquatic biota at concentrations above 100 |ig/L.
668
-------
Summary of Biological Effects Tissue Concentrations for Selenium
Species: Concentration, Units in1:
Taxa Sediment Water
Plants
Chlorella vulgaris,
Green algae
Invertebrates
Brachionus
calyciflorus, Rotifer
Daphnia magna,
Cladoceran
Tissue (Sample Type)
7.4 mg/kg
(whole body)5
15 mg/kg
(whole body)5
6.5 mg/kg
(whole body)5
3 mg/kg
(whole body)5
25 mg/kg
(whole body)5
2.94 mg/kg
(whole body)5
10.2 mg/kg
(whole body)5
2.94 mg/kg
(whole body)5
Toxicity:
Effects
Growth,
LOED
Mortality,
ED 100
Growth,
LOED
Growth,
LOED
Mortality,
LOED
Growth,
LOED
Physiological,
LOED
Physiological,
LOED
Ability to Accumulate2: Source:
Log Log
BCF BAF BSAF Reference
[10]
[10]
[10]
[15]
[15]
[16]
[16]
[16]
Comments3
L; reduced growth
L; lethal body
burden
L; reduction in
population biomass
L; increased
biomass over
controls
L; mortality
L; reduced growth
L; decreased whole
body chloride
concentration
L; increased whole
body calcium content
ON
ON
-------
2j Summary of Biological Effects Tissue Concentrations for Selenium
Species: Concentration, Units in1:
Taxa Sediment Water Tissue (Sample Type)
6.34 mg/kg
(whole body)5
10.2 mg/kg
(whole body)5
6.34 mg/kg
(whole body)5
6.34 mg/kg
(whole body)5
102 mg/kg
(whole body)5
4.22 mg/kg
(whole body)5
0.26 mg/kg
(whole body)5
10.2 mg/kg
(whole body)5
6.34 mg/kg
(whole body)5
2.94 mg/kg
(whole body)5
Toxicity:
Effects
Reproduction,
LOED
Growth, NA
Growth, NA
Physiological,
NA
Reproduction,
NA
Growth,
NOED
Growth,
NOED
Mortality,
NOED
Mortality,
NOED
Mortality,
NOED
Ability to Accumulate2: Source:
Log Log
BCF BAF BSAF Reference
[16]
[16]
[16]
[16]
[16]
[16]
[16]
[16]
[16]
[16]
Comments3
L; delayed time to
first brood,
decreased intrinsic
rate of natural
increase
L; reduced growth
L; reduced growth
L; increased whole
body calcium content
L; delayed time to
first brood,
decreased intrinsic
rate of natural
increase
L; no effect on
growth
L; no effect on
growth
L; no effect on
mortality
L; no effect on
mortality
L; no effect on
mortality
-------
Summary of Biological Effects Tissue Concentrations for Selenium
Species: Concentration, Units in1:
Taxa Sediment Water
Chironomus decorus,
Midge
Tissue (Sample Type)
4.22 mg/kg
(whole body)5
0.26 mg/kg
(whole body)5
4.22 mg/kg
(whole body)5
0.26 mg/kg
(whole body)5
2.94 mg/kg
(whole body)5
4.22 mg/kg
(whole body)5
0.26 mg/kg
(whole body)5
2 mg/kg
(whole body)5
12.6 mg/kg
(whole body)5
17 mg/kg
(whole body)5
0.51 mg/kg
(whole body)5
Toxicity:
Effects
Mortality,
NOED
Mortality,
NOED
Physiological,
NOED
Physiological,
NOED
Reproduction,
NOED
Reproduction,
NOED
Reproduction,
NOED
Growth,
LOED
Mortality,
ED50
Mortality,
ED50
Growth,
LOED
Ability to Accumulate2: Source:
Log Log
BCF BAF BSAF Reference
[16]
[16]
[16]
[16]
[16]
[16]
[16]
[12]
[19]
[19]
[20]
Comments3
L; no effect on
mortality
L; no effect on
mortality
L; no effect on
whole body ions
L; no effect on
whole body ions
L; no effect on
reproduction
L; no effect on
reproduction
L; no effect on
reproduction
L; reduced growth,
exp_conc = <1.0
L; lethal to 50% of
animals in 48 hours
L; lethal to 50% of
animals in 48 hours
L; reduction in
growth
ON
-J
-------
ON
-J
K>
Summary of Biological Effects Tissue Concentrations for Selenium
Species:
Taxa
Fishes
Oncorhynchus
tshawytscha,
Chinook salmon
Concentration, Units in1:
Sediment Water Tissue (Sample Type)
0.68 mg/kg
(whole body)5
0.66 mg/kg
(whole body)5
2.88 mg/kg
(whole body)5
2.01 mg/kg
(whole body)5
2. 16 mg/kg
(whole body)5
1 .6 mg/kg
(whole body)5
4.64 mg/kg
(whole body)5
Toxicity:
Effects
Growth,
LOED
Growth,
LOED
Growth,
LOED
Growth,
LOED
Growth,
LOED
Growth,
LOED
Growth,
LOED
Ability to Accumulate2: Source:
Log Log
BCF BAF BSAF Reference
[5]
[5]
[5]
[5]
[5]
[5]
[5]
Comments3
L; diet exposure,
reduced weight and
length gain in 30
days
L; diet exposure,
reduced weight and
length gain in 60
days
L; diet exposure,
reduced length after
120 days
L; diet exposure,
reduced weight and
length gain in 60
days
L; diet exposure,
reduced weight and
length gain in 60
days
L; diet exposure,
reduced weight gain
after 120 days
L; diet exposure,
reduced weight and
length gain in 120
days in salt water
-------
Summary of Biological Effects Tissue Concentrations for Selenium
Species: Concentration, Units in1:
Taxa Sediment Water Tissue (Sample Type)
5.88 mg/kg
(whole body)5
1.3 mg/kg
(whole body)5
2.08 mg/kg
(whole body)5
0.52 mg/kg
(whole body)5
4.68 mg/kg
(whole body)5
1.08 mg/kg
(whole body)5
1.02 mg/kg
(whole body)5
1 .06 mg/kg
(whole body)5
Toxicity:
Effects
Mortality,
LOED
Mortality,
LOED
Mortality,
LOED
Mortality,
LOED
Mortality,
LOED
Mortality,
LOED
Growth,
NOED
Growth,
NOED
Ability to Accumulate2: Source:
Log Log
BCF BAF BSAF Reference
[5]
[5]
[5]
[5]
[5]
[5]
[5]
[5]
Comments3
L; diet exposure,
reduced survival in
60 days
L; diet exposure,
reduced survival in
90 days
L; diet exposure, no
effect on survival in
60 days
L; diet exposure, no
effect on survival in
90 days
L; diet exposure,
reduced survival in
60 days
L; diet exposure,
reduced survival in
90 days
L; diet exposure, no
effect on weight or
length gain in 30
days
L; diet exposure, no
effect on weight or
length gain in 60
days
ON
-J
-------
ON
-J
Summary of Biological Effects Tissue Concentrations for Selenium
Species: Concentration, Units in1:
Taxa Sediment Water Tissue (Sample Type)
0.54 mg/kg
(whole body)5
1.6 mg/kg
(whole body)5
1.08 mg/kg
(whole body)5
0.72 mg/kg
(whole body)5
2.52 mg/kg
(whole body)5
2.66 mg/kg
(whole body)5
0.8 mg/kg
(whole body)5
5.76 mg/kg
(whole body)5
Toxicity:
Effects
Growth,
NOED
Growth,
NOED
Growth,
NOED
Growth,
NOED
Growth,
NOED
Mortality,
NOED
Mortality,
NOED
Mortality,
NOED
Ability to Accumulate2: Source:
Log Log
BCF BAF BSAF Reference
[5]
[5]
[5]
[5]
[5]
[5]
[5]
[5]
Comments3
L; diet exposure, no
effect on weight or
length gain in 90
days
L; diet exposure, no
effect on length after
120 days
L; diet exposure, no
effect on weight or
length gain in 90
days
L; diet exposure, no
effect on weight gain
after 120 days
L; diet exposure, no
effect on lenght and
weight gain in salt
water
L; diet exposure, no
effect on survival in
60 days
L; diet exposure, no
effect on survival in
90 days
L; diet exposure, no
effect on survival in
120 days
-------
Summary of Biological Effects Tissue Concentrations for Selenium
Species:
Taxa
Pimephales
promelas,
Fathead minnow
Lepomis
macrochirus,
Bluegill
Concentration, Units in1:
Sediment Water Tissue (Sample Type)
4.64 mg/kg
(whole body)5
12.2 mg/kg
(whole body)5
10.3 mg/kg
(whole body)5
12.2 mg/kg
(whole body)5
15.2 mg/kg
(whole body)5
17.8 mg/kg
(whole body)5
2.4 mg/kg
(whole body)5
15.8 mg/kg (liver)5
2.8 mg/kg
(skeletal muscle)5
6.3 mg/kg (testis)5
Toxicity:
Effects
Mortality,
NOED
Growth,
LOED
Growth,
NOED
Mortality,
NOED
Growth,
LOED
Mortality,
LOED
Mortality,
NOED
Mortality,
LOED
Mortality,
LOED
Mortality,
LOED
Ability to Accumulate2: Source:
Log Log
BCF BAF BSAF Reference
[5]
[16]
[14]
[14]
[10]
[10]
[13]
[7]
[7]
[7]
Comments3
L; diet exposure, no
effect on survival in
120 days
L; reduction in size
and growth of larvae
L; no effect on larval
growth
L; no effect on
mortality
L; reduced growth
of larvae
L; mortality, loss of
weight
L; no effect on
mortality
L
L
L
ON
-J
-------
2j Summary of Biological Effects Tissue Concentrations for Selenium
Species: Concentration, Units in1:
Taxa Sediment Water Tissue (Sample Type)
4.6 mg/kg
(whole body)5
4.6 mg/kg
(whole body)5
4.6 mg/kg
(whole body)5
0.4 mg/kg (brain)5
8.3 mg/kg (gill)5
1 .8 mg/kg (gonad)5
13.7 mg/kg (heart)5
2.2 mg/kg (intestine)5
102 mg/kg (kidney)5
1 1 .4 mg/kg (liver)5
2.4 mg/kg (plasma)5
Toxicity:
Effects
Mortality,
LOED
Growth, NA
Reproduction,
NA
Mortality,
NOED
Mortality,
NOED
Mortality,
NOED
Mortality,
NOED
Mortality,
NOED
Mortality,
NOED
Mortality,
NOED
Mortality,
NOED
Ability to Accumulate2: Source:
Log Log
BCF BAF BSAF Reference
[7]
[7]
[7]
[17]
[17]
[17]
[17]
[17]
[17]
[17]
[17]
Comments3
L
L
L; measurable but
not statistically
significant reduced
survival of embryos
and larvae
L; no effect on
survivorship
L; no effect on
survivorship
L; no effect on
survivorship
L; no effect on
survivorship
L; no effect on
survivorship
L; no effect on
survivorship
L; no effect on
survivorship
L; no effect on
survivorship
-------
Summary of Biological Effects Tissue Concentrations for Selenium
Species: Concentration, Units in1:
Taxa Sediment Water Tissue (Sample Type)
7.2 mg/kg
(red blood cells)5
17.7 mg/kg (spleen)5
1 mg/kg (stomach)5
2.6 mg/kg
(white muscle)5
4.3 mg/kg
(whole body)5
1 .6 mg/kg
(whole body)5
1 .6 mg/kg
(whole body)5
1 .6 mg/kg
(whole body)5
1 .6 mg/kg
(whole body)5
Toxicity:
Effects
Mortality,
NOED
Mortality,
NOED
Mortality,
NOED
Mortality,
NOED
Mortality,
NOED
Cellular,
LOED
Mortality,
LOED
Physiological,
LOED
Behavior,
NOED
Ability to Accumulate2: Source:
Log Log
BCF BAF BSAF Reference
[17]
[17]
[17]
[17]
[17]
[18]
[18]
[18]
[18]
Comments3
L; no effect on
survivorship
L; no effect on
survivorship
L; no effect on
survivorship
L; no effect on
survivorship
L; no effect on
survivorship
L; structural changes
in gill tissue
L; 35% reduction in
survival after 180
days
L; increased
respiratory demands,
lipid depletion
L; no effect on
feeding behavior
ON
-J
-J
-------
ON
-J
oo
Species:
Taxa
Lepomis
macrochirus,
Bluegill
Summary of Biological Effects Tissue Concentrations for Selenium
Concentration, Units in1:
Sediment Water
0.16 mg/L
0.33 mg/L
0.64 mg/L
1.12 mg/L
2.80 mg/L
0.16 mg/L
0.33 mg/L
0.64 mg/L
1.12 mg/L
2.80 mg/L
Tissue (Sample Type)
Day 30:
3.0 |ig/g
3.5 ng/g
4.0 |ig/g
7.0 ng/g
14.3 |ig/g
Day 60:
2.8 ng/g
4.1 |ig/g
5.0 ng/g
9.7 |ig/g
Toxicity: Ability to Accumulate2: Source:
Log Log
Effects BCF BAF BSAF Reference Comments3
Mortality: [6] L
10%
20%
40%
55%
88%
10%
22%
52%
70%
98%
Day 258:
10 |ig/L 9.3 |ig/g (liver)
4.4 |ig/g (ovaries)
3.0 |ig/g (testes)
1.8 |ig/g (muscles)
Day 356:
7.3 |ig/g (liver)
4.5 |ig/g (ovaries)
7.6 |ig/g (testes)
4.2 |ig/g (muscles)
[7]
L
-------
Summary of Biological Effects Tissue Concentrations for Selenium
ON
-J
Species:
Taxa
Lepomis
macrochirus,
Bluegill
Micropterus
salmoides,
Largemouth bass
Concentration, Units in1:
Sediment Water Tissue (Sample Type)
8.4 (j.g/L water,
0.8 |ig/g diet:
1 M-g/g
10.5 |ig/L water,
4.6 |ig/g diet:
10.5 |ig/L water,
8.4 |ig/g diet:
10.1 |ig/L water,
16.8 |ig/gdiet:
10 |ig/g
1 1 .0 |ig/L water,
33.3 |ig/g diet:
19 |ig/g
0.4 mg/kg (brain)5
6.2 mg/kg (gill)5
1 .7 mg/kg (gonad)5
12 mg/kg (heart)5
2.1 mg/kg (intestine)5
Toxicity:
Effects
Mortality,
NOED
Mortality,
NOED
Mortality,
NOED
Mortality,
NOED
Mortality,
NOED
Ability to Accumulate2: Source:
Log Log
BCF BAF BSAF Reference Comments3
[8] L
[17] L; no effect on
survivorship
[17] L; no effect on
survivorship
[17] L; no effect on
survivorship
[17] L; no effect on
survivorship
[17] L; no effect on
survivorship
-------
io Summary of Biological Effects Tissue Concentrations for Selenium
Species: Concentration, Units in1:
Taxa Sediment Water Tissue (Sample Type)
8.6 mg/kg (kidney)5
10 mg/kg (liver)5
3.2 mg/kg (plasma)5
8 mg/kg
(red blood cells)5
16.4 mg/kg (spleen)5
1 .3 mg/kg (stomach)5
1 .4 mg/kg
(white muscle)5
3 mg/kg
(whole body)5
Toxicity:
Effects
Mortality,
NOED
Mortality,
NOED
Mortality,
NOED
Mortality,
NOED
Mortality,
NOED
Mortality,
NOED
Mortality,
NOED
Mortality,
NOED
Ability to Accumulate2: Source:
Log Log
BCF BAF BSAF Reference
[17]
[17]
[17]
[17]
[17]
[17]
[17]
[17]
Comments3
L; no effect on
survivorship
L; no effect on
survivorship
L; no effect on
survivorship
L; no effect on
survivorship
L; no effect on
survivorship
L; no effect on
survivorship
L; no effect on
survivorship
L; no effect on
survivorship
-------
Summary of Biological Effects Tissue Concentrations for Selenium
Species:
Taxa
Concentration, Units in1: Toxicity:
Sediment Water Tissue (Sample Type) Effects
Ability to Accumulate2: Source:
BSAF Reference
Log
BCF
Log
BAF
Comments3
Wildlife
Anas
platyrhynochos,
Mallard
0 ppm diet:
2.5 ppm (liver)
15 ppm diet:
2.0 ppm (liver)
0/100 ppm diet:
35.0 ppm (liver)
15/100 ppm diet:
53.0 ppm (liver)
0 ppm diet:
0.88 ppm (liver)
females 0.69 ppm,
males 1.1 ppm,
3.5 ppm diet:
3.7 ppm (liver)
females 3.2 ppm,
males 4.3 ppm,
7.0 ppm diet:
6.2 ppm (liver)
females 5.1 ppm,
males 7.3 ppm
[9]
L
[11]
L
1 Concentration units based on wet weight unless otherwise noted.
2 BCF = bioconcentration factor, BAF = bioaccumulation factor, BSAF = biota-sediment accumulation factor.
3 L = laboratory study, spiked sediment, single chemical; F = field study, multiple chemical exposure; other unusual study conditions or observations noted.
4 BDL = below detection limit.
5 This entry was excerpted directly from the Environmental Residue-Effects Database (ERED, www.wes.army.mil/el/ered, U.S. Army Corps of Engineers and U.S.
Environmental Protection Agency). The original publication was not reviewed, and the reader is strongly urged to consult the publication to confirm the information
presented here.
ON
00
-------
BIOACCUMULATION SUMMARY SELENIUM
References
1. Weast handbook of chemistry and physics, 68th edition, 1987-1988, B-125. (Cited in: USEPA.
1995. Hazardous Substances Data Bank (HSDB). National Library of Medicine online (TOXNET).
U.S. Environmental Protection Agency, Office of Health and Environmental Assessment,
Environmental Criteria and Assessment Office, Cincinnati, OH. September.)
2. USEPA. 1995. Integrated Risk Information System (IRIS). National Library of Medicine online
(TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental
Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. September.
3. Schultz, R., and R. Hermanutz. 1990. Transfer of toxic concentrations of selenium from parent to
progeny in the fathead minnow (Pimephales promelas). Bull. Environ. Contain. Toxicol. 45:568-
573.
4. Woock, S.E., W.R. Garrett, W.E. Partin, and W.T. Bryson. 1987. Decreased survival and
teratogenesis during laboratory selenium exposures to bluegills, Lepomis macrochirus. Bull.
Environ. Contam. Toxicol. 39:998-1005.
5. Hamilton, S.J., K.J. Buhl, N.L. Faerber, R.H. Wiedmeyer, and F.A. Bullard. 1990. Toxicity of
organic selenium in the diet to chinook salmon. Environ. Toxicol. Chem. 9:347-358.
6. Cleveland, L., E.E. Little, D.R. Buckler, and R.H. Wiedmeyer. 1993. Toxicity and bioaccumulation
of waterborne and dietary selenium in juvenile bluegill (Lepomis macrochirus). Aquat. Toxicol.
27:265-280.
7. Hermanutz, R.O., K.N. Allen, T.H. Roush, and S.F. Hedtke. 1992. Effects of elevated selenium
concentrations on bluegills (Lepomis macrochirus) in outdoor experimental streams. Environ.
Toxicol. Chem. 11:217-224.
8. Coyle, J.J., D.R. Buckler, C.G. Ingersoll, J.F. Fairchild, and T.W. May. 1993. Effects of dietary
selenium on the reproductive success of bluegills (Lepomis macrochirus). Environ. Toxicol. Chem.
12:551-565.
9. Heinz, G.H. 1993. Re-exposure of mallards to selenium after chronic exposure. Environ. Toxicol.
Chem. 12:1691-1694.
10. Dobbs, M.G., D.S. Cherry, and J. Cairns, Jr. 1996. Toxicity and bioaccumulation of selenium to a
three-trophic level food chain. Environ. Toxicol. Chem. 15:340-347.
11. Stanley, T.R., Jr., G.J. Smith, D.J. Hoffman, G.H. Heinz, and R. Rosscoe. 1996. Effects of boron
and selenium on mallard reproduction and duckling growth and survival. Environ. Toxicol. Chem.
15:1124-1132.
12. Alaimo, J., R.S. Ogle, and A.W. Knight. 1994. Selenium uptake by larval Chironomus decorus from
a Ruppia maritima-based benthic/detrital substrate. Arch. Environ. Contam. Toxicol. 27:441-448.
682
-------
BIOACCUMULATION SUMMARY SELENIUM
13. Barrows, M.E., S.R. Petrocelli, K.J. Macek and JJ. Carroll. 1980. Bioconcentration and elimination
of selected water pollutants by bluegill sunfish (Lepomis macrochirus). in ed. Haque, R. Dynamics,
exposure and hazard assessment of toxic chemicals, pp. 379-392
14. Bennett, W.N., A.S. Brooks, and M.E. Boraas. 1986. Selenium uptake and transfer in an aquatic
food chain and its effects on fathead minnow larvae. Arch. Environ. Contain. Toxicol. 15:513-517.
15. Besser, J.M., TJ. Canfield, and T.W. Lapoint. 1993. Bioaccumulation of organic and inorganic
selenium in laboratory food chain. Environ. Toxicol. Chem. 12:57-72.
16. Ingersoll, C.G., FJ. Dwyer, and T.W. May. 1990. Toxicity of inorganic and organic selenium to
Daphnia magna (Cladocera) and Chironomus riparius (Diptera). Environ. Toxicol. Chem. 9:1171-
1181.
17. Lemly, A.D. 1982. Response of juvenile centrarchids to sublethal concentrations of waterborne
selenium. I. Uptake, tissue distribution, and retention. Aquat. Toxicol. 2:235-252.
18. Lemly, A.D. 1993. Metabolic stress during winter increases the toxicity of selenium to fish. Aquat.
Toxicol. 27:133-158.
19. Maier, K.J., and A.W. Knight., 1993. Comparative and acute toxicity and bioconcentration of
selenium by the midge Chironomus decorus exposed to selenate, selenite, and seleno-dl-methionine.
Arch. Environ. Contain. Toxicol. 25:365-370.
20. Malchow, D.E., A.W. Knight and K.J. Maier. 1995. Bioaccumulation and toxicity of selenium in
Chironomus decorus larvae fed a diet of seleniferous Selenastrum capricornutum. Arch. Environ.
Contam. Toxicol. 29:104-109.
683
-------
684
-------
BIOACCUMULATION SUMMARY SILVER
Chemical Category: METAL
Chemical Name (Common Synonyms): SILVER CASRN: 7440-22-4
Chemical Characteristics
Solubility in Water: Insoluble [1] Half-Life: Not applicable, stable [1]
LogKow: - LogKoc: -
Human Health
Oral RfD: 5 x 10"3 mg/kg/day [2] Confidence: Low, uncertainty factor = 3
Critical Effect: Argyria—permanent, but benign, bluish-gray discoloration of the skin
Oral Slope Factor: No data [2] Carcinogenic Classification: D [2]
Wildlife
Partitioning Factors: Partitioning factors for silver in wildlife were not found in the literature.
Food Chain Multipliers: Food chain mulitpliers for silver in wildlife were not found in the literature.
Aquatic Organisms
Partitioning Factors: Silver in the water column can partition to dissolved and particulate organic
carbon. Important issues related to water column concentrations of silver are water hardness (i.e., calcium
concentration), pH, and metal speciation, since the monovalent form of silver is believed to be responsible
for observed biological effects. In addition, silver is known to form a variety of relatively insoluble (i.e.,
nonbioavailable) complexes, including silver sulfides formed with acid volatile sulfides, that can be
important in controlling the toxicity and bioaccumulation of silver in sediments [8 and 9].
Food Chain Multipliers: Little evidence exists to support the general occurrence of biomagnification
of silver within marine or freshwater food webs [3]. Silver uptake by aquatic organisms appears to be
almost entirely from the dissolved form. When silver was bound to algal cell membranes, it could not
be dislodged by either mechanical disruption or leaching at low pH; therefore, silver bound to algal cells
is likely unassimilable by higher organisms [3].
685
-------
BIOACCUMULATION SUMMARY SILVER
Toxicity/Bioaccumulation Assessment Profile
Silver does not appear to be a highly mobile element under typical conditions in most aquatic habitats.
Tissue residue-toxicity relationships can also vary because organisms may sequester metal in different
forms that might be analytically measurable as tissue residue, but might actually be stored in unavailable
forms within the organism as a form of detoxification [4]. Whole-body residues also might not be
indicative of effects concentrations at the organ level because concentrations in target organs, such as the
kidneys and liver, can be 20 times greater than whole body residues [5]. The application of "clean"
chemical analytical and sample preparation techniques is also critical in the measurement of metal tissue
residues [6]. Exposure of rainbow trout to three different silver salts revealed that silver, introduced as
silver nitrate, was 15,000 and 11,000 times more toxic than silver chloride and silver thiosulfate [11].
However, all three forms of dissolved silver were taken up by rainbow trout and accumulated in the
tissue. Interestingly, extremely high levels of silver were found in livers of fish exposed to silver as silver
chloride and silver thiosulfate. Hogstrand et al. [11] attributed low toxicity to these two forms to
production of metallothionein, a small cysteine-rich, intracellular protein that avidly binds most metals.
686
-------
Summary of Biological Effects Tissue Concentrations for Silver
ON
00
Species:
Taxa
Invertebrates
Busycotypus
canaliculatum,
Channeled whelk
Corbiciila fluminea,
Asiatic clam
Mytilus edulis,
Mussel
Crassostrea
virginica,
Eastern oyster
Concentration, Units in1:
Sediment Water Tissue (Sample Type)
0.1-0.5|ig/L 1.1 |ig/g
1,650 mg/kg
(whole body)4
800 mg/kg
(whole body)4
2,5 10 mg/kg
(whole body)4
1,650 mg/kg
(whole body)4
3.7 mg/kg
(whole body)4
2 |ig/L 2.6 |ig/g
5 |ig/L 6.5 |ig/g
7 \iglL 4.8 |ig/g
Toxicity: Ability to Accumulate2:
Log Log
Effects BCF BAF BSAF
Growth,
LOED
Growth,
NOED
Mortality,
LOED
Mortality,
NOED
Physiological,
LOED
Source:
Reference Comments3
[7] F
[8] L; reduction in
growth
[8] L; no effect on
growth
[8] L; reduced survival
[8] L; no effect on
survival
[12] L; significantly
increased oxygen
consumption at
lowest test
concentration at 25
ppt salinity, number
of replicates is 12 to
20
[9] L
-------
ON
00
oo
Summary of Biological Effects Tissue Concentrations for Silver
Species:
Taxa
Crassostrea
virginica, Oyster
Mercenaria
mercenaria,
Quahog clam
Mya arenaria, Soft
shell clam
Concentration, Units in1:
Sediment Water Tissue (Sample Type)
38 mg/kg (gill)4
12.4 mg/kg (whole
body)4
7.6 mg/kg (gill)4
0.8 mg/kg
(whole body)4
10.4 mg/kg
(whole body)4
Toxicity: Ability to Accumulate2:
Log Log
Effects BCF BAF BSAF
Physiological,
LOED
Physiological,
LOED
Physiological,
LOED
Physiological,
LOED
Physiological,
LOED
Source:
Reference Comments3
[12] L; Significantly
increased oxygen
consumption at
lowest test
Q2] concentration at 25
ppt salinity, number
of replicates is 12 to
20
[12] L; significantly
increased oxygen
consumption at
lowest test
Q2i concentration at 25
ppt salinity, number
of replicates is 12 to
20
[12] L; significantly
increased oxygen
consumption at
lowest test
concentration at 25
ppt salinity, number
of replicates is 12 to
20
-------
Summary of Biological Effects Tissue Concentrations for Silver
Species:
Taxa
Homarus
amencanus,
American lobster
Concentration, Units in1:
Sediment Water Tissue (Sample Type)
0.1-0.5 |ig/L 2.3 |ig/g
Toxicity:
Effects
Ability to Accumulate2:
Log Log
BCF BAF BSAF
Source:
Reference Comments3
[7] F
Fishes
Oncorhyncus mykiss,
Rainbow trout
4.3 |ig/L
7.2
9.3
16 |ig/g (liver),
4|ig/g (gills)
13 |ig/g (liver)
4 |ig/g (gills)
20 |ig/g (liver)
4.8 |ig/g (gills)
[11]
L
Salmo trutta,
Brown trout
1343Bq/ginfood, Day
7: 17.6 Bq/g
269 Bq/g in food,
Day 13: 18.5 Bq/g
296 Bq/g in food,
Day 20: 21.7 Bq/g
Salmo trutta,
Brown trout
289 Bq/g in food,
Day 26: 26.6 Bq/g
273 Bq/g in food,
Day 33: 27.4 Bq/g
[10]
L
ON
oo
-------
ON
VO
O
Summary of Biological Effects Tissue Concentrations for Silver
Species:
Taxa
Concentration, Units in1: Toxicity:
Sediment Water Tissue (Sample Type) Effects
Ability to Accumulate2:
BSAF
Log
BCF
Log
BAF
Source:
Reference Comments3
623.8 Bq/g (liver)
24.9 Bq/g (kidneys)
25.5 Bq/g (viscera)
5.5 Bq/g (gills)
23.9 Bq/g (digestive
tract)
3.2 Bq/g (muscle)
4.4 Bq/g (bone)
2.9 Bq/g (head)
7.2 Bq/g (skin)
[10]
1 Concentration units based on wet weight unless otherwise noted.
2 BCF = bioconcentration factor, BAF = bioaccumulation factor, BSAF = biota-sediment accumulation factor.
3 L = laboratory study, spiked sediment, single chemical; F = field study, multiple chemical exposure; other unusual study conditions or observations noted.
4 This entry was excerpted directly from the Environmental Residue-Effects Database (ERED, www.wes.army.mil/el/ered, U.S. Army Corps of Engineers and U.S.
Environmental Protection Agency). The original publication was not reviewed, and the reader is strongly urged to consult the publication to confirm the information
presented here.
-------
BIOACCUMULATION SUMMARY SILVER
References
1. Weast handbook of chemistry and physics, 68th edition, 1987-1988, B-127. (Cited in: USEPA.
1995. Hazardous Substances Data Bank (HSDB). National Library of Medicine online
(TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental
Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. September.)
2. USEPA. 1995. Integrated Risk Information System (IRIS). National Library of Medicine online
(TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental
Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. September.
3. Connell, D.B., J.G. Sanders, G.F. Riedel, and G.R. Abbe. 1991. Pathways of silver uptake and
trophic transfer in estuarine organisms. Environ. Sci. Technol. 25:921-923.
4. Klerks, P.L., and P.R. Bartholomew. 1991. Cadmium accumulation and detoxification in a Cd-
resistant population of the oligochaete Limnodrilus hojfmeisteri. Aquat. Toxicol 19:97-112.
5. McKinney, J. 1993. Metals bioavailability and disposition kinetics research needs workshop. July
18-19, 1990. Toxicol Environ. Chem. 38:1-71.
6. Schmitt, C.J., and S.E. Finger. 1987. The effects of sample preparation on measured
concentrations of eight elements in edible tissues of fish from streams contaminated by lead
mining. Arch. Environ. Contain. Toxicol. 16:185-207.
7. Greig, R., and JJ. Pereira. 1993. Metal concentrations in American lobster and channeled whelk
from two dredge spoil dump sites in Long Island Sound. Bull. Environ. Contam. Toxicol. 50:626-
632.
8. Diamond, J.M., D.G. Mackler, M. Collins, and D. Gruber. 1990. Derivation of a freshwater silver
criteria for the New River, Virginia using representative species. Environ. Toxicol. Chem. 9:1425-
1434.
9. Sanders, J.G., G.R. Abbe, and G.F. Riedel. 1990. Silver uptake and subsequent effects on growth
and species composition in an estuarine community. Sci. Total Environ. 97/98:761-769.
10. Gamier, J. and J.P. Baudin. 1990. Retention of ingested 110m Ag by a freshwater fish Salmo
truttaL. Water Air Soil Pollut. 50:409-421.
11. Hogstrand, C., F. Galvez, and C.M. Wood. 1996. Toxicity, silver accumulation and
metallothionein induction in freshwater rainbow trout during exposure to different silver salts.
Environ. Toxicol. Chem. 15:1102-1108.
12. Thurberg, P.P., A. Calabrese, and M.A. Dawson. 1974. Effects of silver on oxygen consumption
of bivalves at various salinities. In Pollution and physiology of marine organisms, ed. FJ.
Vernberg et al. Academic Press, New York, NY.
691
-------
692
-------
BIOACCUMULATION SUMMARY TRIBUTYLTIN
Chemical Category: METAL
Chemical Name (Common Synonyms): TRIBUTYLTIN CASRN: 688-73-3
Tributyltin compounds, such as those used in antifouling paints, consist of a tin (Sn) atom covalently
bonded to three butyl (C4H9-) moieties and an associated anion (X). A number of organotin compounds
have been used as ingredients in paints, pesticides, and preservatives, including trialkyltins (e.g.,
bis(tributyltin) oxide (TBTO), bis(tributyltin) sulfide, tributyltin acetate, tributyltin fluoride, tributyltin
naphthenate, and tributyltin resinate), triaryltins (e.g., triphenyltin hydroxide), dialkyltins (e.g., (TBTF1)
dibutyltin dilaurte, dibutyltin isooctylmercaptonacetate, and dibutyltin maleate), and monooctyltins
(e.g., monooctyltin tris isooctyl mercaptoacetate). In aquatic systems, the distribution of TBT species
is dependent on pH and salinity. In seawater, the hydrated TBT cation, tributyltin chloride, (TBTC1)
bis (tributyltin carbonate), and tributyltin hydroxide are in equilibrium. It is widely accepted that
tributyltin toxicity is ascribed to the cation (TBT++) and not to which anion is associated with the
biocide in the neutral compound. Researchers have been inconsistent and at times ambiguous in
reporting concentrations of organotins and in their use of units in the literature [1]. The following
discussion is based on the tributyltin cation (TBT++) and not the various species. The table summarizing
biological effects contains data for the tributyltin cation, as well as for tributyltin chloride, tributyltin
fluoride, tributyltin oxide, and tin. The table identifies the chemical species measured, if the
information was available in the original document reviewed.
Chemical Characteristics
Solubility in Water: <1 to >200 mg/L [2] Half-Life: Sediments: >20 months [3]
Log Kow: 2.2 - 4.4 [2] Log Koc: 4.36 - 5.02 [4]
Human Health
Oral RfD: 3 x 10"5 mg/kg/day [5] Confidence: Low, uncertainty factor = 1000
Critical Effect: Immunotoxicity in rats
Oral Slope Factor (Reference): No data [5] Carcinogenic Classification: No data [5]
Wildlife
Partitioning Factors: Laboratory studies have demonstrated accumulation of TBT in mice and rats,
and butyltin residues were detected recently in the blubber of a number of marine mammal species [2].
However, accurate determination of partitioning factors for TBT in wildlife is difficult because this
compound is rapidly metabolized once it has been taken up by vertebrates. No partitioning factors were
identified for wildlife in the studies reviewed.
Food Chain Multipliers: Biomagnification of butyltins in aquatic systems does not occur, or if it does,
only to a minor extent [2].
693
-------
BIOACCUMULATION SUMMARY TRIBUTYLTIN
Aquatic Organisms
Partitioning Factors: Uptake of TBT from sediment to tissues is a complex, non-linear process, and
may be better approximated by a power function [6]. Uptake and elimination rates vary considerably
by species [4] and the bioavailability of sediment-associated TBT is controlled by a wide range of
parameters (eg., chemical speciation, pH, organic content), further moderating uptake rates [2,6].
Attempts to derive BSAFs with wide-ranging utility are also hampered by the fact that tissues burdens
in aquatic animals have traditionally been correlated with TBT concentrations in the water column,
rather than sediment concentrations.
Once TBT has been incorporated, it tends to partition into multiple tissue compartments. Log BCFs
ranged from 2.70 in carp muscle [7] to 2.32-2.74 in whole rainbow trout [8] and 3.26 in muscle tissue,
3.66 in viscera, and 3.41 in whole body residues of sheepshead minnow [9]. Tsuda et al. [7] found that
BCFs for carp were highest in kidney, followed by gall bladder, liver, and muscle, in that order. In
rainbow trout, BCFs for TBT were highest for peritoneal fat, followed by kidney, liver, and gall
bladder. As with wildlife, TBT can be rapidly metabolized by many aquatic organisms. The rapid
metabolism of TBT possibly explains why apparent uptake rates in bivalves, whose enzyme systems
metabolize butyltins at a much slower rate, are typically higher than in other organisms [2]. Seasonal
variability has been reported for the eastern oyster Crassostrea gigas. The lowest proportion of TBT
in tissues was found in the summer months and associated with either higher biodegradation rates of
TBT in the water column or higher biotransformation rates in oyster tissues [10]. In the studies
reviewed, Log BCF's for marine bivalves range from 4.09 to 5.10 The highest log BCF identified was
for the zebra mussel (Dreissena polymorpha) at 5.95 Reported log BCFs for polychaete worms are
approximately 3.85.
Food Chain Multipliers: Biomagnification of TBT does not appear to be significant in aquatic
systems. Although TBT is accumulated or concentrated to a very high degree in lower trophic level
organisms, dietary uptake in higher trophic level organisms appears to be counteracted by
biotransformation in the liver [2].
Toxicity/Bioaccumulation Assessment Profile
Tri-substituted organotins (such as tributyltin) are most commonly used as pesticides in commercial and
agricultural applications. Tributyltin (TBT) is widely used as a preservative for timber and wood,
textiles, paper, and leather [2]. The use of marine paints containing TBT compounds as toxic additives
has been found to be very effective in eliminating fouling problems [11]. TBT-based antifouling paints
typically contain up to 20 percent by weight of a suitable tributyl or triphenyltin toxicant which is
slowly leached into the surrounding water in the immediate vicinity of the hull. The active lifetime of
these paints is usually 1-2 years, after which time the vessel must be repainted [12].
The toxicity of organotins increases with progressive introduction of organic groups at the tin atom [2].
Thus, the high toxicity of TBT led to its use as a fungicide, bactericide, and algicide. TBT-containing
antifouling paints were recognized as up to 100 times more effective than copper-based antifouling
paints [10]. In fact, studies have demonstrated that TBT is deleterious at concentrations far lower than
those indicated for other marine pollutants [13]. Consequently TBT has been used in antifouling paints
since the early 1960s and gained widespread application on all types of vessels in the 1970s and 1980s
[2]. Shell thickening in oysters (Crassostrea gigas) has been reported in some areas of France since
694
-------
BIOACCUMULATION SUMMARY TRIBUTYLTIN
the outset of its introduction in that country in 1968 [14]. TBT leaching from the ship hulls into the
water appeared to be the major pathway of entry into the aquatic environment [2]. Other sources of
TBT in the aqueous environment include releases of fugitive paint and paint chips from vessel repair
and dry-dock facilities [15]. TBT is likely to partition between suspended particles in the water column
and sediments, although up to 99 percent of the TBT may reside in the sediments. TBT-contaminated
sediments can represent a substantial source of organotin to aquatic receptors [16]. TBT has a
significant lipid solubility and thus a high affinity for bioaccumulation [17]. Some organisms, including
fishes, crustaceans, bivalves, and microorganisms, have the ability to bioconcentrate TBT to
concentrations which are orders of magnitude higher than the exposure concentration [13].
Acute effects of TBT have been observed in the water column at TBT concentrations of 1 ng/L. This
concentration has been associated with reduced reproduction in snails [17]. Histological alterations
were observed in young European minnows exposed to an aqueous TBT concentration of 0.8 ug/L [17].
Reduced growth was noted in long-term exposures of rainbow trout yolk sac fry to 0.2 ug/L TBT,
resulting in an estimated NOEC of 0.04 ug/L [17]. Immunotoxic effects were observed in the guppy
at 0.32 ug/L TBT. In studies of Acartia tonsa, reductions in survival in acute tests were observed at
0.029 ug/L; NOECs and LOECs for survival during chronic tests were 0.024 and 0.017 ug/L,
respectively [18].
As a group, molluscs are among the most sensitive to TBT. Gastropod snails exhibit anatomical
abnormalities referred to as imposex, the superimposition of male characteristics onto a normal female
reproductive system [19]. Growth in oyster spat is inhibited at aqueous concentrations of 0.15 ug/L
and shell thickening has been reported at 0.2 ug/L. Other effects in oysters include abnormal veliger
development, malformation of trocophores, larval anomalies, perturbation in food assimilation, and
high mortality [20]. Some freshwater and marine bivalves are able to tolerate short-term TBT exposure
due to their ability to isolate themselves from the irritating environment by closing their valves.
TBT concentrations in sediments can be from one to several thousand times higher than concentrations
found in the overlying water [21]. Bivalve populations can be completely eliminated when sediment
TBT concentrations exceed 0.8 ug/g [17]. No sediment criteria exist for TBT, and ER-L and ER-M
ranges are unavailable. However, studies indicate that mollusks respond to sediment concentrations
of TBT as low as 10 ng/g, while some copepod crustaceans, echinoderms, polychaetes, tunicates,
phytoplankton, and fish respond to sediment TBT concentrations between 10 and 100 ng/g [21].
695
-------
ON
VO
ON
Summary of Biological Effects Tissue Concentrations for Tributyltin
Species:
Taxa
Invertebrates
Nereis
diversicolor,
Polychaete
Neanthes
arenaceodentata,
Polychaete
Littorina littorea,
Gastropod
mollusk
(Common
winkle)
Concentration, Units in1:
Sediment Water
445 ± 83 68.2 ±
ng/g dw 40.6
(n=5) ng/L3
(n=8)
100
ng/L3
50 ng/L3
500
ng/L4
445±83 ng 68.2±
dw (n = 5) 40.6
ng/L
(n = 8)
Tissue (SampleType)
479 ± 249 ng/g dwf
(pooled, whole body)
(n=5)
6.27|ig/g dw TBT++
(whole body)
<3.0 |ig/g dw TBT++
(whole body)
16.81 |ig/gdwTBT++
(whole body)
l,009±428ng/gdw
(pooled, soft tissue)
(n = 4)
Toxicity: Ability to Accumulate2: Source:
Log Log
Effects BCF BAF BSAF Reference Comments3
3.85 [21] F
Reduced [23] L5
growth and
reproduction
No significant [23] L5
effect on
survival,
growth, or
reproduction
Significant [23] L5
effect on
survival
4.17 [21] F
-------
Summary of Biological Effects Tissue Concentrations for Tributyltin
Species:
Taxa
Littorina littorea,
Periwinkle
Mama
corniiarietis,
Freshwater
gastropod
(Ramshorn snail)
Marisa
cornuarietis,
Freshwater
gastropod
(Ramshorn snail)
Ilyanassa
obsoleta,
Mud snail
Niicella lapillus,
Dog welk
Concentration, Units in1:
Sediment Water Tissue (SampleType)
0.1 mg/kg
TBTC1 (whole body)8
50 ng «800|igSn/gdw
Sn/L4 (soft tissue)
200 ng «1600|igSn/gdw
Sn/L4 (soft tissue)
20 ng/L4 620 ng/g dwf
(soft tissue)
18.7 o":
ng/L4 l,475ngSn/gdw
Toxicity: Ability to Accumulate2: Source:
Log Log
Effects BCF BAF BSAF Reference
Reproduction, [46]
NOED
YDS index 4.234 [32]
constant at
stage 1
YDS index 4.964 [32]
increased
from stage 1
to stage 3
100% [35]
occurrence of
imposex in
females
Imposex d": [36]
77,900
Comments3
L andF
combined;
imposex -
intersex response
(prostate length,
isi); estimated
wet weight
L; equilibrium
reached after 3
to 4 months;
females
accumulate more
than males
L; equilibrium
reached after 3
to 4 months;
females
accumulate more
than males
F
F
ON
VO
-J
l,864ngSn/gdw
(soft tissue)
?:
99,700
-------
Summary of Biological Effects Tissue Concentrations for Tributyltin
Species:
Taxa
Concentration, Units in1:
Toxicity:
Sediment Water Tissue (SampleType) Effects
Ability to Accumulate2:
Log Log
Source:
BCF
BAF
BSAF Reference Comments3
107
ng/L4
0.25 ng
Sn/L4
1-2 ng
Sn/L4
3-5 ng
Sn/L4
20 ng
Sn/L4
d":
2,436 ng Sn/g dw
3,498 ng Sn/g dw
(soft tissue)
0.1 mg/kg
(whole body)
0.1 |ig Sn/g dw
(soft tissue)
0.025 |ig Sn/g dw
(soft tissue)
0.238 - 0.239 |ig Sn/g
dw (soft tissue)
0.602 - 0.569 |ig Sn/g
dw (soft tissue)
1. 464-1. 696 |ig Sn/g
dw (soft tissue)
Sterilization d":
(?) 22,800
Induction of
imposex
Normal
breeding
occurs
Stage 1
(infolding of
pallian cavity
floor)
Imposex
Relative Penis
Size (RPS) =
48%; Vas
Deferens
Sequence
(YDS) =
Stage 4.4
(breeding not
impaired)
RPS = 96.6%;
YDS = Stage
5.1 (breeding
impaired)
RPS = 109%;
YDS = Stage
5.0 (breeding
impaired)
[36]
32,700
[37]
[38]
[38]
L
L
L
[38]
L
[38]
[38]
-------
Summary of Biological Effects Tissue Concentrations for Tributyltin
Species:
Taxa
Niicella lapillus,
Dog welk
Niicella lapillus,
Dog whelk
Concentration, Units in1:
Sediment Water Tissue (SampleType)
100 ng 2.520-3.164|igSn/g
Sn/L4 dw (soft tissue)
<0.5 ng 0.039 - 0.092 |ig Sn/g
Sn/L4 dw (soft tissue)
2mg/kg TBTionand
DBT ion
(whole body)8
1.97mg/kg TBTion
and DBT ion
(whole body)8
Toxicity: Ability to Accumulate2: Source:
Log Log
Effects BCF BAF BSAF Reference
RPS = 90.4%; [38]
YDS = Stage
5.0 (breeding
impaired)
RPS = 3.7%; [38]
YDS = Stage
3.2 (breeding
not impaired)
Development, [36]
NA
Development, [36]
NOED
Comments3
L
F
LandF
combined; paint
on shell; female
penis length
increased; body
burden as tin not
TBT or DBT
LandF
combined; paint
on shell; no
effect in male
penis length;
body burden as
tin not TBT or
DBT
-------
o
o
Summary of Biological Effects Tissue Concentrations for Tributyltin
Species:
Taxa
Concentration, Units in1:
Toxicity:
Ability to Accumulate2:
Source:
Sediment Water Tissue (SampleType) Effects
Log
BCF
Log
BAF
BSAF Reference Comments3
0.0413 mg/kg
TBTC1 (whole body)8
Development,
LOED
1.17 mg/kg
TBTC1 (whole body)8
Reproduction,
LOED
0.733 mg/kg
TBTC1 (whole body)8
Reproduction,
LOED
1.82 mg/kg
TBTC1 (whole body)8
Development,
NA
[36] L and F
combined;
relative penis
size significantly
decreased
(female/male
penis length);
body burden as
tin not TBT or
DBT
[36] L and F
combined;
sterility in
females; body
burden as tin not
TBT or DBT
[36] L and F
combined;
sterility in
females; body
burden as tin not
TBT or DBT
[36] L and F
combined; paint
on shell; no
effect in male
penis length;
body burden as
tin not TBT or
DBT
-------
Summary of Biological Effects Tissue Concentrations for Tributyltin
Species:
Taxa
Thais clavigera,
Whelk
Mytilus edulis,
Blue mussel
Concentration, Units in1:
Sediment Water Tissue (SampleType)
1.33 mg/kg
TBTC1 (whole body)8
0.909 mg/kg
TBTC1 (whole body)8
0.0666 mg/kg TBTC1
(whole body)8
0.013 mg/kg
TBTC1 (whole body)8
0.019-0.047^^
(pooled, soft tissue)
Toxicity: Ability to Accumulate2: Source:
Log Log
Effects BCF BAF BSAF Reference
Development, [36]
NA
Development, [36]
NOED
Development, [36]
NOED
Reproduction, [50]
LOED
Reduced [24]
growth
Comments3
L andF
combined; paint
on shell; female
penis length
increased; body
burden as tin not
TBT or DBT
L andF
combined; paint
on shell; no
effect in male
penis length;
body burden as
tin not TBT or
DBT
LandF
combined; no
increase in penis
length; equals
0.5 ug/g
TBT+DBT;
body burden as
tin not TBT or
DBT
L; degradation
products present
F; 82-day
exposure
-------
-J
o
Summary of Biological Effects Tissue Concentrations for Tributyltin
Species: Concentration
Taxa Sediment
0.08 |ig/g
dw
Mytilus edulis, 0.03 |ig/g
Blue mussel dw
0.02 |ig/g
dw
0.10 |ig/g
dw
0.15 |ig/g
dw
0.04 |ig/g
dw
, Units in1:
Water
200
ng/L4
15 ±8
ng/L4
33 ±27
ng/L4
21 ±8
ng/L4
13 ng/L4
22 ±12
ng/L4
17 ±12
ng/L4
Tissue (SampleType)
2.0 |ig/g dwf
(soft tissue)
4 |ig/g dwf
(soft tissue)
1.5mg/kgf
(soft tissue)
2.20mg/kg TBTO
(soft tissue)
l.SM-g/g*
(whole body)
0.64 |ig/g f
(soft tissue)
0.75 |ig/gf
(soft tissue)
0.34 |ig/gf
(soft tissue)
0.16ng/gf
(soft tissue)
0.66 |ig/gf
(soft tissue)
0.44 |ig/gf
(soft tissue)
Toxicity:
Effects
Threshold for
reduced scope
for growth
Severe
inhibition of
growth,
significantly
reduced
feeding rate,
threshold
concentration
Threshold for
growth rate
inhibition
Reduced
growth in spat
Reduced
growth
Ability to Accumulate2: Source:
Log Log
BCF BAF BSAF Reference
[25]
[26]
[27]
[28]
[29]
[30]
[30]
[30]
[30]
[30]
[30]
Comments3
F; other
contaminants
present
L5
F; 84-day
exposure
L; 45-day
exposure
F6
F
F
F
F
F
F
-------
Summary of Biological Effects Tissue Concentrations for Tributyltin
Species: Concentration
Taxa Sediment
0.08 |ig/g
dw
0.05 |ig/g
dw
0.04 |ig/g
dw
0.11|ig/g
dw
0.07 |ig/g
dw
0.04 |ig/g
dw
0.36 |ig/g
dw
0.15 |ig/g
dw
0.31 |ig/g
dw
Mytilus edulis, 0.10 |ig/g
Blue mussel dw
0.07 |ig/g
dw
0.05 |ig/g
dw
0.27 |ig/g
dw
0.07 |ig/g
dw
, Units in1:
Water
13 ng/L4
8ng/L4
35 ±17
ng/L4
17 ±9
ng/L4
22 ±14
ng/L4
8 ±2
ng/L4
45 ±17
ng/L4
31 ±18
ng/L4
23 ±18
ng/L4
11 ±4
ng/L4
26 ±9
ng/L4
22 ±15
ng/L4
13 ±5
ng/L4
8 ng/L4
Toxicity:
Tissue (SampleType) Effects
0.30 ng/gf
(soft tissue)
0.15ng/gf
(soft tissue)
1.01 ng/gf
(soft tissue)
0.61 ng/gf
(soft tissue)
0.46 ng/gf
(soft tissue)
0.29 ng/gf
(soft tissue)
0.98 ng/gf
(soft tissue)
1.04ng/gf
(soft tissue)
0.38 ^g/gf
(soft tissue)
0.29 ng/gf
(soft tissue)
0.75 ng/gf
(soft tissue)
0.47 ng/gf
(soft tissue)
0.27 ng/gf
(soft tissue)
0.17ng/gf
(soft tissue)
Ability to Accumulate2: Source:
Log Log
BCF BAF BSAF Reference
[30]
[30]
[30]
[30]
[30]
[30]
[30]
[30]
[30]
[30]
[30]
[30]
[30]
[30]
Comments3
F
F
F
F
F
F
F
F
F
F
F
F
F
F
-J
o
-------
Summary of Biological Effects Tissue Concentrations for Tributyltin
Species:
Taxa
Mytilus edulis,
Blue mussel
Concentration
Sediment
0.05 |ig/g
dw
0.02 |ig/g
dw
0.02 |ig/g
dw
0.04 |ig/g
dw
<0.01 |ig/g
dw
0.01 |ig/g
dw
0.02 |ig/g
dw
0.01 |ig/g
dw
0.01 |ig/g
dw
0.05 |ig/g
dw
<0.01 |ig/g
dw
0.66 |ig/g
dw
0.26 |ig/g
dw
0.15 |ig/g
dw
, Units in1:
Water
26 ±12
ng/L4
18 ±13
ng/L4
15 ±12
ng/L4
8 ±2
ng/L4
11 ng/L4
23 ±23
ng/L4
3 ±2
ng/L4
16 ng/L4
6 ±5
ng/L4
6 ±5
ng/L4
2 ng/L4
38 ±21
ng/L4
366 ±29
ng/L4
76 ±43
ng/L4
Toxicity:
Tissue (SampleType) Effects
0.45 |ig/gf
(soft tissue)
0.41 |ig/gf
(soft tissue)
0.19ng/gf
(soft tissue)
0.12ng/gf
(soft tissue)
0.30 |ig/gf
(soft tissue)
0.35 |ig/gf
(soft tissue)
0.07 |ig/gf
(soft tissue)
0.17ng/gf
(soft tissue)
(soft tissue)
o.iing/gf
(soft tissue)
0.05 |ig/gf
(soft tissue)
(soft tissue)
0.82 |ig/gf
(soft tissue)
0.32 |ig/gf
(soft tissue)
Ability to Accumulate2: Source:
Log Log
BCF BAF BSAF Reference
[30]
[30]
[30]
[30]
[30]
[30]
[30]
[30]
[30]
[30]
[30]
[30]
[30]
[30]
Comments3
F
F
F
F
F
F
F
F
F
F
F
F
F
F
-------
Summary of Biological Effects Tissue Concentrations for Tributyltin
Species:
Taxa
Mytilus edulis,
Blue mussel
Concentration
Sediment
0.53 |ig/g
dw
0.08 |ig/g
dw
0.19 |ig/g
dw
0.17 |ig/g
dw
0.07 |ig/g
dw
0.06 |ig/g
dw
0.03 |ig/g
dw
0.04 |ig/g
dw
0.05 |ig/g
dw
0.02 |ig/g
dw
0.03 |ig/g
dw
0.02 |ig/g
dw
4.6 |ig/g dw
10.8 |ig/g
dw
, Units in1:
Water
25 ng/L4
38 ±33
ng/L4
13 ±4
ng/L4
13 ±5
ng/L4
8 ±3
ng/L4
15 ±6
ng/L4
11 ±6
ng/L4
5 ±2
ng/L4
12 ±10
ng/L4
7 ±6
ng/L4
6 ±2
ng/L4
6 ±4
ng/L4
93 ±45
ng/L4
1090
±1850
ng/L4
Toxicity:
Tissue (SampleType) Effects
0.35 ng/gf
(soft tissue)
0.60 |jg/gf
(soft tissue)
0.41 |ig/gf
(soft tissue)
0.20 |jg/gf
(soft tissue)
O.llng/gf
(soft tissue)
0.93 |jg/gf
(soft tissue)
0.58 |ig/gf
(soft tissue)
O.lOfAg/g'
(soft tissue)
0.33 |ig/gf
(soft tissue)
0.23 |ig/gf
(soft tissue)
0.09 |ig/gf
(soft tissue)
0.07 |ig/gf
(soft tissue)
2.57 |ig/gf
(soft tissue)
3.22 |ig/gf
(soft tissue)
Ability to Accumulate2: Source:
Log Log
BCF BAF BSAF Reference
[30]
[30]
[30]
[30]
[30]
[30]
[30]
[30]
[30]
[30]
[30]
[30]
[30]
[30]
Comments3
F
F
F
F
F
F
F
F
F
F
F
F
F
F
-J
o
-------
o
ON
Summary of Biological Effects Tissue Concentrations for Tributyltin
Species:
Taxa
Mytilus edulis,
Mussel
Concentration, Units in1:
Sediment Water Tissue (SampleType)
0.23 ng/g 25 ±7 0.81ng/gf
dw ng/L4 (soft tissue)
2.58 mg/kg
TBTC1 (whole body)8
2.58 mg/kg
TBTC1 (whole body)8
Toxicity: Ability to Accumulate2: Source:
Log Log
Effects BCF BAF BSAF Reference
[30]
Physiological, [53]
LOED
Physiological, [53]
NA
Comments3
F
L; significant
increase in
anoxic heat
dissipation
(j/h/g) at test
concentration
L; 35%
reduction in
anoxia tolerance
as percent of
controls
-------
Summary of Biological Effects Tissue Concentrations for Tributyltin
Species:
Taxa
Concentration, Units in1:
Toxicity:
Sediment Water Tissue (SampleType) Effects
Ability to Accumulate2:
Log Log
Source:
BCF
BAF
BSAF Reference Comments
Mytilus edulis,
Mussel
0.556 mg/kg
TBTC1 (whole body)8
Physiological,
EDS
1.8 mg/kg
TBTC1 (whole body)8
Physiological,
EDS
[26] L; 50% increase
in respiration as
compared to
controls
calculated from
formula in text;
exposure
concentrations
variable because
of rapid uptake
by test organisms
so not measured
or reported
[26] L; 50%reduction
in clearance rate
(feeding rate) as
compared to
controls;
exposure
concentrations
variable because
of rapid uptake
by test organisms
so not measured
or reported
o
-J
-------
o
oo
Summary of Biological Effects Tissue Concentrations for Tributyltin
Species:
Taxa
Concentration, Units in1:
Toxicity:
Sediment Water Tissue (SampleType) Effects
Ability to Accumulate2:
Log Log
Source:
BCF
BAF
BSAF Reference Comments
1.08mg/kg
TBTC1 (whole body)8
Physiological,
LOED
1.08mg/kg
TBTC1 (whole body)8
Physiological,
LOED
0.8 mg/kg
TBTC1 (whole body)8
Physiological,
NOED
[26] L; significant
decrease in
clearance rate
(feeding);
exposure
concentrations
variable because
of rapid uptake
by test organisms
so not measured
or reported
[26] L; significant
decrease in
scope for
growth; exposure
concentrations
variable because
of rapid uptake
by test organisms
so not measured
or reported
[26] L; no significant
decrease in
clearance rate
(feeding);
exposure
concentrations
variable because
of rapid uptake
by test organisms
so not measured
or reported
-------
Summary of Biological Effects Tissue Concentrations for Tributyltin
Species:
Taxa
Concentration, Units in1:
Toxicity:
Sediment Water Tissue (SampleType) Effects
Ability to Accumulate2:
Log Log
Source:
BCF
BAF
BSAF Reference Comments
0.8 mg/kg
TBTC1 (whole body)8
Physiological,
NOED
2 mg/kg
TBTC1 (whole body)8
Physiological,
NOED
[26] L; no significant
decrease in
scope for
growth; exposure
concentrations
variable because
of rapid uptake
by test organisms
so not measured
or reported
[26] L; no significant
change in food
absorption
eficiency;
exposure
concentrations
variable because
of rapid uptake
by test organisms
so not measured
or reported
Area zebra,
Mussel
1.11 |ig/g dwf
(soft tissue)
35%
reduction in
scope for
growth
[25]
-j
o
-------
Summary of Biological Effects Tissue Concentrations for Tributyltin
Species:
Taxa
Dreissena
polymorpha,
Zebra mussel
Dreissena
polymorpha,
Zebra mussel
Concentration, Units in1: Toxicity:
Sediment Water Tissue (SampleType) Effects
70 ng/L4 73.13 |ig/g dw TBT Reduction in
(x; cation (soft tissue) growth after
n = 2) (x;n = 2) 105 days
exposure and
transfer to
clean site
12.7 mg/kg Growth,
TBTC1 (whole body)8 NOED
1.66 mg/kg Growth,
TBTC1 (whole body)8 NOED
Ability to Accumulate2: Source:
Log Log
BCF BAF BSAF Reference Comments3
5.95 [31] F; steady-state
reached after 35
days; 105-day
uptake and
depuration
phases
[31] F; concentration
of TBT in tissues
and water; field
study at marina
with exposure to
TBT and DBT
likely; mean
values provided;
no significant
impact on
growth
[31] F; concentration
of DBT in
tissues and TBT
in water; field
study at marina
with exposure to
TBT and DBT
likely; mean
values provided;
no significant
impact on
growth
-------
Summary of Biological Effects Tissue Concentrations for Tributyltin
Species:
Taxa
Crassostrea
gigas, Pacific
oyster
Concentration, Units in1:
Sediment Water Tissue (SampleType)
0.75 rag/kg'
(whole body)
0.27 |ig/gf
(soft tissue)
2.38mg/kg TBTO
(soft tissue)
0.08|ig/g 15 ±8 1.61|ig/gf
dw ng/L4 (soft tissue)
0.03|ig/g 33 ±27 l.e^g/g'
dw ng/L4 (soft tissue)
0.02 |ig/g 21 ±8 0.62 |ig/gf
dw ng/L4 (soft tissue)
0.10 |ig/g 13 ng/L4 0.36 |ig/gf
dw (soft tissue)
Toxicity: Ability to Accumulate2: Source:
Log Log
Effects BCF BAF BSAF Reference Comments3
Reduction in [33] F
condition
factor and
growth
Reduced [34] F
tissue growth;
shell
thickening
Reduced [28] L; 45-day
growth in spat exposure
Shell [30] F
thickness
index = 4.39;
x tissue
weight = 1.29
Shell [30] F
thickness
index = 4.85;
x tissue
weight = 0.70
Shell [30] F
thickness
index = 6.85;
x tissue
weight = 2.59
Shell [30] F
thickness
index = 9.82;
x tissue
weight = 5.66
-------
Summary of Biological Effects Tissue Concentrations for Tributyltin
Species:
Taxa
Crassostrea
gigas, Pacific
oyster
Concentration
Sediment
0.15 |ig/g
dw
0.04 |ig/g
dw
0.08 |ig/g
dw
0.05 |ig/g
dw
0.04 |ig/g
dw
O.lljig/g
dw
, Units in1:
Water Tissue (SampleType)
22 ±12 l.2Q\jig/g*
ng/L4 (soft tissue)
17 ±12 l.46\ig/g*
ng/L4 (soft tissue)
13 ng/L4 0.44 |ig/gf
(soft tissue)
8 ng/L4 0.33 |ig/gf
(soft tissue)
35 ±17 1.49\ig/g*
ng/L4 (soft tissue)
17 ±9 1.73jj.g/gt
ng/L4 (soft tissue)
Toxicity: Ability to Accumulate2: Source:
Log Log
Effects BCF BAF BSAF Reference Comments3
Shell [30] F
thickness
index = 4.78;
x tissue
weight = 1.26
Shell [30] F
thickness
index = 4.67;
x tissue
weight = 0.67
Shell [30] F
thickness
index = 8. 10;
x tissue
weight = 2.62
Shell [30] F
thickness
index = 10.2;
x tissue
weight = 2.84
Shell [30] F
thickness
index = 5.14;
x tissue
weight = 0.97
Shell [30] F
thickness
index = 5.29;
x tissue
weight = 0.84
-------
Summary of Biological Effects Tissue Concentrations for Tributyltin
Species:
Taxa
Crassostrea
gigas, Pacific
oyster
Concentration
Sediment
0.07 |ig/g
dw
0.04 |ig/g
dw
0.36 |ig/g
dw
0.15 |ig/g
dw
0.31 |ig/g
dw
0.10 |ig/g
dw
, Units in1:
Water Tissue (SampleType)
22 ±14 0.61|ig/gt
ng/L4 (soft tissue)
8 ±2 0.38 |ig/gf
ng/L4 (soft tissue)
45 ±17 1.24|ig/gf
ng/L4 (soft tissue)
31 ±18 1.57 |ig/gf
ng/L4 (soft tissue)
23 ±18 0.50
ng/L4
1 1 ±4 0.45 |ig/gf
ng/L4 (soft tissue)
Toxicity: Ability to Accumulate2: Source:
Log Log
Effects BCF BAF BSAF Reference Comments3
Shell [30] F
thickness
index = 8.07;
x tissue
weight = 2.23
Shell [30] F
thickness
index = 9.83;
x tissue
weight = 2.90
Shell [30] F
thickness
index = 4.95;
x tissue
weight = 0.77
Shell [30] F
thickness
index = 5.04;
x tissue
weight = 0.49
e weight = [30] F
2.39
Shell [30] F
thickness
index = 10.2;
x tissue
weight = 2.77
-------
Summary of Biological Effects Tissue Concentrations for Tributyltin
Species: Concentration
Taxa Sediment
0.07 |ig/g
dw
0.05 ng/g
dw
0.27 |ig/g
dw
0.07 ng/g
dw
0.05 |ig/g
dw
0.02 |ig/g
dw
, Units in1:
Water
26 ±9
ng/L4
22 ±15
ng/L4
13 ±5
ng/L4
8 ng/L4
26 ±12
ng/L4
18 ±13
ng/L4
Tissue (SampleType)
0.74 ng/gf
(soft tissue)
1.26ng/gf
(soft tissue)
0.34 |ig/gf
(soft tissue)
0.31 ng/gf
(soft tissue)
0.80 |ig/gf
(soft tissue)
0.98 |ig/gf
(soft tissue)
Toxicity: Ability to Accumulate2: Source:
Log Log
Effects BCF BAF BSAF Reference Comments3
Shell [30] F
thickness
index = 5.06;
x tissue
weight = 1 .24
Shell [30] F
thickness
index = 5.24;
x tissue
weight = 1 .24
Shell [30] F
thickness
index = 9.83;
x tissue
weight = 2.44
Shell [30] F
thickness
index = not
sampled; x
tissue weight
= not sampled
Shell [30] F
thickness
index = 5.39;
x tissue
weight = 1.18
Shell [30] F
thickness
index = 5.29;
x tissue
weight = 1.14
-------
Summary of Biological Effects Tissue Concentrations for Tributyltin
Species: Concentration
Taxa Sediment
0.02 |ig/g
dw
Crassostrea 0.04 jj,g/g
gigas, dw
Pacific oyster
<0.01 |ig/g
dw
0.01 |ig/g
dw
0.02 |ig/g
dw
0.02 |ig/g
dw
, Units in1:
Water Tissue (SampleType)
15 ±12 0.24 |ig/gf
ng/L4 (soft tissue)
8 ±2 0.27 |ig/gf
ng/L4 (soft tissue)
1 1 ng/L4 0.37 |ig/gf
(soft tissue)
23 ±23 0.56 |ig/gf
ng/L4 (soft tissue)
10 ± O.Hiig^
ng/L4 (soft tissue)
3+2 0.11 |ig/gf
ng/L4 (soft tissue)
Toxicity: Ability to Accumulate2: Source:
Log Log
Effects BCF BAF BSAF Reference Comments3
Shell [30] F
thickness
index = 9.00;
x tissue
weight = 2.50
Shell [30] F
thickness
index = 8.62;
x tissue
weight = 5.92
Shell [30] F
thickness
index = 9.63;
x tissue
weight = 1.39
Shell [30] F
thickness
index = 6.48;
x tissue
weight = 1 .44
Shell [30] F
thickness
index = not
sampled; x
tissue weight
= not sampled
Shell [30] F
thickness
index = 19.8;
x tissue
weight = 5.96
-------
Summary of Biological Effects Tissue Concentrations for Tributyltin
Species:
Taxa
Crassostrea
gigas, Pacific
oyster
Concentration
Sediment
0.01 |ig/g
dw
0.01 |ig/g
dw
0.05 |ig/g
dw
<0.01 |ig/g
dw
0.66 |ig/g
dw
0.26 |ig/g
dw
, Units in1:
Water
16 ng/L4
6 ±5
ng/L4
6 ±5
ng/L4
2 ng/L4
38 ±21
ng/L4
366 ±29
ng/L4
Tissue (SampleType)
0.18ng/gf
(soft tissue)
0.28 |ig/gf
(soft tissue)
0.08 |ig/gf
(soft tissue)
0.08 |ig/gf
(soft tissue)
2.26 |ig/gf
(soft tissue)
2.18ng/gf
(soft tissue)
Toxicity: Ability to Accumulate2: Source:
Log Log
Effects BCF BAF BSAF Reference Comments3
Shell [30] F
thickness
index = 12.4;
x tissue
weight = 2.72
Shell [30] F
thickness
index = 9.64;
x tissue
weight = 2.06
Shell [30] F
thickness
index = 23.3;
x tissue
weight = 4.11
Shell [30] F
thickness
index = 2 1.0;
x tissue
weight = 9.28
Shell [30] F
thickness
index = 4.95;
x tissue
weight = 1.00
Shell [30] F
thickness
index = 3.96;
x tissue
weight = 0.97
-------
Summary of Biological Effects Tissue Concentrations for Tributyltin
Species: Concentration
Taxa Sediment
0.15 |ig/g
dw
0.53 |ig/g
dw
0.08 |ig/g
dw
0.19 |ig/g
dw
0.17 |ig/g
dw
0.07 |ig/g
dw
, Units in1:
Water
76 ±43
ng/L4
25 ng/L4
38 ±33
ng/L4
13 ±4
ng/L4
13 ±5
ng/L4
8 ±3
ng/L4
Tissue (SampleType)
1.34^
(soft tissue)
0.65 |ig/gf
(soft tissue)
0.88 |ig/gf
(soft tisue)
LSSjig/g'
(soft tisue)
0.50 |ig/gf
(soft tisue)
0.26 |ig/gf
(soft tissue)
Toxicity: Ability to Accumulate2: Source:
Log Log
Effects BCF BAF BSAF Reference Comments3
Shell [30] F
thickness
index = 6.87;
x tissue
weight = 2.53
Shell [30] F
thickness
index = 14.9;
x tissue
weight = 3.65
Shell [30] F
thickness
index = 10.6;
x tissue
weight = 1 .56
Shell [30] F
thickness
index = 5.98;
x tissue
weight = 0.89
Shell [30] F
thickness
index = 12.5;
x tissue
weight = 3. 19
Shell [30] F
thickness
index = 14.7;
x tissue
weight = 7.09
-J
-J
-------
-J
oo
Species: Concentration
Taxa Sediment
0.06 |ig/g
dw
0.03 ng/g
dw
Summary of Biological Effects Tissue Concentrations for Tributyltin
, Units in1:
Water
15 ±6
ng/L4
11 ±6
ng/L4
Tissue (SampleType)
1.39|ig/f
(soft tissue)
1.44^*
(soft tissue)
Toxicity: Ability to Accumulate2: Source:
Log Log
Effects BCF BAF BSAF Reference Comments3
Shell [30] F
thickness
index = 7.56;
x tissue
weight = 1.77
Shell [30] F
thickness
index = 5.41;
x tissue
weight = 1.32
Crassostrea
gigas, Pacific
oyster
0.04
dw
0.05 |ig/g
dw
0.02 |ig/g
dw
0.03 |ig/g
dw
5 ±2
ng/L4
12 ±10
ng/L4
7 ±6
ng/L4
6 ±2
ng/L4
0.21
(soft tissue)
0.30
(soft tissue)
0.49 |ig/gf
(soft tissue)
0.25 ^ig/gf
(soft tissue)
Shell
thickness
index = 13.1;
x tissue
weight = 8.07
Shell
thickness
index =10.6;
x tissue
weight = 1.56
Shell
thickness
index = 12.4;
x tissue
weight = 1.24
Shell
thickness
index = 25.7;
x tissue
weight = 5.22
[30]
[30]
[30]
[30]
-------
Summary of Biological Effects Tissue Concentrations for Tributyltin
Species: Concentration, Units in1:
Taxa Sediment Water
0.02 |ig/g 6 ±4
dw ng/L4
4.6 |ig/g dw 93 ±45
ng/L4
10.8 |ig/g 1,090
dw ±1,850
ng/L4
l.l|ig/gdw 82 ±9
ng/L4
0.23 |ig/g 25 ±7
dw ng/L4
Crassostrea
gigas, Oyster
Tissue (SampleType)
0.13ng/gf
(soft tissue)
6.35 ng/gf
(soft tissue)
3.65 ng/gf
(soft tissue)
5.60 ng/gf
(soft tissue)
1.28ng/gf
(soft tissue)
22 mg/kg
TBTF1 (whole body)8
Toxicity: Ability to Accumulate2: Source:
Log Log
Effects BCF BAF BSAF Reference Comments3
Shell [30] F
thickness
index = 189;
x tissue
weight = 6.23
Shell [30] F
thickness
index = 3.21;
x tissue
weight = 0.37
Shell [30] F
thickness
index = 8.06;
x tissue
weight = 0.1 2
Shell [30] F
thickness
index = 4.34;
x tissue
weight = 0.95
Shell [30] F
thickness
index = 6.73;
x tissue
weight = 1.24
Morphology, [45] L and F
ED 100 combined;
malformation of
shells
-------
Summary of Biological Effects Tissue Concentrations for Tributyltin
Species:
Taxa
Crassostrea
gigas, Oyster
Crassostrea
gigas, Oyster
Concentration, Units in1:
Sediment Water Tissue (SampleType)
5mg/kg
TBTF1 (whole body)8
22 mg/kg
TBTF1 (whole body)8
5 mg/kg
TBTF1 (whole body)8
0.75 mg/kg
TBTC1 (whole body)8
3.7 mg/kg
TBTO (whole body)8
Toxicity: Ability to Accumulate2: Source:
Log Log
Effects BCF BAF BSAF Reference
Morphology, [45]
LOED
Mortality, [45]
ED 100
Mortality, NA [45]
Growth, NA [47]
Growth, [52]
ED 100
Comments3
L andF
combined;
malformation of
shells
LandF
combined; 100%
mortality after
170 days
L andF
combined; 30%
mortality after
110 days
F; 44% reduction
in condition
factor and
growth
L; no growth
(weight increase
or length) in
high test
concentration
-------
Summary of Biological Effects Tissue Concentrations for Tributyltin
Species:
Taxa
Concentration, Units in1:
Toxicity:
Ability to Accumulate2:
Source:
Sediment Water Tissue (SampleType) Effects
Log
BCF
Log
BAF
BSAF Reference Comments3
4.89 mg/kg
TBTO (whole body)8
Growth,
ED 100
[52]
1.71 mg/kg
TBTO (whole body)8
4.89 mg/kg
TBTO (whole body)8
Growth,
ED 100
Growth, NA
[52]
[52]
1.71 mg/kg
TBTO (whole body)8
Growth, NA
[52]
L; no growth
(length) in
high test
concentration
(with sediment
present at 30
mg/L)
L; no growth
(length) in
low test
concentration
L; 92%
reduction in
growth (weight
increase)in
high test
concentration
relative to
control
L; 70%
reduction in
growth (weight
increase)in
low test
concentration
relative to
control
-------
Summary of Biological Effects Tissue Concentrations for Tributyltin
Species:
Taxa
Concentration, Units in1:
Toxicity:
Ability to Accumulate2:
Source:
Sediment Water Tissue (SampleType) Effects
Log
BCF
Log
BAF
BSAF Reference Comments3
1.3mg/kg
TBTO (whole body)8
Growth, NA
1.71 mg/kg
TBTO (whole body)8
Growth, NA
1.71 mg/kg
TBTO (whole body)8
Mortality,
NOED
3.7 mg/kg
TBTO (whole body)8
Physiological,
NA
[52] L; 47%
reduction in
growth (weight
increase)in
low test
concentration
with 30 mg/L
sediment present
relative to
control
[52] L; 70%
reduction in
growth (length)
in low test
concentration
with 30 mg/L
sediment present
relative to
control
[52] L; no mortality
in low test
concentration
(both with and
without sediment
present)
[52] L; 63%
reduction in
condition index
relative to
control in
high test
concentration
-------
Summary of Biological Effects Tissue Concentrations for Tributyltin
Species:
Taxa
Ostrea edulis,
Oyster
Ostrea edulis,
Oyster
Concentration, Units in1:
Sediment Water Tissue (SampleType)
4.89 mg/kg
TBTO(whole body)8
1.71 mg/kg
TBTO(whole body)8
1.3 mg/kg
TBTO (whole body)8
0.53 mg/kg
TBTO (soft tissue)
0.75 mg/kg
TBTO (soft tissue)
Toxicity: Ability to Accumulate2: Source:
Log Log
Effects BCF BAF BSAF Reference
Physiological, [52]
NA
Physiological, [52]
NA
Physiological, [52]
NA
No effect on [28]
growth in spat
Reduced [28]
growth in spat
Comments3
L; 42%
reduction in
condition index
relative to
control in
high test
concentration
with 30 mg/L
sediment present
L; 18%
reduction in
condition index
relative to
control in
low test
concentration
L; 11%
reduction in
condition index
relative to
control in
low test
concentration
with 30 mg/L
sediment present
L; 45-day
exposure
L; 45-day
exposure
-------
Summary of Biological Effects Tissue Concentrations for Tributyltin
Species:
Taxa
Saccostria
commercialis,
Sydney rock
oyster
Saccostria
commercialis,
Sydney rock
oyster
Concentration, Units in1:
Sediment Water Tissue (SampleType)
0.012 mg/kg
TBTC1 (whole body)8
0.04 mg/kg
TBTC1 (whole body)8
HOngSn/g'1
(soft tissues)
107 ng Sn/g'1
(soft tissues)
86 ng Sn/g'1
(soft tissues)
98 ng Sn/g'1
(soft tissues)
87 ng Sn/g-1
(soft tissues)
350 ng Sn/g-1
(soft tissues)
Toxicity:
Effects
Morphology,
LOED
Morphology,
LOED
Shell
deformations;
shell curl
Shell
deformations;
shell curl
Shell
deformations;
shell curl
Shell
deformations;
shell curl
Shell
deformations;
shell curl
Shell
deformations;
shell curl
Ability to Accumulate2: Source:
Log Log
BCF BAF BSAF Reference Comments3
[51] F
[51] F
[39] F
[39] F
[39] F
[39] F
[39] F
[39] F
Cerastoderma
edule, Cockle
445 ± 83
ng/g dw
(n=5)
68.2 ±
40.6
ng/L4
(n=8)
4,128 ng/g, dwf
(pooled, soft tissue)
(n=l)
4.78
[21]
-------
Summary of Biological Effects Tissue Concentrations for Tributyltin
Species:
Taxa
Macoma
balthica, Clam
Merceneria
mercenaria,
Hard shell clam
Venerupis
decussata,
Clam
Venerupis
semidecussata,
Clam
Mya arenaria,
Soft shell clam
Petricola
pholadiformis,
American
piddock
Concentration
Sediment
445 ± 83
ng/g dw
(n=5)
445 ± 83
ng/g dw
(n=5)
445 ± 83
ng/g dw
(n = 5)
445 ± 83
ng/g dw
(n = 5)
, Units in1:
Water
68.2 ±
40.6
ng/L4
(n=8)
68.2 ±
40.6
ng/L4
(n=8)
68.2 ±
40.6
ng/L4
(n = 8)
68.2 ±
40.6
ng/L4
(n = 8)
Toxicity: Ability to Accumulate2: Source:
Log Log
Tissue (SampleType) Effects BCF BAF BSAF Reference Comments3
4,587 ± 2,793 ng/g 4.83 [21] F
dwf
(pooled, soft tissue)
(n=4)
8,649 ng/g dwf 5.10 [21] F
(pooled, soft tissue)
(n=l)
2.64 mg/kg TBTO Reduced [28] L; 45-day
(soft tissue) growth in spat exposure
1.48 mg/kg TBTO No effect on [28] L; 45-day
(soft tissue) spat growth exposure
36,807 ±9,800 5.73 [21] F
ng/g dwf
(pooled, soft tissue)
(n = 4)
838 ± 108 ng/g dwf 4.09 [21] F
(pooled, soft tissue)
(n = 2)
-------
-J
K>
ON
Summary of Biological Effects Tissue Concentrations for Tributyltin
Species:
Taxa
Scrobicularia
plana, Clam
Scorbicularia
plana, Clam
Scorbicularia
plana, Clam
Concentration
Sediment
445 ± 83
ng/g dw
(n = 5)
0.03 |ig/g
dw
|ig/g dw
0.03 ng/g
dw
(n=3)
0.039 |ig/g
dw
(n=3)
0.22 ng/g
dw
(n=3)
0.12 |ig/g
dw
(n=6)
0.11|ig/g
dw
0.02 |ig/g
dw
0.126 |ig/g
dw
, Units in1:
Water
68.2 ±
40.6
ng/L4
(n=8)
4.0-17.5
ng/L4
7.0-10.8
ng/L4
15.2-
51.6
ng/L4
17.2-
51.3
ng/L4
0.6-213
ng/L4
10.9-
33.2
ng/L4
7.4
ng/L4
2.7
ng/L4
230
ng/L4
Toxicity:
Tissue (SampleType) Effects
3,375 ± 232 ng/g dwf
(pooled, soft tissue)
(n = 4)
0.635 |ig Sn/g dw
(soft tissues)
0.263 |ig Sn/g dw
(soft tissues)
2.04 |ig Sn/g dw
(soft tissues)
1.12|igSn/gdw
(soft tissues)
2.05 |ig Sn/g dw
(soft tissues)
1.69 |ig Sn/g dw
(soft tissues)
1.51 |ig Sn/g dw
(soft tissues)
0.62 |ig Sn/g dw
(soft tissues)
5.09 |ig Sn/g dw
(soft tissues)
Ability to Accumulate2: Source:
Log Log
BCF BAF BSAF Reference
4.69 [21]
[40]
[40]
[40]
[40]
[40]
[40]
[40]
[40]
[40]
Comments3
F
F
F
F
F
F
F
F
F
F
2.91 mg/kg TBTO
(soft tissue)
Reduced
growth in spat
[28]
L; 45-day
exposure
-------
Summary of Biological Effects Tissue Concentrations for Tributyltin
Species:
Taxa
Concentration, Units in1: Toxicity: Ability to Accumulate2: Source:
Log Log
Sediment Water Tissue (SampleType) Effects BCF BAF BSAF Reference Comments3
Hyalella azteca,
Amphipod
4.8nM3 HOnmol/gdw
(whole body)
4 week LC50
[22]
L; 1 week to
reach
equilibrium in
tissues
Fishes
Oncorhynchus
mykiss, Rainbow
trout
1.41 |ig
Sn/L
0.42 jig
Sn/L
1.21mgSn/kg
(liver)
0.34 mg Sn/kg
(gall bladder)
2.30 mg Sn/kg
(kidney)
1.38 mg Sn/kg
(carcass)
5.56 mg Sn/kg
(peritoneal fat)
1.04 mg Sn/kg
(gill)
0.67 mg Sn/kg
(blood)
0.50 mg Sn/kg
(gut)
0.32 mg Sn/kg
(muscle)
2.20 mg Sn/kg
(brain)
96-hr LC50
406
[8]
[8]
L; 15-dy
exposure period
-j
K>
-J
-------
Summary of Biological Effects Tissue Concentrations for Tributyltin
Species:
Taxa
Oncorhynchus
mykiss,
Rainbow trout
Concentration, Units in1:
Sediment Water Tissue (SampleType)
0.11 mg/kg
TBTO (whole body)
0.35 mg/kg
TBTO (whole body)
0.1 3 mg/kg
TBTO (whole body)
0.27 mg/kg TBTO
(whole body)
Toxicity:
Effects
Behavior,
LOED
Growth,
LOED
Growth,
LOED
Growth,
LOED
Ability to Accumulate2: Source:
Log Log
BCF BAF BSAF Reference Comments3
[43] L; significantly
increased
swimming
behavior
(distances and
directions of)
[43] L; significantly
lower weight
increase at
lowest test
concentration
[43] L; significantly
increased
swimming
behavior
(distances and
directions of)
[43] L; significantly
lower weight
increase at
lowest test
concentration;
residue from
-------
Summary of Biological Effects Tissue Concentrations for Tributyltin
Species:
Taxa
Oncorhynchus
mykiss,
Rainbow trout
Concentration, Units in1: Toxicity: Ability to Accumulate2: Source:
Log Log
Sediment Water Tissue (SampleType) Effects BCF BAF BSAF Reference Comments3
0.6 ng 2.5|igTBTO/g Histopatho- [44] L; 28-day
TBTO/ (whole body)7 logical effects exposure
L4 Spleen: 20%
had
lymphocytic
depletion;
20% increased
erythrophagia;
Gills: 10%
had cell
necrosis
within primary
lamellae, 30%
within
secondary
lamellae;
Pseudobranch:
30% had cell
necrosis
within
pseudobranch-
ial tissue
-------
Summary of Biological Effects Tissue Concentrations for Tributyltin
Species:
Taxa
Concentration, Units in1:
Toxicity:
Ability to Accumulate2:
Source:
Sediment Water Tissue (SampleType) Effects
Log
BCF
Log
BAF
BSAF Reference Comments3
1.0 jig
TBTO/
L4
2.75 |ig TBTO/g
(whole body)7
Histopatho-
logical effects
Spleen: 90%
had
lymphocytic
depletion;
50% increased
erythrophagia;
Gills: 20%
had cell
necrosis
within primary
lamellae, 50%
within
secondary
lamellae;
Pseudobranch:
50% had cell
necrosis
within
pseudobranch-
ial tissue
[44]
L; 28-day
exposure
-------
Summary of Biological Effects Tissue Concentrations for Tributyltin
Species:
Taxa
Oncorhynchus
mykiss,
Rainbow trout
Concentration, Units in1: Toxicity: Ability to Accumulate2: Source:
Log Log
Sediment Water Tissue (SampleType) Effects BCF BAF BSAF Reference Comments3
2.0 ng 5.5|igTBTO/g Histopatho- [44] L; 28-day
TBTO/L (whole body)7 logical effects exposure
Spleen: 30%
had
lymphocytic
depletion;
70% increased
erythrophagia;
Gills: 40%
had cell
necrosis
within primary
lamellae, 50%
within
secondary
lamellae;
Pseudobranch:
20% had cell
necrosis
within oral
mucosa, 30%
had cell
necrosis
within
pseudobranch-
ial tissue
Oncorhynchus
mykiss,
Rainbow trout
13.1mg/kgTBTO
oxide (whole body)8
Mortality,
ED50
[49]
L; median lethal
dose
-------
Summary of Biological Effects Tissue Concentrations for Tributyltin
Species:
Taxa
Concentration, Units in1:
Toxicity:
Ability to Accumulate2:
Source:
Sediment Water Tissue (SampleType) Effects
Log
BCF
Log
BAF
BSAF Reference Comments3
Oncorhynchus
mykiss,
Rainbow trout
4.0 ng
TBTO/
L4
7.0 |ig TBTO/g
(whole body)7
Histopatho-
logical effects;
Spleen: 100%
had
lymphocytic
depletion;
90% increased
erythrophagia;
Gills: 100%
had cell
necrosis
within primary
lamellae, 80%
within
secondary
lamellae;
Pseudobranch:
60% had cell
necrosis
within oral
mucosa, 70%
had cell
necrosis
within
pseudobranch-
ial tissue
[44]
L; 28-day
exposure
-------
Species:
Taxa
Cyprinodon
variegatus,
Sheepshead
minnow
Summary of Biological Effects
Concentration, Units in1:
Sediment Water Tissue (SampleType)
40,800 mg/kg
TBTO (liver)8
1,2 10 mg/kg
TBTO (muscle)8
2,480 mg/kg
TBTO (viscera)8
2,600 mg/kg
TBTO (whole body)8
Tissue Concentrations for Tributyltin
Toxicity: Ability to Accumulate2: Source:
Log Log
Effects BCF BAF BSAF Reference
Development, [9]
NOED
Development, [9]
NOED
Development, [9]
NOED
Development, [9]
NOED
Comments3
L; TBTO as tin;
no significant
response for
length or weight
of Fl generation
fish (parental
exposure)
L; TBTO as tin;
no significant
response for
length or weight
of Fl generation
fish (parental
exposure)
L; TBTO as tin;
no significant
response for
length or weight
of Fl generation
fish (parental
exposure)
L; TBTO as tin
in whole body of
Fl generation;
no significant
response for
length or weight
of Fl generation
fish (parental
exposure)
-------
Si Summary of Biological Effects
Species: Concentration, Units in :
Taxa Sediment Water Tissue (SampleType)
40,800 mg/kg
TBTO (liver)8
1,2 10 mg/kg
TBTO (muscle)8
2,480 mg/kg
TBTO (viscera)8
2,600 mg/kg
TBTO (whole body)8
40,800 mg/kg
TBTO (liver)8
Tissue Concentrations for Tributyltin
Toxicity: Ability to Accumulate2: Source:
Log Log
Effects BCF BAF BSAF Reference
Growth, [9]
NOED
Growth, [9]
NOED
Growth, [9]
NOED
Growth, [9]
NOED
Reproduction, [9]
NOED
Comments3
L; TBTO as tin;
no significant
response for
length or weight
L; TBTO as tin;
no significant
response for
length or weight
L; TBTO as tin;
no significant
response for
length or weight
L; TBTO as tin
in whloe body of
Fl generation;
no significant
response for
length or weight
in adults
L; TBTO as tin;
no significant
response for
number of eggs
spawned per day
per female, or
hatching success
-------
Summary of Biological Effects Tissue Concentrations for Tributyltin
Species:
Taxa
Concentration, Units in1:
Toxicity:
Ability to Accumulate2:
Source:
Sediment Water Tissue (SampleType) Effects
Log
BCF
Log
BAF
BSAF Reference Comments3
l,210mg/kg
TBTO (muscle)8
2,480 mg/kg
TBTO (viscera)8
2,600 mg/kg
TBTO (whole body)8
Reproduction,
NOED
[9]
Reproduction,
NOED
[9]
Reproduction,
NOED
[9]
L; TBTO as tin;
no significant
response for
number of eggs
spawned per day
per female, or
hatching success
L; TBTO as tin;
no significant
response for
number of eggs
spawned per day
per female, or
hatching success
L; TBTO as tin
in whloe body of
Fl generation;
no significant
response for
number of eggs
spawned per day
per female, or
hatching success
in adults
Ictalurus
punctatus,
Channel catfish
0.1 mg/kg (whole
body tissue residue
concentrations)
Significant
(P<0.05)
suppression of
humoral
response
[41]
-------
Summary of Biological Effects Tissue Concentrations for Tributyltin
Species:
Taxa
Poecilia
reticulata,
Guppy
Stenotomus
chrysops,
Scup
Concentration, Units in1:
Sediment Water Tissue (SampleType)
0.7 mg/kg TBTO
(whole body tissue
residue
concentrations)
202 mg/kg
TBTC1 (liver)8
16.3 mg/kg
TBTC1 (whole body)8
8 mg/kg
TBTC1 (liver)8
14.7 mg/kg
TBTC1 (liver)8
202 mg/kg
TBTC1 (liver)8
3.3 mg/kg
TBTC1 (whole body)8
Toxicity: Ability to Accumulate2: Source:
Log Log
Effects BCF BAF BSAF Reference
Histopatho- [42]
logical
changes
Physiological, [48]
LOED
Physiological, [48]
LOED
Cellular, [48]
NOED
Cellular, [48]
NOED
Cellular, [48]
NOED
Cellular, [48]
NOED
Comments3
L; statistically
significant
reduction of
hepatic enzyme
activity
L; statistically
significant
reduction of
hepatic enzyme
activity
L; no effect
on liver
histopathology
L; no effect
on liver
histopathology
L; no effect
on liver
histopathology
L; no effect
on liver
histopathology
-------
Summary of Biological Effects Tissue Concentrations for Tributyltin
Species: Concentration, Units in1:
Taxa Sediment Water Tissue (SampleType)
8.1 mg/kg
TBTC1 (whole body)8
16.3 mg/kg
TBTC1 (whole body)8
8 mg/kg
TBTC1 (liver)8
14.7 mg/kg
TBTC1 (liver)8
3.3 mg/kg
TBTC1 (whole body)8
8.1 mg/kg
TBTC1 (whole body)8
Toxicity: Ability to Accumulate2: Source:
Log Log
Effects BCF BAF BSAF Reference
Cellular, [48]
NOED
Cellular, [48]
NOED
Physiological, [48]
NOED
Physiological, [48]
NOED
Physiological, [48]
NOED
Physiological, [48]
NOED
Comments3
L; no effect
on liver
histopathology
L; no effect
on liver
histopathology
L; statistically
insignificant
reduction of
hepatic enzyme
activity
L; statistically
insignificant
reduction of
hepatic enzyme
activity
L; statistically
insignificant
reduction of
hepatic enzyme
activity
L; statistically
insignificant
reduction of
hepatic enzyme
activity
-J
u>
-J
1 Concentration units based on wet weight unless otherwise noted.
2 BCF = bioconcentration factor, BAF = bioaccumulation factor, BSAF = biota-sediment accumulation factor.
-------
3 L = laboratory study, spiked sediment, single chemical; F = field study, multiple chemical exposure; other unusual study conditions or observations noted.
4 Surface water or aqueous concentration; not pore water.
5 Laboratory toxicity test, co-occurrence of multiple contaminants with listed contaminant.
6 Outdoor microcosm or artificial stream test, co-occurrence of multiple contaminants with listed contaminant.
7 Residue concentration estimated from graphical material.
8 This entry was excerpted directly from the Environmental Residue-Effects Database (ERED, www.wes.army.mil/el/ered, U.S. Army Corps of Engineers and U.S.
Environmental Protection Agency). The original publication was not reviewed, and the reader is strongly urged to consult the publication to confirm the information
presented here.
f Type of tributyltin species not reported.
Conversion Factors:
[TBT] * 0.41 = [Sn] [TBTO] * 0.97 = [TBT]
[TBT] * 1.12 = [TBT Cl] [Sn] * 2.74 = [TBT Cl]
[TBT Cl * 0.36 = [Sn] [Sn] *2.44 = [TBT]
[TBT Cl] * 0.89 = [TBT]
-------
BIOACCUMULATION SUMMARY TRIBUTYLTIN
References
1. Champ, M. A., and P. F. Selgman. 1996. An introduction to organotin compound and their
use in antifouling coatings. In Organotin, ed. M.A. Champ and P. F. Seligman, pp. 1-25.
Chapman and Hall, London.
2. Pent, K. 1996. Ecotoxicology of organotin compounds. Crit. Rev. Toxicol. 26(1):1-117.
3. Maguire, R.J., and RJ. Tkacz. 1985. Degradation of the tri-n-butyltin species in water and
sediment from Toronto Harbor. J. Agric. Food Chem. 33:947-953.
4. Meador, J.P., C.A. Krone, D.W. Dyer, and U. Varanasi. 1997. Toxicity of sediment-associated
tributyltin to infaunal invertebrate species: species comparison and the role of organic carbon.
Mar. Environ. Res. 43(3):219-241
5. USEPA. 1996. Integrated Risk Information System (IRIS). National Library of Medicine
online (TOXNET). U.S. Environmental Protection Agency, Office of Health and
Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH.
September.
6. USEPA. 1996. Recommendations for a screening level for tributyltin in Puget Sound
sediment. USEPA Region 10 Document Control Number 4000-09-01-AADE, 13-01-AADC,
33-01-AAAN.
7. Tsuda, T., Nakanishi, H., Aoki, S., and Takebayahi, J. 1987. Determination of butyltin and
phenyltin coumpounds in biological and sediment samples by electron-capture gas
chromatography. /. Chromatogr. 387:361-370.
8. Martin, R.C., D.G. Dixon, RJ. Maguire, P.V. Hodson, and RJ. Tkacz. 1989. Acute toxicity,
uptake, depuration, and tissue distribution of tri-n-butyltin in rainbow trout, Salmo gairdneri.
Aquatic Toxicol. 15:37.
9. Ward G.S., G.C. Cramm, P.R. Parrish, H. Trachman, and A. Schlesinger. 1981.
Bioaccumulation and chronic toxicity of bis(tributyltin)oxide (TBTO): Tests with a saltwater
fish. Aquatic Toxicology and Hazard Assessment: Fourth Conference, ed. D.R. Branson and
K.L. Dickson, pp. 183-200. ASTM Special Technical Publication 737, American Society for
Testing and Materials, Philadelphia, PA.
10. Wade, T. L., B. Garcia-Romero, and J. M. Brooks. 1988. Tributyltin contamination in bivalves
from United States coastal estuaries. Environ. Sci. Technol 22(12): 1488-1493.
11. Craig, P. J. 1986. Organometallic compounds in the environment: Principles and reactions,
pp. 111-159. John Wiley and Sons, New York, NY.
12. Davies, A. G., and PJ. Smith. 1982. In Comprehensive organometallic chemistry, ed. E.W.
Able, F.G.A Stone, and G. Wilkinson, p. 519. Pergamon Press, Oxford, United Kingdom.
739
-------
BIOACCUMULATION SUMMARY TRIBUTYLTIN
13. Clark, E. A., R.M. Sterritt, and J.N. Lester. 1988. The fate of tributyltin in the aquatic
environment. Environ. Set Tech, M., J.P. Berthome, E. Polanco-Torres, C. Azieu, J.M.
Deslous-Paoli, D. Razet, and J. Gamier. 1981. Anomalies de croissance de la coquille de
Crassostrea gigas dans le basin de Marennes-Oleron. Bilan de trois annees d'observation.
ICES Shellfish and Benthos Committee. CM 1981/K:13.
15. Uhler, A. D., G.S. Durell, W.G. Steinhauer, and A.M. Spellacy. 1993. Tributyltin levels in
bivalve mollusks from the East and West coasts of the United States: results from the 1988-
1990 National Status and Trends Mussel Watch project. Environ. Toxicol Chem. 12:139-153.
16. Huggett, R. J., M.A. Unger, and D.A. Westbrook. 1986. Organotin concentrations in the
southern Chesapeake Bay. In Proceedings, Oceans 1986 Conference, Organotin Symposium,
Vol. 4., pp. 1262-1265, Washington, DC, September 23-25, 1986.
17. Fent, K., and J. Hunn. 1995. Organotins in freshwater harbors and rivers: Temporal
distribution, annual trends and fate. Environ. Toxicol. Chem. 14:1123-1132.
18. Bushong, S. J., M.C. Ziegenfuss, M.A. Unger, and L.W. Hall. 1990. Chronic tributyltin
toxicity experiments with the Chesapeake Bay copepod, Acartia tonsa. Environ. Toxicol.
Chem. 9:359-366.
19. Smith, B.S. 1981. Tributyltin compounds induce male characteristics on female mud snails
Nassarius obsoletus = Ilyanassa obsoleta. J. Appl. Toxicol. 1:141-144.
20. UNEP. 1989. Assessment oforganotin compounds as marine pollutants in the Mediterranean.
Athens: Mediterranean Action Plan 1989. United Nations Environment Programme.
21. Bryan, G. W., and P.E. Gibbs. 1991. Impact of low concentrations of tributyltin (TBT) on
marine organisms: A review. In Metal ecotoxicology: Concepts and applications, ed. M.C.
Newman and A.W. Mclntosh, pp. 323-262. Lewis Publishers, Chelsea, MI.
22. Borgmann, U., Y.K. Chau, P.T.S. Wong, M. Brown, and J. Yaromich. 1996. Tributyltin
accumulation and toxicity to Hyalella azteca. In Proceedings of the Workshop on Organotin
Compounds in the Canadian Aquatic Environment, ed. R.J. Maguire, Y.K. Chau, and J.A.J.
Thompson, National Water Research Institute, Sidney, British Columbia, February 19-20,1996.
23. Moore, D. W., T.M. Dillon, and B.C. Suedel. 1991. Chronic toxicity of tributyltin to the
marine polychaete worm, Neanthes arenaceodentata. Aquat. Toxicol. 21:181-198.
24. Salazar, M. H., P.B. Duncan, S.M. Salazar, and K.A. Rose. 1995. In-situ bioassays using
transplanted mussels: H Assessing contaminated sediment at a Superfund site in Puget Sound.
In Third Symposium on Environmental Toxicology and Risk Assesment, ed. J.S. Hughes, G.R.
Biddinger, and E. Mones, pp. 242-263. American Society for Testing and Materials,
Philadelphia, PA.
25. Page, D.S., and J. Widdows. 1991. Temporal and spatial variation in levels of alkyltins in
mussel tissues: A lexicological intepretation of field data. Mar. Environ. Res. 32:113-129.
740
-------
BIOACCUMULATION SUMMARY TRIBUTYLTIN
26. Widdows, J., and D.S. Page. 1993. Effects of tributyltin and dibutyltin on the physiological
energetics of the mussel, Mytilus edulis. Mar. Environ. Res. 35:233-249.
27. Salazar, M. H., and S. M. Salazar. 1995. Chapter 15: Mussels as bioindicators: Effects of
TBT on survival, bioaccumulation and growth under natural conditions. In Tributyltin:
Environmental fate and effects, ed. M.A. Champ and P.F. Seligman, pp. 305-330. Chapman
and Hall, New York, NY.
28. Thain, J. E. 1986. Toxicity of TBT to bivalves: Effects on reproduction, growth and survival.
In Proceedings, Oceans 1986 Conference, Organotin Symposium, Vol. 4, pp. 1306-1313.
Washington, DC, September 23-25, 1986.
29. Salazar, M.H., and S.M. Salazar. 1988. Tributyltin and mussel growth in San Diego Bay. In
Proceedings, Oceans 1988 Conference, International Organotin Symposium, Vol. 4, pp. 1188-
1197.
30. Waite, M.E., MJ. Waldock, J.E. Thain, D.S. Smith, D. S., and S.M. Milton. 1991. Reductions
in TBT concentrations in UK estuaries following legislation in 1986 and 1987. Mar. Environ.
Res. 32:89-111.
31. van Slooten, K.B. and J. Tarradellas. 1994. Accumulation, depuration, and growth effects of
tributyltin in the freshwater bivalve Dreissena polymorpha under field conditions. Environ.
Toxicol. Chem. 13:755-762.
32. Schulte-Oehlmann, U., P. Fioroni, J. Oehlmann, and E. Stroben. 1995. Marisa cornuarietis
(Gastropoda, Prosobranchia): A potential TBT bioindicator for freshwater environments.
Ecotoxicology 4:372-384.
33. Davies, I. M., J. Drinkwater, and J.C. McKie. 1988. Effects of tributyltin compounds from
antifoulants on Pacific oysters Crassostrea gigas in Scottish Sea Lochs, U. K. Aquaculture
74(3-4):319-330.
34. Waldock, M.J., M.E. Waite, and J.E. Thain. 1992. Improvements in bioindicator performance
in UK estuaries following the control of the use of antifouling paints. ICES/MEQC Memo
CM1992/E32.
35. Bryan, G.W., P.E. Gibbs, R.J. Huggett, L.A. Curtis, D.S. Bailey, and D.M. Dauer. 1989.
Effects of tributyltin pollution on the mud snail, Ilyanassa obsoleta, from the York River and
Sarah Creek, Chesapeake Bay. Mar. Pollut. Bull. 20(9):458-462.
36. Bryan, G.W., P.E. Gibbs, G.R. Burt, and L.G. Hummerstone. 1987. The effects of tributyltin
(TBT) accumulation on adult dog-whelks, Nucella lapillus: Long-term field and laboratory
experiments. /. Mar. Biol Assoc. UK. 67(3):525-544.
37. Gibbs, P.E., G.W. Bryan, P.L. Pascoe, and G. R. Burt. 1987. The use of the dog-whelk,
Nucella lapillus, as an indicator of tributyltin (TBT) contamination. /. Mar. Biol. Assoc. UK.
67(3):507-524.
741
-------
BIOACCUMULATION SUMMARY TRIBUTYLTIN
38. Gibbs, P.E. and G.W. Bryan. 1995. Reproductive failure and population decline of the
gastropod Nucella lapillus resulting from imposex caused by tributyltin pollution. In
Tributyltin: Environmental fate and effects, ed. M.A. Champ and P.P. Seligman. Chapman and
Hall, New York, NY.
39. Batley, G.E., C. Fuhua, C.I. Brockbank, and KJ. Flegg. 1989. Accumulation of tributyltin by
the Sydney rock oyster, Saccostrea commercialis. Aust. J. Mar. Freshwater Res. 40:49-54.
40. Langston, W.J., and G.R. Burt. 1991. Bioavailability and effects of sediment-bound TBT in
deposit feeding clams, Scrobicularia plana. Mar. Environ. Res. 32(1991):61-77.
41. Rice, C.D., M.M. Barnes, and T.C. Ardel. 1995. Immunotoxicity in channel catfish, Ictalurus
punctatus, following exposure to tributyltin. Arch. Environ. Contain. Toxicol. 28:464-470.
42. Wester, P.W., J.H. Canton, A.A.J. Van lersel, E.I. Krajnc, and H.A.M.G. Vaessen. 1990. The
toxicity of bis(tri-n-butyltin) oxide (TBTO) and di-n-butyltin dichloride (DBTC) in the small
fish species Oryzias latipes (medaka) and Poecilia reticulata (guppy). Aquat. Toxicol. 16:53-
72.
43. Triebskorn, R., H.R. Kohler, J. Flemming, T. Braunbeck, R.-D. Negele, and H. Rahmann.
1994. Evaluation of bis(tri-n-butyltin) oxide (TBTO) neurotoxicity in rainbow trout
(Onchorhynchus mykiss). I. Behaviour, weight increase, and tin content. Aquat. Toxicol.
30:189-197.
44. Schwaiger, J., F. Bucher, H. Ferling, W. Kalbfus, and R.-D. Negele. 1992. A prolonged
toxicity study on the effects of sublethal concentrations of bis(tri-n-butyltin)oxide (TBTO):
Histopathological and histochemical findings in rainbow trout (Oncorhynchus mykiss). Aquat.
Toxicol. 23:31-48.
45. Alzieu, C., and M. Heral. 1984. Ecotoxicological effects of organotin compounds on oyster
culture. In Ecotoxicological testing for the marine environment, ed. G. Persoone, E. Jaspers
and C. Claus, pp. 187-196. State University of Ghent and Institute of Scientific Research,
Bredene, Belgium.
46. Bauer, B., P. Fioroni, I. Ide, S. Liebe, J. Oehlmann, E. Stroben, and B. Watermann. 1995. TBT
wffects on the female genital system on Littorina littorea: A possible indicator of tributyltin
pollution. Hydrobiologia 309: 15-27, 1995.
47. Davies, I.M., J. Drinkwater, J.C. Mckie and P. Balls. 1987. Effects of the use of tributyltin
antifoulants in mariculture. In Proceedings, Oceans 1987 Conference, International Organotin
Symposium, Vol. 4, pp. 1477-1481.
48. Fent, K., and J.J. Stegeman. 1992. Effects of tributyltin in vivo on hepatic cytochrome P450
forms in marine fish. Aquat. Toxicol. 24:219-240.
49. Hodson, P.V., D.G. Dixon, and K.L.E. Kaiser. 1988. Estimating the acute toxicity of
waterborne chemicals in trout from measurements of median lethal dose and the octanol-water
partition coefficient. Environ. Toxicol. Chem. 7:443-454.
742
-------
BIOACCUMULATION SUMMARY TRIBUTYLTIN
50. Horiguchi, T., H. Shiraishi, M. Shimizu, and M. Morita. 1997. Effects of triphenyltin chloride
and five other organotin compounds on the development of imposex in the rock shell, Thais
clavigera. Environmental Pollution, 95(1):85-91.
51. Scammell, M.S., G.E. Batley, and C.I. Brockbank. 1991. A field study of the impact on oysters
of tributyltin introduction and removal in a pristine lake. Arch. Environ. Contain. Toxicol. 20:
276-281.
52. Waldock, M.J., and J.E. Thain. 1983. Shell thickening in Crassostrea gigas: Organotin
antifouling or sediment induced? Mar. Pollut. Bull. 14: 411-415.
53. Wang, W.X., J. Widdows, and D.S. Page. 1992. Effects of organic toxicants on the anoxic
energy metabolism of the mussel Mytilus edulis. Mar. Environ. Res. 34: 327-331.
743
-------
744
-------
BIOACCUMULATION SUMMARY TERBUFOS
Chemical Category: PESTICIDE (ORGANOPHOSPHATE)
Chemical Name (Common Synonyms): TERBUFOS CASRN: 13071-79-9
Chemical Characteristics
Solubility in Water: 15 ppm [ 1 ] Half-Life: No data [2]
Log Kow: No data [3] Log Koc: —
Human Health
Oral RfD: 1.3 x 10~4 mg/kg/day [4] Confidence: Not available, uncertainty factor
= 10
Critical Effect: Inhibition of plasma cholinesterase observed in dogs
Oral Slope Factor: No data [5] Carcinogenic Classification: D [6]
Wildlife
Partitioning Factors: Partitioning factors for terbufos in wildlife were not found in the literature.
Food Chain Multipliers: Food chain multipliers for terbufos in wildlife were not found in the
literature.
Aquatic Organisms
Partitioning Factors: Partitioning factors for terbufos in aquatic organisms were not found in the
literature.
Food Chain Multipliers: Food chain multipliers for terbufos in aquatic organisms were not found in
the literature.
Toxicity/Bioaccumulation Assessment Profile
Terbufos, an organophosphate pesticide, is the active ingredient of Counter [7]. The application of
Counter at the rate of 1.45 kg per hectare resulted in low-level exposure sufficient to induce blood
plasma cholinesterase depressions, but generally not at levels sufficient to cause increased mortality to
bobwhites and cottontails [8]. Turbofos is highly toxic to mammals. The acute oral LD50 for mice (Mus
musculus) was 3.5 mg/kg [9], whereas 63 percent of exposed deer mice [7] were killed at 2.48 mg/kg
dose. The residue of terbufos in live earthworms (1.73 mg/kg) was significantly lower than the residue
(18.1 mg/kg) in dead organisms after a 32-day exposure [10].
745
-------
BIOACCUMULATION SUMMARY TERBUFOS
Acute toxicity, expressed as the 96-h LC50 of terbufos to aquatic species, ranged from 4.7 |ig/L for
Menidia beryllina to 390 |ig/L for Pimephales promelas [11]. Terbufos toxicity in the aquatic
environment is influenced by pH and other physicochemical factors [12]. Experiments conducted with
rainbow trout and Gammarus showed that terbufos was least toxic at pH 7.5, and more toxic at higher
and lower pH. The accumulation factor (AF) for terbufos was influenced by salinity and temperature
[13]. The AF for grass shrimp ranged from 20 at 30 ppt salinity and 22°C to 64 at 25 ppt salinity and
17°C, while the AF for sheepshead minnows ranged from 71 at 15 ppt salinity and 22°C to 287 at 15
ppt salinity and 17°C.
746
-------
Invertebrates
Gammarus
pseudolimnaeus,
Amphipod
Summary of Biological Effects Tissue Concentrations for Terbufos
Species:
Taxa
Concentration, Units in1: Toxicity:
Sediment Water Tissue (Sample Type) Effects
Ability
Log
BCF
to Accumulate2: Source:
Log
BAF
BSAF Reference Comments3
0.168 mg/kg
(whole body)4
Mortality,
ED50
[1
L; lethal to
50% of
animals in
96 hours
Palaemonetes
pugio, Grass
shrimp
0.07 mg/kg
(whole body)4
Mortality,
ED 100
[13]
L; mortality
Fishes
Oncorhynchus
mykiss, Rainbow
trout
4.08 mg/kg
(whole body)4
Mortality,
ED50
[12]
L; lethal to
50% of
animals in
96 hours
Cyprinodon
variegatus,
Sheepshead
minnow
0.11 mg/kg
(whole body)4
Mortality,
ED 100
[13]
L; mortality
1 Concentration units based on wet weight unless otherwise noted.
2 BCF = bioconcentration factor, BAF = bioaccumulation factor, BSAF = biota-sediment accumulation factor.
3 L = laboratory study, spiked sediment, single chemical; F = field study, multiple chemical exposure; other unusual study conditions or observations noted.
4 This entry was excerpted directly from the Environmental Residue-Effects Database (ERED, www.wes.army.mil/el/ered, U.S. Army Corps of Engineers and U.S.
Environmental Protection Agency). The original publication was not reviewed, and the reader is strongly urged to consult the publication to confirm the information
presented here.
-------
BIOACCUMULATION SUMMARY TERBUFOS
References
1. Weast handbook of chemistry andphysics, 68th edition, 1987-1988, B-73. (Cited in: USEPA.
1995. Hazardous Substances Data Bank (HSDB). National Library of Medicine online
(TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental
Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. September.)
2. USEPA. 1989. Chemical fate rate constants for SARA section 313 chemicals and Superfund
Health Manual chemicals. Prepared by Chemical Hazard Assessment Division, Syracuse
Research Corporation, for U.S. Environmental Protection Agency, Office of Toxic Substances,
Exposure Evaluation Division, Washington, DC, and Environmental Criteria and Assessment
Office, Cincinnati, OH. August 11.
3. Karickhoff, S.W., and J.M. Long. 1995. Internal report on summary of measured, calculated,
and recommended log Kow values. Draft. Prepared by U.S. Environmental Protection Agency,
Office of Research and Development, Environmental Research Laboratory-Athens, for E.
Southerland, Office of Water, Office of Science and Technology, Standards and Applied
Science Division, Washington, DC. April 10.
4. USEPA. 1993. Reference dose tracking report. U.S. Environmental Protection Agency, Office
of Pesticide Programs, Health Effects Division, Washington, DC.
5. USEPA. 1997. Integrated Risk Information System (IRIS). National Library of Medicine online
(TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental
Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. June.
6. USEPA. 1992. Classification list of chemicals evaluated for carcinogenicity potential. U.S.
Environmental Protection Agency, Office of Pesticide Programs, Washington, DC.
7. Block, E.K., T.E. Lacher, Jr., and R.J. Kendall. 1993. Effects of the organophosphate pesticide
Counter on laboratory deer mice (Peromyscus maniculatus). Environ. Toxicol. Chem. 12:377-
383.
8. Tank, S.L., L.W. Brewer, M.J. Hooper, G.P. Cobb HI, and R.J. Kendall. 1993. Survival and
pesticide exposure of northern bobwhites (Colinus virginianus) and eastern cottontails
(Sylvilagus floriJanus) on agricultural fields treated with Counter 15G. Environ. Toxicol.
Chem. 12:2113-2120.
9. Berg, G.L. 1982. Farm Chemicals. In Farm chemicals handbook. Meister, Willoughby, OH.
10. Cobb, G.P., E.H. Hoi, P.W. AUen, J.A. Gagne, and R.J. Kendall. 1995. Uptake, metabolism and
toxicity of terbufos in the earthworm (Lumbricus terrestris) exposed to Counter-15G in
artificial soils. Environ. Toxicol. Chem. 14:279-285.
11. Hemmer, M.J., D.P. Middaugh, and V. Comparetta. 1992. Comparative acute sensitivity of
larval topsmelt, Atherinops affinis, and inland silverside, Menidia beryllina, to 11 chemicals.
Environ. Toxicol. Chem. 11:401-408.
748
-------
BIOACCUMULATION SUMMARY TERBUFOS
12. Howe, G.E., L.L. Marking, T.D. Bills, JJ. Rach, and F.L. Mayer, Jr. 1994. Effects of water
temperature and pH on toxicity of terbufos, trichlorfon, 4-nitrophenol and 2,4-dinitrophenol
to the amphipod (Gammarus pseudolimnaeus) and rainbow trout (Oncorhynchus mykiss).
Environ. Toxicol Chem. 13:51-66.
13. Brecken-Folse, J.A., F.L. Mayer, L.E. Pedigo, and L.L. Marking. 1994. Acute toxicity of 4-
nitrophenol, 2,4-dintrophenol, terbufos, and trichlorfon to grass shrimp (Palaemonetes spp.)
and sheepshead minnows (Cyrprinodon variegatus) as affected by salinity and temperature.
Environ. Toxicol. Chem. 13:67-77.
749
-------
750
-------
BIOACCUMULATION SUMMARY
TOTAL PCBs
Chemical Category: POLYCHLORINATED BIPHENYLS
Chemical Name (Common Synonyms): Total PCBs
CASRN: 1336-36-3
Chemical Characteristics
Solubility in Water: See Aroclors
and congeners [1]
Log Kow: —
Half-Life: No data [2,3], See Aroclors
congeners
LogKoc: —
Human Health
Oral RfD: See Aroclors and congeners [4]
Critical Effect: See Aroclors and congeners
Oral Slope Factor: No data [4]
Confidence:
Carcinogenic Classification: 2A [4]
Wildlife
Partitioning Factors: BSAFs were calculated for red-winged blackbird and tree swallow eggs during
a study in the Great Lakes are; with values ranging from 4.2 to 133, as reported in the attached table.
BSAFs for tree swallow nestlings were 6.7 and 9.5.
Food Chain Multipliers: The most toxic congeners have been shown to be selectively accumulated
from organisms at one trophic level to the next [5]. At least three studies have concluded that PCBs
have the potential to biomagnify in food webs based on aquatic organisms and predators that feed
primarily on aquatic organisms [6,7,8]. The results from Biddinger and Gloss [6] and USAGE [8]
generally agreed that highly water-insoluble compounds (including PCBs) have the potential to
biomagnify in these types of food webs. Thomann's [9] model also indicated that highly water-
insoluble compounds (log kow values 5 to 7) showed the greatest potential to biomagnify.
Biomagnification factors of 32 and 93 were determined for total PCBs from alewife to herring gull eggs
and from alewife to whole body herring gull, respectively [10]. A study of arctic marine food chains
measured total PCB biomagnification factors of 3.7 to 8.8 for fish to seal, 7.4 to 13.9 for seal to bear,
and 49.2 for fish to bear [11].
Aquatic Organisms
Partitioning Factors: A log BCF of 3.62 was measured for perch in a Swedish lake [40]. In a study
of several lakes in central Ontario, BSFs for zooplankton ranged from 1.0 to 9.1. Log BAFs for fish
ranged from -0.22 to 0.97, as reported in the summary table, and BSFs from 0.13 to 30 were noted.
751
-------
BIOACCUMULATION SUMMARY
TOTAL PCBs
Log BAFs for crayfish ranged -0.70 to 0.89 and BSFs ranged from 2.0 to 23.7 in the Ontario lakes
study [35]. Log BAFs for clams in that study ranged from -0.05 to 0.32 with BSF values from 2.1 to
10.4.
Food Chain Multipliers: Polychlorinated biphenyls have been demonstrated to biomagnify through
the food web. Oliver and Niimi [12], studying accumulation of PCBs in various organisms in the Lake
Ontario food web, reported concentrations of total PCBs in phytoplankton, zooplankton, and several
species of fish. Their data indicated a progressive increase in tissue PCB concentrations moving from
organisms lower in the food web to top aquatic predators (see following table). In a study of PCB
accumulation in lake trout (Salvelinus namaycush) of Lake Ontario, Rasmussen et al. [13] reported that
each trophic level contributed about a 3.5-fold biomagnification factor to the PCB concentrations in the
trout. In a study of several lakes in Ontario, log biomagnification factors for transfer from zooplankton
to fish ranged from 0.00 to 0.97, as reported in the attached summary table for total PCBs.
Observed and Relative Concentrations of PCBs in Organisms of the Lake Ontario Food
Web [12]
Species
Phytoplankton
Mysids
Pontoporeia affinis
Oligochaetes
Sculpin
Alewife
Smelt
Salmonids
Observed Concentrations (ng/g ww)
50
330
790
180
1600
1300
1400
4300
Relative Concentration
1
6.6
15.8
3.6
32
26
28
86
Toxicity/Bioaccumulation Assessment Profile
PCBs are a group (209 congeners/isomers) of organic chemicals, based on various substitutions of
chlorine atoms on a basic biphenyl molecule. These manufactured chemicals have been widely used
in various processes and products because of the extreme stability of many isomers, particularly those
with five or more chlorines [14]. A common use of PCBs was as dielectric fluids in capacitors and
transformers. In the United States, Aroclor is the most familiar registered trademark of commercial
PCB formulations. Generally, the first two digits in the Aroclor designation indicate that the mixture
contains biphenyls, and the last two digits give the weight percent of chlorine in the mixture.
As a result of their stability and their general hydrophobic nature, PCBs released to the environment
have dispersed widely throughout the ecosystem [14]. PCBs are among the most stable organic
compounds known, and chemical degradation rates in the environment are thought to be slow. As a
result of their highly lipophilic nature and low water solubility, PCBs are generally found at low
concentrations in water and at relatively high concentrations in sediment [15]. Individual PCB
752
-------
BIOACCUMULATION SUMMARY TOTAL PCBs
congeners have different physical and chemical properties based on the degree of chlorination and
position of chlorine substitution, although differences with degree of chlorination are more significant
[15]. Solubilities and octanol-water partition coefficients for PCB congeners range over several orders
of magnitude [16]. Octanol-water partition coefficients, which are often used as estimators of the
potential for bioconcentration, are highest for the most chlorinated PCB congeners.
Dispersion of PCBs in the aquatic environment is a function of their solubility [15], whereas PCB
mobility within and sorption to sediment are a function of chlorine substitution pattern and degree of
chlorination [17]. The concentration of PCBs in sediments is a function of the physical characteristics
of the sediment, such as grain size [18,19] and total organic carbon content [18,19,20,21]. Fine
sediments typically contain higher concentrations of PCBs than coarser sediments because of more
surface area [15]. Mobility of PCBs in sediment is generally quite low for the higher chlorinated
biphenyls [17]. Therefore, it is common for the lower chlorinated PCBs to have a greater dispersion
from the original point source [15]. Limited mobility and high rates of sedimentation could prevent
some PCB congeners in the sediment from reaching the overlying water via diffusion [17].
The persistence of PCBs in the environment is a result of their general resistance to degradation [16].
The rate of degradation of PCB congeners by bacteria decreases with increasing degree of chlorination
[22]; other structural characteristics of the individual PCBs can affect susceptibility to microbial
degradation to a lesser extent [16]. Photochemical degradation, via reductive dechlorination, is also
known to occur in aquatic environments; the higher chlorinated PCBs appear to be most susceptible
to this process [21].
Due to the toxicity, high Kow values, and highly persistent nature of many PCBs, they possess a high
potential to bioaccumulate and exert reproductive effects in higher-trophic-level organisms. Aquatic
organisms have a strong tendency to accumulate PCBs from water and food sources. The log
bioconcentration factor for fish is approximately 4.70 [23]. This factor represents the ratio of
concentration in tissue to the ambient water concentration. Aquatic organisms living in association
with PCB-contaminated sediments generally have tissue concentrations equal to or greater than
the concentration of PCB in the sediment [23]. Once taken up by an organism, PCBs partition
primarily into lipid compartments [15]. Thus, differences in PCB concentration between species and
between different tissues within the same species may reflect differences in lipid content [15]. PCB
concentrations in polychaetes and fish have been strongly correlated to their lipid content [24].
Elimination of PCBs from organisms is related to the characteristics of the specific PCB congeners
present. It has been shown that uptake and depuration rates in mussels are high for lower-chlorinated
PCBs and much lower for higher-chlorinated congeners [25,26]. In some species, tissue
concentrations of PCBs in females can be reduced during gametogenesis because of PCB transfer to
the more lipophilic eggs. Therefore, the transferred PCBs are eliminated from the female during
spawning [27,28]. Fish and other aquatic organisms biotransform PCBs more slowly than other
species, and they appear less able to metabolize, or excrete, the higher chlorinated PCB congeners
[27]. Consequently, fish and other aquatic organisms may accumulate more of the higher-chlorinated
PCB congeners than are found in the environment [15].
The acute toxicity of PCBs appears to be relatively low, but results from chronic toxicity tests indicate
that PCB toxicity is directly related to the duration of exposure [29]. Toxic responses have been noted
to occur at concentrations of 0.03 and 0.014 |ig/L in marine and freshwater environments, respectively
[29]. The LC50 for grass shrimp exposed to PCBs in marine waters for 4 days was 6.1 to 7.8 ug/L
753
-------
BIOACCUMULATION SUMMARY TOTAL PCBs
[29]. Chronic toxicity of PCBs presents a serious environmental concern because of their resistance
to degradation [30], although the acute toxicity of PCBs is relatively low compared to that of other
chlorinated hydrocarbons. Sediment contaminated with PCBs has been shown to elicit toxic responses
at relatively low concentrations. Sediment bioassays and benthic community studies suggest that
chronic effects generally occur in sediment at total PCB concentrations exceeding 370 |ig/kg [31].
A number of field and laboratory studies provide evidence of chronic sublethal effects on aquatic
organisms at low tissue concentrations [16]. Field and Dexter [16] suggest that a number of marine
and freshwater fish species have experienced chronic toxicity at PCB tissue concentrations of less than
1.0 mg/kg and as low as 0.1 mg/kg. Spies et al. [32] reported an inverse relationship between PCB
concentrations in starry flounder eggs in San Francisco Bay and reproductive success, with an effective
PCB concentration in the ovaries of less than 0.2 mg/kg. Monod [33] also reported a significant
correlation between PCB concentrations in eggs and total egg mortality in Lake Geneva char. PCBs
have also been shown to cause induction of the mixed function oxidase (MFO) system in aquatic
animals, with MFO induction by PCBs at tissue concentrations within the range of environmental
exposures [16].
754
-------
Summary of Biological Effects Tissue Concentrations for Total PCBs
Species:
Taxa
Invertebrates
Zooplankton,
(species not named
specifically)
Concentration, Units in1:
Sediment Water
Boshkung 0.93 ng/L
Lake: 27.2; 356
(TOC
normalized)
Hg/kg (dw)
Wood Lake: 1.85 ng/L
15.2; 156
(TOC
normalized)
|ig/kg (dw)
St. Nora Lake: 1.60 ng/L
12; 227 (TOC
normalized)
|ig/kg (dw)
Opeongo Lake: 1 .23 ng/L
53.9; 546
(TOC
normalized)
|ig/kg (dw)
Skugog Lake:
Rice Lake:
Clear Lake:
Toxicity:
Tissue (Sample Type) Effects
11.6, 392 (lipid
normalized) |ig/kg4
3.56, 1030 (lipid
normalized) |ig/kg
4.36, 1550 (lipid
normalized) |ig/kg
6. 11, 766 (lipid
normalized) |ig/kg
Ability to Accumulate2: Source:
Log Log
BCF BAF BSAF Reference Comments3
1.6 [34,35] F; seven lakes in
central Ontario; water
samples are filtered
samples collected
from the water
column at 1 m depth;
BSF values appear in
the BSAF column;
BSF was calculated
as the concentration
of total PCBs (lipid
6.7 basis) divided by the
concentration in
surface sediment
(organic carbon
basis)
9.1
8.5
1.0
-------
Summary of Biological Effects Tissue Concentrations for Total PCBs
Species:
Taxa
Nephtys incisa,
Polychaete worm
Nereis incisa,
Polychaete worm
Concentration, Units in1:
Sediment Water
Stations:
MIC = 385
|ig/kg (dw)
M2B = 325
|ig/kg (dw)
M4 = 1060
|ig/kg (dw)
M5 = 2.73
|ig/kg (dw)
M8 = 1290 |ig
(dw)
M89B = 559
|ig/kg (dw)
Station:
MIC = 385
|ig/kg (dw)
Toxicity:
Tissue (Sample Type) Effects
Stations:
MlC = 314|ig/kg
M2B = 143 ng/kg
M4 = 349|ig/kg
M5 =279|ig/kg
M8 =872|ig/kg
M89B= 153 |ig/kg
Station:
MIC = 326 ng/kg
Ability to Accumulate2: Source:
Log Log
BCF BAF BSAF Reference Comments3
[36] F; sediment samples
from the New York
Bight; total PCB
concentrations were
quantified as a sum of
Aroclor 1242 and
1254
[36] F; sediment samples
from the New York
Bight; total PCB
concentrations were
quantified as a sum of
Aroclor 1242 and
1254
-------
Summary of Biological Effects Tissue Concentrations for Total PCBs
Species:
Taxa
Concentration, Units in1:
Toxicity:
Ability to Accumulate2:
Log Log
Sediment Water Tissue (Sample Type) Effects BCF BAF BSAF
Source:
Reference Comments3
Nereis virens,
Sand worm
Day 180:
4,310±640
|ig/kg (dw)
Day 180:
522±178 |ig/kg
[36] L; sediment from
Passaic River from
four stations was
composited for
bioaccumulation
study with
commercial species;
TOC was 5.7%.
sediment and tissue
(whole body)
concentrations are
mean and SD
concentrations of
three replicate tests
Ninoe nigripes,
Polychaete worm
Stations:
M5 = 2.73
|ig/kg (dw)
M89A= 13.3
|ig/kg (dw)
Ref=33.1
|ig/kg (dw)
Stations:
M5 =48.9|ig/kg
M89A = 402 |ig/kg
MXRef = 176 |ig/kg
[36] F; sediment samples
from the New York
Bight; total PCB
concentrations were
quantified as a sum of
Aroclor 1242 and
1254
-------
Summary of Biological Effects Tissue Concentrations for Total PCBs
Species:
Taxa
Pherusa affinis,
Polychaete worm
Concentration, Units in1:
Sediment Water
Stations:
MIC = 385
|ig/kg (dw)
M4B = 201
|ig/kg (dw)
Tissue
Toxicity:
(Sample Type) Effects
Stations:
MIC = 129 ng/kg
M4B = 107 |ig/kg
Ability to Accumulate2: Source:
Log Log
BCF BAF BSAF Reference Comments3
[36] F; sediment samples
from the New York
Bight; total PCB
concentrations were
quantified as a sum of
Aroclor 1242 and
1254
Polinices duplicatus, Station:
Moon snail M5 = 2.73
|ig/kg (dw)
Station:
M5 = 78.1|ig/kg
[36] F; sediment samples
from the New York
Bight; total PCB
concentrations were
quantified as a sum of
Aroclor 1242 and
1254
Mytilus edulis, 0.14-45|ig/kg 0.045-1.8 2.7-3.2 ng/g
Mussel dw ng/L
Mytilus edulis,
Mussel
0.6 mg/kg
(whole body)5
1.4 mg/kg
(whole body)5
Mortality, NA
Mortality, NA
[64] L; no significant
decrease in anoxic
survival time (control
13 days)
[64] L; decreased anoxic
survival time (control
10.7 days)
-------
Summary of Biological Effects Tissue Concentrations for Total PCBs
Species:
Taxa
Clams
(species not named
specifically)
Concentration, Units in1:
Sediment Water
Boshkung 0.93 ng/L
Lake: 27.2, 356
(TOC
normalized)
Hg/kg (dw)
Wood Lake: 1.85 ng/L
15.2, 156
(TOC
normalized)
|ig/kg (dw)
St. Nora Lake: 1.60 ng/L
12, 227 (TOC
normalized)
|ig/kg (dw)
Opeongo Lake: 1 .23 ng/L
53.9, 546
(TOC
normalized)
|ig/kg (dw)
Rice Lake:
Toxicity: Ability to Accumulate2:
Log Log
Tissue (Sample Type) Effects BCF BAF BSAF
1 .4 mg/kg Physiological,
(whole body)5 NOED
8.16, 2330 (lipid 0.59 6.5
normalized)
l-ig/kg
4.63, 1670 (lipid 0.20 10.4
normalized)
M-8/kg
3.57, 1590 (lipid 0.00 6.9
normalized)
l-ig/kg
6.32, 1630 (lipid 0.32 2.1
normalized)
M-g/kg
-0.05 6.9
Source:
Reference Comments3
[64] L; no significant
changes in adenylate
energy charge or
glycogen content
[34,35] F; six lakes in central
Ontario; water
samples are filtered
samples collected
from the water
column at 1 m depth;
BSF values appear in
the BSAF column;
BSF was calculated
as the concentration
of total PCBs (lipid
basis) divided by the
concentration in
surface sediment
(organic carbon
basis)
Clear Lake
0.46
2.7
-------
ON
O
Summary of Biological Effects Tissue Concentrations for Total PCBs
Species:
Taxa
Corbicula fluminea,
Asian clam
Concentration,
Sediment
2.3 ng/g dw
3.3 ng/g dw
Units in1:
Water
surface
water:
43.2 ng/L
6.4 ng/L
Toxicity:
Tissue (Sample Type) Effects
7,
7,
.6
.2
Hg/g
M-g/g
of lipid
of lipid
Ability
Log
BCF
to Accumulate2:
Log
BAF BSAF
Source:
Reference
[38]
Comments3
F; Rio Santiago
Rio de la Plata,
Argentina
and
Spisula solidissima, Station:
Clam MSB = ND
|ig/kg (dw)
Station:
M5B = 38.1|ig/kg
[36] F; Sediment samples
from the New York
Bight; total PCB
concentrations were
quantified as a sum of
Aroclor 1242 and
1254.
Macoma nasuta,
Clam
Day 180:4310
± 640 |ig/kg
(dw)
Day 120:
68.9 ±10.3|ig/kg
Macoma nasuta,
Bent nose clam
1.7mg/kg
(whole body)5
Behavior,
NOED
[36] L; sediment from
Passaic River from
four stations was
composited for
bioaccumulation
study with
commercial species;
TOC was 5.7%;
sediment and tissue
whole body
concentrations are
mean and SD
concentrations of
three replicate tests
[45] L; no effect on
burrowing behavior
-------
Summary of Biological Effects Tissue Concentrations for Total PCBs
Species:
Taxa
Mercenaria
mercenaria,
Clam
Pitar morrhuana,
Clam
Mya truncata,
Bivalves:
Concentration, Units in1:
Sediment Water
Stations:
M7 = 12.8
Hg/kg (dw)
MXRef=33.1
(J.g/kg (dw)
Station:
M4B = 201
(J.g/kg (dw)
surface
water:
Toxicity:
Tissue (Sample Type) Effects
1 .7 mg/kg Mortality,
(whole body)5 NOED
Stations:
M7 =48.7|ig/kg
MX>Ref=95.7|ig/kg
Station:
M4B = 37.2|ig/kg
Ability to Accumulate2: Source:
Log Log
BCF BAF BSAF Reference Comments3
[45] L; no effect on
mortality
[36] F; sediment samples
from the New York
Bight; total PCB
concentrations were
quantified as a sum of
Aroclor 1242 and
1254
[37] F; sum of 47
congeners in
Orchomene sp.,
Amphipod
0.14-45 ng/kg 0.045-1.8 0.89-2.2 ng/g
dw ng/L
0.14-45 g/kg
dw
0.045-1.8 32-36 ng/g
ng/L
Cambridge Bay,
Northwest
Territories, Canada;
sediment samples
collected from 65
sites over 3 years
-J
ON
-------
Summary of Biological Effects Tissue Concentrations for Total PCBs
Species:
Taxa
Palaemonetes pugio,
Grass shrimp
Concentration, Units in1: Toxicity:
Sediment Water Tissue (Sample Type) Effects
Mean of day 0 Day 28:
and day 180 147±42|ig/kg
replicates:
3,550±1,070
|ig/kg (dw)
Ability to Accumulate2: Source:
Log Log
BCF BAF BSAF Reference Comments3
[36] TOC was 5.7%;
sediment and tissue
whole body
concentrations are
mean and SD
concentrations of
three replicate tests;
early removal of
shrimp to avoid
preying upon other
species (28-day
exposure, not yet
steady state)
My sis relicta,
Opossum Shrimp
1.9 mg/kg
(whole body)5
Behavior,
NOED
[56] L; no effect on
feeding behavior
-------
Summary of Biological Effects Tissue Concentrations for Total PCBs
Species:
Taxa
Concentration, Units in1:
Toxicity:
Ability to Accumulate2:
Sediment
Water Tissue (Sample Type) Effects
Log
BCF
Log
BAF
BSAF
Source:
Reference Comments3
Procambams sp.;
Crayfish
Scugog Lake
Rice Lake
Clear Lake
0.41 23.7 [35] F; three lakes in
-0.70 2.0 central Ontario; water
0.89 7.3 samples are filtered
samples collected
from the water
column at 1 m depth;
BSF values appear in
the BSAF column;
BSF was calculated
as the concentration
of total PCBs (lipid
basis) divided by the
concentration in
surface sediment
(organic carbon
basis)
Callinectes sapidus,
Crab
Station:
M5 =2.73|ig/kg
(dw)
Station: M5 = 69.9
|ig/kg (muscle)
M5=l,870|ig/kg
(hepatopancreas)
[36] F; sediment samples
from the New York
Bight; total PCB
concentrations were
quantified as a sum of
Aroclor 1242 and
1254
Chironomus
riparius, Midge
3.3 mg/kg (whole
body)5
1.1 mg/kg (whole
body)5
Behavior,
NOED
Behavior,
NOED
[57] L; no effect on
swimming behavior
[57] L; no effect on
swimming behavior
-------
o! Summary of Biological Effects
Species: Concentration, Units in1:
Taxa Sediment Water Tissue (Sample Type)
0.3 mg/kg (whole
body)5
Ephemera danica, 1 .5 mg/kg (whole
Mayfly body)5
1 .5 mg/kg (whole
body)5
Tissue Concentrations for Total PCBs
Toxicity: Ability to Accumulate2:
Log Log
Effects BCF BAF BSAF
Behavior,
NOED
Growth,
NOED
Mortality,
NOED
Source:
Reference
[57]
[63]
[63]
Comments3
L; no effect on
swimming behavior
L
L
Asterias rubens,
Starfish
19.2 mg/kg (gonad)5 Reproduction,
LOED
0.146 mg/kg (gonad)5 Development,
LOED
0.324 mg/kg (gonad)5 Development,
LOED
[47] L; concentrations are
ug/g lipid gonadal
indices evaluated
[48] L; estimated wet
weight adult males
[48] L; estimated wet
weight adult females
Fishes
Oncorhynchus
mykiss,
Rainbow trout
50 mg/kg (whole
body)5
100 mg/kg (whole
body)5
200 mg/kg (whole
body)5
Physiological,
LOED
Physiological,
NA
Physiological,
NA
[53]
[53]
[53]
L; mixed function
oxidase induction,
including
benzo(a)pyrene
hydroxylase
induction
-------
Summary of Biological Effects Tissue Concentrations for Total PCBs
Species:
Taxa
Oncorhynchus
tnykiss,
Rainbow trout
Concentration, Units in1:
Sediment Water Tissue (Sample Type)
0.29 mg/kg (whole
body)5
0.56 mg/kg (whole
body)5
1.3 mg/kg (fat)5
2.2 mg/kg (Fat)5
2.2 mg/kg (fat)5
1.3 mg/kg (fat)5
1.7 mg/kg (fat)5
1.3 mg/kg (fat)5
Toxicity: Ability to Accumulate2:
Log Log
Effects BCF BAF BSAF
Physiological,
ED50
Physiological,
ED50
Physiological,
ED30
Physiological,
ED30
Physiological,
ED30
Physiological,
ED30
Physiological,
ED35
Physiological,
ED35
Source:
Reference
[54]
[54]
[61]
[61]
[61]
[61]
[61]
[61]
Comments3
L; internal dose used
as tissue
concentration;
induction of aryl
hydrocarbon
hydroxylase (AHH)
L; 30% decrease in
hemoglobin content
relative to control
L; 30% increase in
liver size relative to
control
L; 30% decrease in
hemoglobin content
relative to control
L; 30% increase in
liver size relative to
control
L; 35% increase in
kidney size relative to
control
L; 35% increase in
kidney size relative to
control
-j
ON
-------
ON
ON
Summary of Biological Effects Tissue Concentrations for Total PCBs
Species:
Taxa
Oncorhynchus
kisutch,
Coho salmon
Oncorhynchus
tshawytscha,
Chinook salmon
Concentration, Units in1:
Sediment Water Tissue (Sample Type)
2.2 mg/kg (fat)5
1.3 mg/kg (fat)5
645 mg/kg (whole
body)5
43 mg/kg (carcass)5
43 mg/kg (carcass)5
9.8 mg/kg (carcass)5
9.8 mg/kg (carcass)5
3.5 mg/kg
(whole body)5
3.5 mg/kg
(whole body)5
Toxicity: Ability to Accumulate2:
Log Log
Effects BCF BAF BSAF
Growth, ED40
Growth, ED40
Mortality,
ED100
Morphology,
LOED
Physiological,
LOED
Morphology,
NOED
Physiological,
NOED
Cellular,
LOED
Growth,
NOED
Source:
Reference
[61]
[61]
[60]
[55]
[55]
[55]
[55]
[52]
[52]
Comments3
L; 40% decrease in
growth relative to
control
L; 40% decrease in
growth relative to
control
L; radiolabeled -
contaminated food
fed
L; decrease in
hepatosomatic index
L; lipid levels in
carcass decreased
L; no decrease in
hepatosomatic index
L; no effect on lipid
levels in carcass
L; structure changes
in intestine cells,
increased exfoliation
of mucosa, mucosal
cell inclusions
L; no effect on
weight gain
-------
Summary of Biological Effects Tissue Concentrations for Total PCBs
Species:
Taxa
Salmo salar,
Atlantic salmon
Salmonids
Concentration, Units in1:
Sediment Water Tissue (Sample Type)
30 mg/kg
(whole body)5
Toxicity:
Effects
Mortality,
NOED
Ability
Log
BCF
to Accumulate2:
Log
BAF BSAF
7.81 (log 1.85
BAF)
Source:
Reference
[46]
[12]
Comments3
L; no effect on
mortality
F
Salvelinus
namaycush,
Lake trout
0.31 mg/kg (eggs)
Salvelinus
namaycush,
Lake trout
Boshkung 0.93 ng/L
Lake: 27.2; 356
(TOC
normalized)
|ig/kg (dw)
St. Nora Lake: 1.6 ng/L
12; 227 (TOC
normalized)
|ig/kg (dw)
Opeongo Lake: 1.23 ng/L
53.9; 546
(TOC
normalized)
|ig/kg (dw)
87.6, 1,550 (lipid
normalized) |ig/kg
17.4, 2,460 (lipid
normalized) |ig/kg
48.8, 2,100 (lipid
normalized) |ig/kg
Egg hatchabil-
ity reduced by
57% and fry
survival reduced
by 19% relative
to the control.
0.41 4.3
0.20 10.7
0.43 3.*
[39] L; Total PCB was
measured as Aroclor
1284; total DDT in
eggs was 0.15 mg/kg
which was also
significantly higher
than in controls
[34,35] F; four lakes in
central Ontario; water
samples are filtered
samples collected
from the water
column at 1 m depth;
BSF values appear in
the BSAF column;
BSF was calculated
as the concentration
of total PCBs (lipid
basis) divided by the
concentration in
surface sediment
(organic carbon
basis)
-------
ON
oo
Summary of Biological Effects Tissue Concentrations for Total PCBs
Species:
Taxa
Salvenliniis
namaycush,
Lake trout
Concentration, Units in1:
Sediment Water Tissue (Sample Type)
Clear Lake:
2.3 mg/kg
(whole body)5
2.4 mg/kg
(whole body)5
1.8 mg/kg
(whole body)5
0.76 mg/kg
(whole body)5
2.1 mg/kg
(whole body)5
0.76 mg/kg
(whole body)5
Toxicity:
Effects
Growth,
LOED
Growth,
LOED
Growth,
LOED
Growth,
NOED
Growth,
NOED
Growth,
NOED
Ability to Accumulate2: Source:
Log Log
BCF BAF BSAF Reference
0.97 8.8
[58]
[58]
[58]
[58]
[58]
[58]
Comments3
L; PCB dosed with
acetone carrier;
enhanced growth
(weight only; not
length)
L; PCB dosed with
acetone carrier;
enhanced growth
(weight and length)
L; PCB with no
acetone carrier;
enhanced growth
(weight and length)
L; PCB dosed with
acetone carrier; no
effect on growth
(weight or length)
L; PCB with no
acetone carrier; no
effect on growth
(weight or length)
L; on growth (weight
or length)
-------
Summary of Biological Effects Tissue Concentrations for Total PCBs
Species: Concentration, Units in1:
Taxa Sediment Water Tissue (Sample Type)
0.76 mg/kg
(whole body)5
2.3 mg/kg
(whole body)5
2.4 mg/kg
(whole body)5
0.76 mg/kg
(whole body)5
2.1 mg/kg
(whole body)5
1.8 mg/kg
(whole body)5
1.5 mg/kg (eggs)5
Toxicity: Ability to Accumulate2:
Log Log
Effects BCF BAF BSAF
Mortality,
NOED
Mortality,
NOED
Mortality,
NOED
Mortality,
NOED
Mortality,
NOED
Mortality,
NOED
Reproduction,
LOED
Source:
Reference
[58]
[58]
[58]
[58]
[58]
[58]
[59]
Comments3
L; PCB dosed with
acetone carrier; no
effect on mortality
L; PCB dosed with
acetone carrier; no
effect on mortality
L; PCB dosed with
acetone carrier; no
effect on mortality
L; PCB with no
acetone carrier; no
effect on mortality
L; PCB with no
acetone carrier; no
effect on mortality
L; PCB with no
acetone carrier; no
effect on mortality
L
Myoxocephaliis
quadircornis,
Four horn sculpin
surface
water:
0.14-45|ig/kg 0.045-1.8 7.3-230 ng/g (whole
dw ng/L body excluding liver)
12-1,300 (liver)
[37]
F; 2-4 individuals of
each species of
sculpin were pooled
to make a sample
from each site
-------
-J
o
Summary of Biological Effects Tissue Concentrations for Total PCBs
Species:
Taxa
Myoxocephalus
scorpiiis,
Short-horn sculpin
Concentration, Units in1:
Sediment Water
0.14-45|ig/kg 0.045-1.8
dw ng/L
Toxicity:
Tissue (Sample Type) Effects
1.4-38 ng/g (whole
body excluding liver)
5.5-220 (liver)
Ability to Accumulate2: Source:
Log Log
BCF BAF BSAF Reference Comments3
Gadosogac, 0.14-45|ig/kg 0.045-1.8 4.4-39 ng/g (whole
Greenland cod dw ng/L body excluding liver)
100-2,500 (liver)
F; analyzed as
individual fish
Salvelinus alpinus,
Arctic char
Prochilodus
platensis
0.14-45|ig/kg 0.045-1.8 3.4-3.5 ng/g (whole
dw ng/L body excluding liver)
5.1-7.8 (liver)
3 ng/g dw 13.8 ng/L 6.7, 17.8, 9.2 |ig/g of
lipid (muscle)
[38]
F; analyzed as
individual fish
F; Rio Santiago and
Rio de la Plata,
Argentina
Pimelodits albicans 3 ng/g dw
13.8 ng/L 3.3 |ig/g of lipid
(muscle)
Oligoscarcus jenynsi 58 ng/g dw
42.3 ng/L 4.1 |ig/g of lipid
(muscle)
Carassius auratus,
Goldfish
253 mg/kg
(whole body)5
271 mg/kg
(whole body)5
Mortality, ED50
Mortality, ED50
[51] L; lethal body burden
[51] L; lethal body burden
-------
Summary of Biological Effects Tissue Concentrations for Total PCBs
Species:
Taxa
Notemigonvs
crysoleiicas, Golden
shiner
Concentration, Units in1:
Sediment Water
Boshkung 0.93 ng/L
Lake: 27.2; 356
(TOC
normalized)
|ig/kg (dw)
Wood Lake: 1.85 ng/L
15.2; 156
(TOC
normalized)
|ig/kg (dw)
St. Nora Lake: 1.60 ng/L
12; 227 (TOC
normalized)
|ig/kg (dw)
Toxicity: Ability to Accumulate2:
Log Log
Tissue (Sample Type) Effects BCF BAF BSAF
293 mg/kg Mortality, ED50
(whole body)5
324 mg/kg Mortality, ED50
(whole body)5
250 mg/kg Mortality, ED50
(whole body)5
256 mg/kg Mortality, ED50
(whole body)5
250 mg/kg Behavior,
(whole body)5 LOED
250 mg/kg Morphology,
(whole body)5 LOED
5.44,642 (lipid 0.04 1.8
normalized) |ig/kg
4.25, 1170 (lipid 0.04 7.3
normalized) |ig/kg
5.20,683 (lipid -0.22 3.0
normalized) |ig/kg
Source:
Reference Comments3
[51] L; lethal body burden
[51] L; lethal body burden
[51] L; lethal body burden
[51] L; lethal body burden
[51] L; loss of appetite,
lack of coordination
[51] L; color changes
[34,35] F; six lakes in central
Ontario; water
samples are filtered
samples collected
from the water
column at 1 m depth;
BSE values appear in
the BSAF column;
BSE was calculated
as the concentration
of total PCBs (lipid
basis) divided by the
concentration in
surface sediment
(organic carbon
basis)
-------
Summary of Biological Effects Tissue Concentrations for Total PCBs
Species:
Taxa
Concentration, Units in1: Toxicity:
Sediment Water Tissue (Sample Type) Effects
Ability to Accumulate2:
Log
BCF
Log
BAF
BSAF
Source:
Reference Comments
OpeongoLake: 1.23ng/L 11.9,482 (lipid
53.9; 546 normalized) |ig/kg
(TOC
normalized)
|ig/kg (dw)
Rice Lake:
-0.22
0.9
-0.40
2.9
Clear Lake:
-1.00
0.13
Phoxiniis phoxinus,
Minnow
1.6 mg/kg
(whole body)5
170 mg/kg
(whole body)5
170 mg/kg
(whole body)5
15 mg/kg
(whole body)5
170 mg/kg
(whole body)5
Behavior,
LOED
Growth,
LOED
Mortality,
LOED
Reproduction,
LOED
Reproduction,
NA
[43] L; changes in feeding
behavior
[43] L; increased growth
[43] L; doubling of
mortality rate
compared to controls
after 300 days
[43] L; reduction in time
to hatch, fry death
[43] L; 85% reduction in
hatchability of eggs
-------
Summary of Biological Effects Tissue Concentrations for Total PCBs
Species:
Taxa
Pimephales
notatus, Bluntnose
minnow
Lepomis
macrochirus,
Concentration, Units in1:
Sediment Water
Boshkung 0.93 ng/L
Lake: 27.2; 356
(TOC
normalized)
|ig/kg (dw)
Wood Lake: 1.85 ng/L
15.2; 156
(TOC
normalized)
|ig/kg (dw)
St. Nora Lake: 1.60 ng/L
12; 227 (TOC
normalized)
|ig/kg (dw)
Opeongo Lake: 1 .23 ng/L
53.9; 546
(TOC
normalized)
|ig/kg (dw)
Scugog Lake:
Clear Lake:
Toxicity: Ability to Accumulate2:
Log Log
Tissue (Sample Type) Effects BCF BAF BSAF
9.78, 1130 (lipid 0.28 3.1
normalized) |ig/kg
6.24, 446 (lipid -0.40 2.8
normalized) |ig/kg
10.4, 993 (lipid -0.22 4.3
normalized) |ig/kg
7.96, 893 (lipid 0.08 1.6
normalized) |ig/kg
0.23 13.2
1.20 13.8
0.6 mg/kg Physiological,
(muscle)5 ED50
Source:
Reference Comments3
[34,35] F; six lakes in central
Ontario; water
samples are filtered
samples collected
from the water
column at 1 m depth;
BSF values appear in
the BSAF column;
BSF was calculated
as the concentration
of total PCBs (lipid
basis) divided by the
concentration in
surface sediment
(organic carbon
basis)
[49] L; inhibition of Mg-
ATPase activity
Bluegill
-------
Summary of Biological Effects Tissue Concentrations for Total PCBs
Species:
Taxa
Concentration, Units in1:
Toxicity:
Ability to Accumulate2:
Sediment
Water Tissue (Sample Type) Effects
Log
BCF
Log
BAF
BSAF
Source:
Reference Comments3
Morone saxatilis,
Striped bass
4.4 mg/kg
(whole body)5
Growth,
NOED
[65] L; parental exposure
to PCBs in field, then
post yolk absorption
exposure of immature
to PCB contaminated
brine shrimp; no
significant change in
growth
Micropterus
dolomieu,
Smallmouth bass
356
Boshkung
Lake: 27.2
(TOC
normalized)
Hg/kg (dw)
Wood Lake:
15.2; 156
(TOC
normalized)
|ig/kg (dw)
St. Nora Lake:
12; 227 (TOC
normalized)
|ig/kg (dw)
Opeongo Lake
53.9; 546
(TOC
normalized)
|ig/kg (dw)
Scugog Lake:
Rice Lake:
Clear Lake:
9.3 ng/L
1.85ng/L
1.60 ng/L
1.23 ng/L
25.5, 2420 (lipid
normalized) |ig/kg
6.17, 1160 (lipid
normalized)|ig/kg
35.4, 2910 (lipid
normalized)|ig/kg
4.77, 2200 (lipid
normalized)|ig/kg
0.6 6.7
0,04 7.3
0.28
0.46
-0.22
0.26
0.60
12.7
4.0
5.1
15.5
3.8
[34,35] F; seven lakes in
central Ontario; water
samples are filtered
samples collected
from the water
column at 1 m depth;
BSF values appear in
the BSAF column;
BSF was calculated
as the concentration
of total PCBs (lipid
basis) divided by the
concentration in
surface sediment
(organic carbon
basis)
-------
Summary of Biological Effects Tissue Concentrations for Total PCBs
Species:
Taxa
Percaflavescens,
Yellow perch
Concentration, Units in1:
Sediment Water
Boshkung 0.93 ng/L
Lake: 27.2; 356
(TOC
normalized)
|ig/kg (dw)
Wood Lake: 1.85 ng/L
15.2; 156
(TOC
normalized)
|ig/kg (dw)
St. Nora Lake: 1.60 ng/L
12; 227 (TOC
normalized)
|ig/kg (dw)
Opeongo Lake: 1 .23 ng/L
53.9; 546
(TOC
normalized)
|ig/kg (dw)
Scugog Lake:
Rice Lake:
Clear Lake:
Toxicity:
Tissue (Sample Type) Effects
11.4, 4260 (lipid
normalized) |ig/kg
8.76, 3440 (lipid
normalized) |ig/kg
8.43, 3 140 (lipid
normalized) |ig/kg
4.98, 33 10 (lipid
normalized) |ig/kg
Ability to Accumulate2:
Log Log
BCF BAF BSAF
0.86 11.8
0.52 26.8
0.30 13.7
0.63 6.0
0.52 30
-0.30 4.4
0.84 6.6
Source:
Reference Comments3
[34,35] F; seven lakes in
central Ontario; water
samples are filtered
samples collected
from the water
column at 1 m depth;
BSF values appear in
the BSAF column;
BSF was calculated
as the concentration
of total PCBs (lipid
basis) divided by the
concentration in
surface sediment
(organic carbon
basis)
-------
-J
ON
Summary of Biological Effects Tissue Concentrations for Total PCBs
Species:
Taxa
Concentration, Units in1:
Toxicity:
Ability to Accumulate2:
Log Log
Sediment Water Tissue (Sample Type) Effects BCF BAF BSAF
Source:
Reference Comments3
Percafluviatilis,
Perch
Surface 825 ng/g 3.62
water: (geometric mean)
8.6 ng/L (513-1,244)
(geometric
mean)
(4.2-20.8)
[40] F; fat % = 2.3, SD =
0.6. Fish and water
were sampled in Lake
Jarnsjon, Sweden.
PCBs in water were
measured
continuously in
summer and autumn
(concentration
reflects both
dissolved and
particulate). Ten fish
were collected.
Fundulus
heteroclitus,
Mummichog
10 mg/kg
(whole body)5
32 mg/kg
(whole body)5
100 mg/kg
(whole body)5
0.32 mg/kg
(whole body)5
1 mg/kg
(whole body)5
3.2 mg/kg
(whole body)5
Physiological,
LOED
Physiological,
LOED
Physiological,
not applicable
Physiological,
NOED
Physiological,
NOED
Physiological,
NOED
[50] L; induction of
ethoxyresorufin O-
deethylase (EROD)
[50] L; induction of
cytochrome P4501a
[50] L; hepatic enzyme
induction (P4501 &
EROD)
[50] L; no induction of
hepatic enzymes
[50] L; no induction of
hepatic enzymes
[50] L; no induction of
hepatic enzymes
-------
Summary of Biological Effects Tissue Concentrations for Total PCBs
Species:
Taxa
Platyichthes
stellatus,
Starry flounder
Concentration, Units in1:
Sediment Water Tissue (Sample Type)
<0.2 mg/kg (eggs)
Toxicity:
Effects
Reduced
reproductive
success
Ability
Log
BCF
to Accumulate2:
Log
BAF BSAF
Source:
Reference
[32]
Comments3
F; field-collected fish
injected with carp
pituitary extract to
induce final stages of
gametogenesand
spawning; in the
field, the fish were
exposed to sediments
contaminated with
PCBs, DDT, and
PAHs
Pleuronectes
americanus,
Winter flounder
7.1 mg/kg
(whole body)5
Growth,
LOED
[44] L; reduced length and
weight of larvae
Limanda limanda,
Dab
0.0181 mg/kg
(muscle)5
0.0181 mg/kg
(muscle)5
Biochemical,
LOED
Biochemical,
LOED
[62] L; total cytochrome
P450 levels
significantly different
from control / sum of
CB 77,105,118,156)
[62] L; 7-ethoxyresorutin-
O-deethylase
(EROD) activity
significantly different
from control/sum of
CB congeners 77,
105, 118, 156)
-------
Summary of Biological Effects Tissue Concentrations for Total PCBs
Species:
Taxa
Concentration, Units in1:
Toxicity:
Ability to Accumulate2:
Sediment
Water Tissue (Sample Type) Effects
Log
BCF
Log
BAF
BSAF
Source:
Reference Comments3
Wildlife
0.0181 mg/kg
(muscle)5
Biochemical,
LOED
[62] L; Cytochrome
P4501a(CYPIA)
levels significantly
different from
control/sum of CB
congeners??, 105,
118, 156)
Haliaeetus
leucocephalus,
Bald eagle
fish tissue (diet in
natural system):
interior fish = 0.2
mg/kg
shoreline fish =2.1
mg/kg
NOAEC at 4.0
mg/kg (egg),
0.14 mg/kg
(fish);
egg lethality
from diet of
interior fish at
0.2 mg/kg,
shoreline fish at
2.1 mg/kg
[10]
-------
Summary of Biological Effects Tissue Concentrations for Total PCBs
Species:
Taxa
Agelaius phoeniceus,
Red-winged
blackbird (eggs)
Tachycineta bicolor,
Tree swallow
(nestlings)
(eggs)
Concentration, Units in1:
Sediment Water
7.4 ng/g
TOC=2.5%
32.6 ng/g
TOC=21.0%
68.2 ng/g
TOC=7.5%
147.7 ng/g
TOC=12%
28.1 ng/g
TOC-18.5%
144.1 ng/g
TOC=11.5%
2.3 ng/g
TOC-10.5%
2.9 ng/g
TOC=13.8%
8.0 ng/g
TOC=11.1%
11.1 ng/g
TOC-23.9%
144.1 ng/g
TOC=11.5%
2.9 ng/g
TOC=13.8%
144.1 ng/g
TOC=11.5%
2.9 ng/g
TOC=13.8%
Toxicity:
Tissue (Sample Type) Effects
223.5 ng/g
50.1 ng/g
54.6 ng/g
52.7 ng/g
163.5 ng/g
247.8 ng/g
105.9 ng/g
64.9 ng/g
108.3 ng/g
8 1.8 ng/g
(whole body minus
feet, beak, wings, and
feathers)
754.5 ng/g
11. 2 ng/g
1,0 19.7 ng/g
254.6 ng/g
Ability to Accumulate2:
Log Log
BCF BAF BSAF
16.4
5.8
6.0
4.2
22.4
6.6
102.8
64.4
31.3
38.3
9.5
6.7
15.2
133.1
Source:
Reference Comments3
[41] F; Great Lakes/St.
Lawrence River
basin; 12 wetlands
sites; sediment
concentration
reported as wet
weight concentration
which may be a typo-
graphical error
[41] F; Great Lakes/St.
Lawrence River
basin; 12 wetlands
sites; sediment
concentration
reported as wet
weight concentration
which may be a typo-
graphical error
-------
So Summary of Biological Effects Tissue Concentrations for Total PCBs
Species: Concentration, Units in1: Toxicity: Ability
Log
Taxa Sediment Water Tissue (Sample Type) Effects BCF
to Accumulate2: Source:
Log
BAF
BSAF Reference Comments3
Mustela vison,
Ranch mink, (fed
PCB -contaminated
Cypriniis carpio
carp)
NOAEL (control
group)
0.09 |ig PCBs/g liver
tissue
<5.00 pg TEQ/g liver
tissue
LOAEL(10%carpin
diet group)
2.19|igPCBs/gliver
tissue
496 pg TEQ/g liver
tissue
In general, carp diets caused impaired
reproduction and/or reduced survival
of kits; compared to controls. Kits
body weight was significantly reduced
in the 20 and 40% carp groups; kit
body weight and survival in the 10 and
20% carp groups were significantly
reduced at three and six weeks of age.
Females fed 40% carp whelped the
fewest number of kits, all of which
were stillborn or died within 24 hours.
Weight of kits and % kit survival to
age 6 weeks were inversely
proportional to % carp in
mothers'diets; physical abnormalities
and a dose-related decrease in relative
organ weights were also observed in
kits
[43] L; concentration of
total PCBs in carp
/percent carp in diet
per treatment group:
0.015mg-PCBs/kg-
diet/0%
0.72 mg-PCBs/kg-
diet/10%
1.53mg-PCBs/kg-
diet/20%
2.56 mg-PCBs/kg-
diet/40%; carp also
contained 2,3,7,8-
TCDD with resulting
diet concentrations of
1.03, 19.41,40.02,
and 80.76 ng-
TEQs/kg diet in the
0, 10, 20, and 40%
diet exposures; mink
exposed prior to and
throughout
reproductive period
1 Concentration units based on wet weight unless otherwise noted.
2 BCF = bioconcentration factor, BAF = bioaccumulation factor, BSAF = biota-sediment accumulation factor.
3 L = laboratory study, spiked sediment, single chemical; F = field study, multiple chemical exposure; other unusual study conditions or observations noted.
4 Wet weight calculated assuming a dry weight of 25% of the total weight in paper.
5 This entry was excerpted directly from the Environmental Residue-Effects Database (ERED, www.wes.army.mil/el/ered, U.S. Army Corps of Engineers and U.S.
Environmental Protection Agency). The original publication was not reviewed, and the reader is strongly urged to consult the publication to confirm the information
presented here.
-------
BIOACCUMULATION SUMMARY TOTAL PCBs
References
1. Eisler, R. 1986. Poly chlorinated biphenyl hazards to fish, wildlife, and invertebrates: A synoptic
review. U.S. Fish Wildl. Serv. Biol. Rep. 85(1.7).
2. Mackay, D., W.Y. Shiu, and K.C. Ma. 1992. Illustrated handbook of physical-chemical
properties and environmental fate for organic chemicals. Vol. 1, Monoaromatic hydrocarbons,
chlorobenzenes, and PCBs. Lewis Publishers, Boca Raton, FL.
3. USEPA. 1989. Chemical fate rate constants for SARA section 313 chemicals and Sup erfund
Health Evaluation Manual chemicals. Prepared by Chemical Hazard Assessment Division,
Syracuse Research Corporation, for U.S. Environmental Protection Agency, Office of Toxic
Substances, Exposure Evaluation Division, Washington, DC, and Environmental Criteria and
Assessment Office, Cincinnati, OH. August 11.
4. USEPA. 1995. Integrated Risk Information System (IRIS). National Library of Medicine online
(TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental
Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. September.
5. Jones, P.O., J.P. Giesy, T.J. Kubiak, D.A. Verbrugge, J.C. Newstead, J.P. Ludwig, D.E. Tillit,
R. Crawford, N. De Galan, and G.T. Ankley. 1993. Biomagnification of bioassay-derived 2, 3,
7, 8-tetrachlorodibenzo-p-dioxin equivalents. Chemosphere 26:1203-1212.
6. Biddinger, G.R., and S.P. Gloss. 1984. The importance of trophic transfer in the bioaccumulation
of chemical contaminants in aquatic ecosystems. Residue Rev. 91:103-145.
7. Kay, S.H. 1984. Potential for biomagnification of contaminants within marine and freshwater
food webs. Technical Report D-84-7. U.S. Army Corps of Engineers, Waterways Experiment
Station, Vicksburg, MS.
8. USAGE. 1995. Trophic transfer and biomagnification potential of contaminants in aquatic
ecosystems. Environmental Effects of Dredging, Technical Notes EEDP-01-33. U.S. Army
Corps of Engineers, Waterways Experiment Station, Vicksburg, MS.
9. Thomann, R.V. 1989. Bioaccumulation model of organic chemical distribution in aquatic food
chains. Environ. Sci. Technol. 23:699.
10. Braune, B.M., And R.J. Norstrom. 1989. Dynamics of organochlorine compounds in herring
gulls: III. Tissue distribution and bioaccumulation in Lake Ontario Gulls. Environ. Toxicol.
Chem. 8:957-968.
11. Muir, D.C.G., R.J. Norstrom, and M. Simon. 1988. Organochlorine contaminants in arctic
marine food chains: Accumulation of specific polychlorinated biphenyls and chlordane-related
compounds. Environ. Sci. Technol. 22:1071-1079.
12. Oliver, E.G., and AJ. Niimi. 1988. Trophodynamic analysis of polychlorinated biphenyl
congeners and other chlorinated hydrocarbons in the Lake Ontario ecosystem. Environ. Sci.
Technol. 22:388-397.
781
-------
BIOACCUMULATION SUMMARY TOTAL PCBs
13. Rasmussen, J.B., DJ. Rowan, D.R.S. Lean, and J.H. Carey. 1990. Food chain structure in
Ontario lakes determines PCB levels in lake trout (Salvelinus namaycush) and other pelagic fish.
Can. J. Fish. Aquat. Sci. 47:2030-2038.
14. Rand, G. M., P. G. Wells, and L. S. McCarty. 1995. Chapter 1. Introduction to aquatic
toxicology. In Fundamentals of aquatic toxicology: Effects, environmental fate, and risk
assessment, ed. G. M. Rand, pp. 3-67. Taylor and Francis, Washington, DC.
15. Phillips, DJ.H. 1986. Use of organisms to quantify PCBs in marine and estuarine environments.
In PCBs and the Environment, ed. J.S. Waid, pp.127-182. CRC Press, Inc., Boca Raton, FL.
16. Field, L. J., and R. N. Dexter. 1998. A discussion of PCB target levels in aquatic sediments.
Unpublished document. January 11.
17. Fisher, J.B., R.L. Petty, and W. Lick. 1983. Release of polychlorinated biphenyls from
contaminated lake sediments: Flux and apparent diffusivities of four individual PCBs. Environ.
Pollut. 5B: 121-132.
18. Pavlou, S.P., and R.N. Dexter. 1979. Distribution of polychlorinated biphenyls (PCB) in
estuarine ecosystems: Testing the concept of equilibrium partitioning in the marine environment.
Environ. Sci. Technol. 13:65-71.
19. Lynch, T.R., and H.E. Johnson. 1982. Availability of hexachlorobiphenyl isomer to benthic
amphipods from experimentally contaminated sediments. In Aquatic Toxicology and Hazard
Assessment: Fifth Conference, ASTM STP 766, ed. J.G. Pearson, R.B. Foster, and W.E. Bishop,
pp. 273-287. American Society of Testing and Materials, Philadelphia, PA.
20. Chou, S.F.J., and R.A. Griffin. 1986. Solubility and soil mobility of polychlorinated biphenyls.
In PCBs and the environment, ed. J.S. Waid, Vol. 1, pp. 101-120. CRC Press, Inc., Boca Raton,
FL.
21. Sawhney, B.L. 1986. Chemistry and properties of PCBs in relation to environmental effects.
In PCBs and the environment, ed. J.S. Waid, pp. 47-65. CRC Press, Inc., Boca Raton, FL.
22. Furukawa, K. 1986. Modification of PCBs by bacteria and other microorganisms. In PCBs and
the Environment, ed. J.S. Waid, Vol. 2, pp. 89-100. CRC Press, Inc. Boca Raton, FL.
23. Neff, J.M. 1984. Bioaccumulation of organic micropollutants from sediments and suspended
particulates by aquatic animals. Fres. Z. Anal. Chem. 319:132-136.
24. Shaw, G. R., and D. W. Connell. 1982. Factors influencing concentrations of polychlorinated
biphenyls in organisms from an estuarine ecosystem. Aust. J. Mar. Freshw. Res. 33:1057-1070.
25. Tanabe, S., R. Tatsukawa, and D.J.H. Phillips. 1987. Mussels as bioindicators of PCB pollution:
A case study on uptake and release of PCB isomers and congeners in green-lipped mussels
(Perna viridis) in Hong Kong waters. Environ. Pollut. 47:41-62.
782
-------
BIOACCUMULATION SUMMARY TOTAL PCBs
26. Pruell, R. J., J. L. Lake, W. R. Davis, and J. G. Quinn. 1986. Uptake and depuration of organic
contaminants by blue mussels (Mytilus edulis) exposed to environmentally contaminated
sediments. Mar. Biol 91:497-508.
27. Lech, J.J., and R.E. Peterson. 1983. Biotransformation and persistence of polychlorinated
biphenyls (PCBs) in fish. In PCBs: Human and environmental hazards, ed. P.M. D'ltri and M.A.
Kamrin, pp. 187-201. Ann Arbor Science Publishers, Inc., Ann Arbor, MI.
28. Stout, V.F. 1986. What is happening to PCBs? Elements of effective environmental monitoring
as illustrated by an analysis of PCB trends in terrestrial and aquatic organisms. In PCBs and the
Environment, ed. J.S. Waid. CRC Press, Inc., Boca Raton, FL.
29. USEPA. 1980. Ambient water quality criteria document: Polychlorinated biphenyls. EPA
440/5-80-068. (Cited in USEPA. 1996. Hazardous Substances Data Bank (HSDB). National
Library of Medicine online (TOXNET). U.S. Environmental Protection Agency, Office of Health
and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH.
February.)
30. Mearns, A.J., M. Malta, G. Shigenaka, D. MacDonald, M. Buchman, H. Harris, J. Golas, and G.
Lauenstein. 1991. Contaminant trends in the Southern California Bight: Inventory and
assessment. Technical Memorandum NOAA ORCA 62. National Oceanic and Atmospheric
Administration. Seattle, WA.
31. 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. NOAA Tech. Memo. NOS
OMA 52. National Oceanic and Atmospheric Administration, Seattle, WA.
32. Spies, R. B., D. W. Rice, Jr., P. A. Montagna, and R. R. Ireland. 1985. Reproductive success,
xenobiotic contaminants and hepatic mixed-function oxidase (MFO) activity in Platichthys
stellatus populations from San Francisco Bay. Mar. Environ. Res. 17:117-121.
33. Monod, G. 1985. Egg mortality of Lake Geneva char (Salvelinus alpinus) contaminated by PCB
and DDT derivatives. Bull. Environ. Contain. Toxicol. 35:531-536.
34. Macdonald, C.R., and C.D. Metcalf. 1991. Concentration and distribution of PCB congeners in
isolated Ontario lakes contaminated by atmospheric deposition. Can. J. Fish. Aquat. Sci. 48:371-
381.
35. Macdonald, C.R., C. D. Metcalfe, G. C. Balch, and T. L. Metcalfe. 1993. Distributions of PCB
congeners in seven lake systems: Interactions between sediment and food-web transport. Environ.
Toxicol. Chem. 12:1991-2003.
36. Pruell, R.J., N.I. Rubinstein, B.K. Taplin, J.A. LiVolsi, and C.B. Norwood. 1990. 2,3,7,8-
TCDD, 2, 3, 7, 8-TCDF and PCBs in marine sediments and biota: Laboratory and field studies.
Final Report to U.S. Army Corps of Engineers, New York District. U.S. Environmental
Protection Agency, Environmental Research Laboratory, Narragansett, RI.
783
-------
BIOACCUMULATION SUMMARY TOTAL PCBs
37. Bright, D.A., S.L. Grundy, and K.J. Reimer. 1995. Differential bioaccumulation of non-ortho
substituted and other PCB congeners in coastal arctic invertebrates and fish. Environ. Set
Technol 29:2504-2512.
38. Columbo, J.C., M.F. Khalil, M. Arnac, and A.C. Horth. 1990. Distribution of chlorinated
pesticides and individually polychlorinated biphenyls in biotic and abiotic compartments of the
Rio de la Plata, Argentina. Environ. Sci. Technol. 24(498-505).
39. Mac, M.J., and C.C. Edsall. 1991. Environmental contaminants and the reproductive success of
lake trout in the Great Lakes: An epidemiological approach. /. Toxicol Environ. Contain.
Toxicol. 27:368-375.
40. Bremle, G., L. Okla, and P. Larsson. 1995. Uptake of PCBs in fish in a contaminated river
system: Bioconcentration factors measured in the field. Environ. Sci. Technol. 29:2010-2015.
41. Bishop, C.A., M.D. Koster, A.A. Chek, D.J.T. Hussell, and K. Jock. 1995. Chlorinated
hydrocarbons and mercury in sediments, red-winged blackbirds (Agelaius phoeniceus) and tree
swallows (Tachycineta bicolor) from wetlands in the Great Lakes-St. Lawrence River basin.
Environ. Toxicol. Chem. 14:491-501.
42. Heaton, S.N., S.J. Bursian, J.P. Giesy, D.E. Tillitt, J.A. Render, P.O. Jones, D.A. Verbrugge, T.J.
Kubiak, and R.J. Aulerich. 1995. Dietary exposure of mink to carp from Saginaw Bay,
Michigan. 1. Effects on reproduction and survival, and the potential risks to wild mink
populations. Arch. Environ. Contain. Toxicol. 28:334-343.
43. Bengtsson, B.E. 1980. Long-term effects of PCB (Clophen A50) on growth, reproduction and
swimming performance in the minnow, Phoxinus phoxinus. Water Res. 14:681-687.
44. Black, D.E., O.K. Phelps, and R.L. Lapan. 1988. The effect of inherited contamination on egg
and larval winter flounder, Pseudopleuronectes americanus. Mar. Environ. Res. 25:45-62.
45. Boese, B.L., M. Winsor, H. Lee Li, S. Echols, J. Pelletier, and R. Randall. 1995. PCB congeners
and hexachlorobenzene biota sediment accumulation factors for Macoma nasuta exposed to
sediments with different total organic carbon contents. Environ. Toxicol. Chem. 14:303-310.
46. Carlberg, G.E., K. Martinsen, A. Kringstad, E. Gjessing, M. Grande, T. Kallqvist and J.U. Skare.
1986. Influence of aquatic humus on the bioavailability of chlorinated micropollutants in Atlantic
salmon. Arch. Environ. Contain. Toxicol. 15:543-548.
47. Den Besten, P.J., H.J. Herwig, A.C. Smaal, D.I. Zandee, and P.A. Voogt. 1990. Interference of
polychlorinated biphenyls (Clophen A50) with gametogenesis in the sea star, IL. Aquat. Toxicol.
18:231-246.
48. Den Besten, P.J., H.J. Herwig, D.I. Zandee, and P.A. Voogt. 1989. Effects of cadmium and PCBs
on reproduction of the sea star Asterias rubens: Aberrations in the early development. Exotox.
Environ. Saf. 18:173-180.
784
-------
BIOACCUMULATION SUMMARY TOTAL PCBs
49. Desaiah, D., L.K. Cutkomp, H.H. Yap, and R.B. Koch. 1972. Inhibition of oligomycin-sensitive
and -insensitive magnesium adenosine triphosphatase activity in fish by polychlorinated
biphenyls. Biochem. Pharmacol. 21:857-865.
50. Gallagher, K., P.A. Van Veld, R.C. Hale, and JJ.Stegeman. 1995. Induction of cytochrome
P4501a in the mummichog (Fundulus heteroclitus) by the polychlorinated terphenyl formulation
Aroclor 5432. Environ. Toxicol Chem. 14:405-409.
51. Hattula, M.L. and O. Karlog. 1972. Toxicity of polychlorinated biphenyls (PCB) to goldfish. Acta
Pharmacol Toxicol. 31:238-240.
52 Hawkes, J.W., E.H. Gruger, Jr., and O.P. Olson. 1980. Effects of petroleum hydrocarbons and
chlorinated biphenyls on the morphology of the intestine of chinook salmon (Onchorhynchus
tshawytscha). Environ. Res. 23:149-161.
53. Hermens, J.L., S.P. Bradbury and SJ. Broderius. 1990. Influence of cytochrome P450 mixed-
function oxidase induction on the acute toxicity to rainbow trout (Salmo gairdneri) of primary
aromatic amines. Ecotox. Environ. Saf. 20:156-166.
54. Janz, D.M., and C.D. Metcalfe. 1991. Relative induction of aryl hydrocarbon hydroxylase by
2,3,7,8-TCDD and two coplanar PCBs in rainbow trout (Oncorhynchus mykiss). Environ.
Toxicol. Chem. 10:917-923.
55. Leatherland, J.F., B.A. Sonstegard, and N.V. Holdrient. 1979. Effect of dietary mirex and PCBs
on hepatosomatic index, liver lipid, carcass lipid and PCB and mirex bioaccumulation in yearling
coho salmon, Oncorhynchus kisutch. Comp. Biochem. Physiol. 63c:243-246.
56. Lester, D.C., and A. Mcintosh. 1994. Accumulation of polychlorinated biphenyl congeners from
Lake Champlain sediments by Mysis relicta. Environ. Toxicol. Chem. 13:1825-1841.
57. Lydy, M.J., K.A. Bruner, D.M. Fry, and S.W. Fisher. 1990. Effects of sediment and the route of
exposure on the toxicity and accumulation of neutral lipophilic and moderately water soluble
metabolizable compounds in the midge, Chironomus Riparius. In Aquatic toxicology and risk
assessment, W.G. Landis et al., Vol 13, pp. 140-164.
58. Mac, M.J., and J.G. Seelye. 1981. Potential influence of acetone in aquatic bioassays testing the
dynamics and effects of PCBs. Bull. Environ. Contain. Toxicol. 27:359-367.
59. Mac, M.J., and T.R. Swartz. 1992. Investigations into the effects of PCB congeners on
reproduction in lake trout from the Great Lakes. Chemosphere 25 (1-2):189-192.
60. Mayer, F.L., P.M. Mehrle, and H.O. Sanders. 1977. Residue dynamics and biological effects of
polychlorinated biphenyls in aquatic organisms. Arch. Environ. Contain. 5:501-511.
61. Poels, C.L.M., M.A. van Der Gaag, J.F.J. van de Kerkhoff, 1980. An investigation into the long-
term effect of Rhine water on rainbow trout. Water Res. 14:1029-1033.
785
-------
BIOACCUMULATION SUMMARY TOTAL PCBs
62 Sleiderink, H.M., J.M. Everaarts, A. Goksoyr, and J.P. Boon. 1995. Hepatic cytochrome P4501A
induction in dab (Limanda limandd) after oral dosing with the polychlorinated biphenyl mixture
Clophen A40. Environ. Toxicol Chem. 14(4):679-687.
63. Sodergren, A., and B. Svensson. 1973. Uptake and accumulation of DDT and PCB by
Ephemera danica (Ephemeroptera) in continuous-flow systems. Bull. Environ. Contain. Toxicol.
9(6).
64. Velduizen-Tsoerkan, M.B., D.A. Holwerda, and D.I. Zandee. 1991. Anoxic survival time and
metabolic parameters as stress indices in sea mussels exposed to cadmium or polychlorinated
biphenyls. Arch. Environ. Contain. Toxicol. 20: 259-265.
65. Westin, D.T., C.E. Olney, and B.A. Rogers. 1983. Effects of parental and dietary PCBs on
survival, growth, and body burdens of larval striped bass. Bull. Environm. Contam. Toxicol.
30:50-57.
786
-------
BIOACCUMULATION SUMMARY
TOXAPHENE
Chemical Category: PESTICIDE (ORGANOCHLORINE)
Chemical Name (Common Synonyms): TOXAPHENE
CASRN: 8001-35-2
Chemical Characteristics
Solubility in Water: 3.0 mg/Lat room
temperature [1].
Log Kow: 5.50 [3]
Half-Life: No data [2]
Log Koc: 5.41 L/kg organic carbon
Human Health
Oral RfD: 3.6 x 10'4 mg/kg/day [4]
Confidence: Not available, uncertainty
factor = 100.
Critical Effect: Hepatocellular tumors in mice and thyroid tumors in rats
Oral Slope Factor: 1.1 x 10+0 per(mg/kg)/day [5] Carcinogenic Classification: B2 [5]
Wildlife
Partitioning Factors: Partitioning factors for toxaphene in wildlife were not found in the literature.
Food Chain Multipliers: Food chain multipliers for toxaphene in wildlife were not found in the
literature.
Aquatic Organisms
Partitioning Factors: Toxaphene is a complex mixture of more than 180 chlorinated bornanes. The
composition of toxaphene which changes markedly appears to be caused by chemical transformation
processes [6]. Toxaphene persistence and degradation in water and biota is modified by numerous and
disparate biological and abiotic factors [7]. In lakes, toxaphene persistence was related to depth,
stratification, and turnover. Toxaphene can persist in water from several months to more than nine years
[8]. Log BCFs for toxaphone ranged from 3.52 for white mullet [10] to 4.72 for fathead minnow [7], as
reported in the following table.
Food Chain Multipliers: Biomagnification of toxaphene was demonstrated in 16 species collected in
lakes in northeastern Louisiana [9]. The highest residues (1.7 to 5.5 mg/kg ww) were measured among
tertiary consumers, such as green-backed heron, spotted gar, and largemouth bass. Secondary consumers
(bluegill, blacktail shiner) contained lower toxaphene residues (0.9 to 1.2 mg/kg ww), whereas primary
consumers, including crayfish and shad, contained lowest levels (0.6 to 1.0 mg/kg ww).
787
-------
BIOACCUMULATION SUMMARY TOXAPHENE
Toxicity/Bioaccumulation Assessment Profile
Since toxaphene represents a complex mixture of nearly 200 compounds, it is difficult to relate observed
toxicity to a specific complex of toxaphene compounds. Fewer than 6 percent of the total number of
toxaphene components have been isolated and individually examined for toxicity [10]. Isensee et al. [11]
separated toxaphene into nine fractions on a silica gel column. Only the first two fractions and last two
fractions revealed reduced toxicity compared with the unfractionated toxaphene, while the middle five
fractions were as toxic as or more toxic than the original pesticide. Although chlorinated hydrocarbons
have low solubility in water, they are readily absorbed by oils, waxes, and fats [12]. Therefore, toxaphene
is generally more toxic to aquatic organisms than are other insecticides and herbicides. Acute toxicity
for freshwater fish species range from 3 to 50 |ig/L [13]. A concentration as low as 5 |ig/L toxaphene
can reduce a population of small fish in lakes without affecting the population of large fish [14].
Freshwater fishes of the Arroyo Colorado accumulated up to 31.5 mg/kg wet weight while fish-eating
birds contained only up to 3 mg/kg of toxaphene [15]. Unlike fishes, avian species readily metabolize and
excrete toxaphene.
Toxaphene compounds have been found in environmental samples and tissues in the Canadian Northern
Territories. The toxicity of toxaphene components present in fish and mammals from Yukon Territory
is unknown [16]. Toxaphene components are present in northern animals in concert with a suite of other
organic contaminants, but neither the risks to the animals bearing the residues nor the risks to people
consuming the animals are known.
788
-------
Summary of Biological Effects Tissue Concentrations for Toxaphene
Species: Concentration, Units in1:
Taxa Sediment Water
Invertebrates
Crassostrea
virginica, Eastern
oyster
Crassostrea
virginica, Eastern
oyster
Palaemonetes pugio,
Grass shrimp
Toxicity:
Tissue (Sample Type) Effects
85 mg/kg Growth, ED27
(whole body)4
47 mg/kg Growth, ED34
(whole body)4
199 mg/kg Growth, ED64
(whole body)4
409 mg/kg Growth, ED96
(whole body)4
2.7 mg/kg Mortality, ED25
(whole body)4
3.3 mg/kg Mortality, ED53
(whole body)4
9.7 mg/kg Mortality, ED68
(whole body)4
Ability to Accumulate2: Source:
Log Log
BCF BAF BSAF Reference
4.52 [7]
[18]
[18]
[18]
[18]
[18]
[18]
[18]
Comments3
F
L; tissue
analyses on
survivors
L; tissue
analyses on
survivors
L; tissue
analyses on
survivors
L; tissue
analyses on
survivors
L; tissue
analyses on
survivors
L; tissue
analyses on
survivors
L; tissue
analyses on
survivors
-------
vo Summary of Biological
Species: Concentration, Units in1:
Taxa Sediment Water Tissue (Sample
4.8 mg/kg
(whole body)4
8.1 mg/kg
(whole body)4
Penaeiis duorarum, 0.36 mg/kg
Pink shrimp (whole body)4
0.54 mg/kg
(whole body)4
0.83 mg/kg
(whole body)4
1.7 mg/kg
(whole body)4
Effects Tissue Concentrations for Toxaphene
Toxicity: Ability to Accumulate2:
Log Log
Type) Effects BCF BAF BSAF
Mortality, ED70
Mortality, ED75
Mortality, ED 15
Mortality, ED20
Mortality, ED65
Mortality, ED90
Source:
Reference Comments3
[18] L; tissue
analyses on
survivors
[18] L; tissue
analyses on
survivors
[18] L; tissue
analyses on
survivors
[18] L; tissue
analyses on
survivors
[18] L; tissue
analyses on
survivors
[18] L; tissue
analyses on
survivors
Fishes
Salvelinusfontinalis,
Brook trout
4.00
[7]
-------
Summary of Biological Effects Tissue Concentrations for Toxaphene
Species: Concentration, Units in1:
Taxa Sediment Water
Salvelinusfontinalis,
Brook trout
Tissue (Sample Type)
1 mg/kg
(whole body)4
3.7 mg/kg
(whole body)4
0.4 mg/kg
(whole body)4
0.6 mg/kg
(whole body)4
9.2 mg/kg
(whole body)4
38 mg/kg
(whole body)4
4.5 mg/kg
(whole body)4
Toxicity:
Effects
Development, LOED
Development, LOED
Growth,
LOED
Growth,
LOED
Development, NA
Development, NA
Development, NA
Ability to Accumulate2: Source:
Log Log
BCF BAF BSAF Reference
[21]
[21]
[21]
[21]
[21]
[21]
[21]
Comments3
L; backbone
development
adversely
affected,
collagen
content
decreased
L; reduced
growth of fry
L; backbone
development
adversely
affected,
collagen
content
decreased
L; backbone
development
adversely
affected,
collagen
content
decreased
-------
Summary of Biological Effects Tissue Concentrations for Toxaphene
Species: Concentration, Units in1:
Taxa Sediment Water Tissue (Sample Type)
18 mg/kg
(whole body)4
2.2 mg/kg
(whole body)4
8.3 mg/kg
(whole body)4
1.8 mg/kg
(whole body)4
2.6 mg/kg
(whole body)4
0.9 mg/kg
(whole body)4
1 .4 mg/kg
(whole body)4
0.2 mg/kg
(whole body)4
2.6 mg/kg
(whole body)4
Toxicity: Ability to Accumulate2:
Log Log
Effects BCF BAF BSAF
Development, NA
Development, NA
Development, NA
Growth, NA
Growth, NA
Growth, NA
Growth, NA
Development, NOED
Development, NOED
Source:
Reference
[21]
[21]
[21]
[21]
[21]
[21]
[21]
[21]
[21]
Comments3
L; backbone
development
adversely
affected,
collagen
content
decreased
L; reduced
growth of fry
L; reduced
growth of fry
L; no effect
on backbone
development
Pimephales
promelas, Fathead
minnow
52000
[7]
-------
Summary of Biological Effects Tissue Concentrations for Toxaphene
Species:
Taxa
Pimephales
promelas, Fathead
minnow
Concentration, Units in1:
Sediment Water Tissue (Sample Type)
5.9 mg/kg
(whole body)4
5.9 mg/kg
(whole body)4
52 mg/kg
(whole body)4
13 mg/kg
(whole body)4
22 mg/kg
(whole body)4
52 mg/kg
(whole body)4
13 mg/kg
(whole body)4
Toxicity:
Effects
Development, LOED
Growth,
LOED
Mortality, LOED
Development, NA
Development, NA
Development, NA
Growth, NA
Ability to Accumulate2: Source:
Log Log
BCF BAF BSAF Reference
[20]
[20]
[20]
[20]
[20]
[20]
[20]
Comments3
L; significant
reduction in
bone
development,
bone collagen
in 150 days
L; significant
reduction in
growth, both
length and
weight
L; increased
mortality after
150 days
L; significant
reduction in
bone
development,
bone collagen
in 150 days
L; significant
reduction in
growth, both
length and
weight
-------
-~J
-f^
Summary of Biological Effects Tissue Concentrations for Toxaphene
Species: Concentration, Units in1:
Taxa Sediment Water
Cyprinodon
variegatus,
Sheepshead minnow
Cyprinodon
variegatus,
Sheepshead minnow
Cyprinodon
variegatus,
Sheepshead minnow
Toxicity:
Tissue (Sample Type) Effects
22 mg/kg Growth, NA
(whole body)4
52 mg/kg Growth, NA
(whole body)4
4.1 mg/kg Mortality, ED25
(whole body)4
35 mg/kg Mortality, ED85
(whole body)4
2.4 mg/kg Mortality, NOED
(whole body)4
10 mg/kg Behavior,
(whole body)4 LOED
Ability to Accumulate2: Source:
Log Log
BCF BAF BSAF Reference
[20]
[20]
4.32-4.49 [17]
[18]
[18]
[18]
[22]
Comments3
L; significant
reduction in
growth, both
length and
weight
L; significant
reduction in
growth, both
length and
weight
L
L; tissue
analyses on
survivors
L; tissue
analyses on
survivors
L; tissue
analyses on
survivors
L; decreased
swimming
activity
-------
Summary of Biological Effects Tissue Concentrations for Toxaphene
Species:
Taxa
Fundulus similis,
Longnose killifish
Fundulus similis,
Longnose killifish
Concentration, Units in1:
Sediment Water Tissue (Sample Type)
36 mg/kg
(whole body)4
36 mg/kg
(whole body)4
10 mg/kg
(whole body)4
19.3 mg/kg
(whole body)4
10 mg/kg
(whole body)4
0.9 mg/kg
(whole body)4
46.6 mg/kg
(whole body)4
24.7 mg/kg
(whole body)4
34 mg/kg
(whole body)4
Toxicity:
Effects
Behavior, NA
Mortality, NA
Mortality, NOED
Mortality, ED 15
Mortality, ED 17
Mortality, ED25
Mortality, EDS 5
Mortality, EDS 5
Mortality, ED53
Ability to Accumulate2: Source:
Log Log
BCF BAF BSAF Reference
[22]
[22]
[22]
4.59 [17]
[18]
[18]
[18]
[18]
[18]
[18]
Comments3
L; decreased
swimming
activity
L; 90%
mortality in
28 days
L; no effect
on mortality
L
L; fish are fry
(test 2)
L; fish are fry
(test 1)
L; fish are
adults
L; fish are fry
(test 2)
L; fish are
juveniles
L; fish are fry
(test 1)
-------
Summary of Biological Effects Tissue Concentrations for Toxaphene
Species: Concentration, Units in1:
Taxa Sediment Water
Leiostomus 0.7 \ig/L
mnthiims, Spot 0.8 \iglL,
2.4 ng/L
Mugil curema, 0.7 \ig/L
White mullet
0.8 ng/L
2.4 ng/L
4.1 Hg/L
Lagodow
rhomboides, Pinfish
Toxicity:
Tissue (Sample Type) Effects
102 mg/kg Mortality, ED95
(whole body)4
0.5 mg/kg Mortality,
(whole body)4 NOED
8 mg/kg Mortality,
(whole body)4 NOED
8.8 mg/kg Mortality,
(whole body)4 NOED
2.9 |ig/g wet wt
0.9 |ig/g wet wt
8.4 |ig/g wet wt
4.0 |ig/g wet wt
2.6 |ig/g wet wt
10.4 |ig/g wet wt
27.0 |ig/g wet wt
1.9 mg/kg Mortality, ED25
(whole body)4
Ability to Accumulate2: Source:
Log Log
BCF BAF BSAF Reference
[18]
[18]
[18]
[18]
3.61 [10]
[10]
[10]
3.76 [10]
3.52 [10
3.63 [10]
3.82 [10]
[18]
Comments3
L; fish are
juveniles
L; fish are
adults
L; fish are fry
(test 1)
L; fish are fry
(test 2)
L
L
L
L
L
L
L
L; tissue
analyses on
survivors
-------
Summary of Biological Effects Tissue Concentrations for Toxaphene
Species: Concentration, Units in1:
Taxa Sediment Water
Ictaliims punctatus,
Channel catfish
Tissue (Sample Type)
1.6mg/kg
(whole body)4
1.2mg/kg
(whole body)4
1.8mg/kg
(whole body)4
1.2mg/kg
(whole body)4
0.8 mg/kg
(whole body)4
1.8 mg/kg
(whole body)4
14 mg/kg
(whole body)4
5.4 mg/kg
(whole body)4
14 mg/kg
(whole body)4
5.4 mg/kg
(whole body)4
Toxicity: Ability to Accumulate2:
Log Log
Effects BCF BAF BSAF
Mortality,
NOED
Cellular,
LOED
Growth,
LOED
Physiological, LOED
Cellular, NA
Cellular, NA
Cellular, NA
Cellular, NA
Growth, NA
Growth, NA
Source:
Reference
[18]
[19]
[19]
[19]
[19]
[19]
[19]
[19]
[19]
[19]
Comments3
L; tissue
analyses on
survivors
L; skin and
liver lesions
L; reduction
in growth
L; hepatic
enzyme
induction
L; skin and
liver lesions
L; skin and
liver lesions
L; skin and
liver lesions
L; skin and
liver lesions
L; reduction
in growth
L; reduction
in growth
-J
vo
-J
-------
Summary of Biological Effects Tissue Concentrations for Toxaphene
Species: Concentration, Units in1:
Taxa Sediment Water Tissue (Sample Type)
0.8 mg/kg
(whole body)4
1.8 mg/kg
(whole body)4
14 mg/kg
(whole body)4
5.4 mg/kg
(whole body)4
1.2 mg/kg
(whole body)4
0.8 mg/kg
(whole body)4
Toxicity:
Effects
Physiological, NA
Physiological, NA
Physiological, NA
Physiological, NA
Growth,
NOED
Growth,
NOED
Ability to Accumulate2: Source:
Log Log
BCF BAF BSAF Reference
[19]
[19]
[19]
[19]
[19]
[19]
Comments3
L; hepatic
enzyme
induction
L; hepatic
enzyme
induction
L; hepatic
enzyme
induction
L; hepatic
enzyme
induction
L; no effect
on growth
L; no effect
on growth
1 Concentration units based on wet weight unless otherwise noted.
2 BCF = bioconcentration factor, BAF = bioaccumulation factor, BSAF = biota-sediment accumulation factor.
3 L = laboratory study, spiked sediment, single chemical; F = field study, multiple chemical exposure; other unusual study conditions or observations noted.
4 This entry was excerpted directly from the Environmental Residue-Effects Database (ERED, www.wes.army.mil/el/ered, U.S. Army Corps of Engineers and U.S.
Environmental Protection Agency). The original publication was not reviewed, and the reader is strongly urged to consult the publication to confirm the information
presented here.
-------
BIOACCUMULATION SUMMARY TOXAPHENE
References
1. Worthing. 1987. Pesticide manual, 8th ed., p. 119. (Cited in: USEPA. 1995. Hazardous
Substances Data Bank (HSDB). National Library of Medicine online (TOXNET). U.S.
Environmental Protection Agency, Office of Health and Environmental Assessment,
Environmental Criteria and Assessment Office, Cincinnati, OH. September.)
2. USEPA. 1989. Chemical fate rate constants for SARA section 313 chemicals and Superfund
Health Manual chemicals. Prepared by Chemical Hazard Assessment Division, Syracuse
Research Corporation, for U.S. Environmental Protection Agency, Office of Toxic Substances,
Exposure Evaluation Division, Washington, DC, and Environmental Criteria and Assessment
Office, Cincinnati, OH. August 11.
3. Karickhoff, S.W., and J.M. Long. 1995. Internal report on summary of measured, calculated,
and recommended log Kow values. Draft. Prepared by U.S. Environmental Protection Agency,
Office of Research and Development, Environmental Research Laboratory-Athens, for E.
Southerland, Office of Water, Office of Science and Technology, Standards and Applied Science
Division, Washington, DC. April 10.
4. USEPA. 1996. Toxaphene: Drinking water health advisory. U.S. Environmental Protection
Agency, Office of Water, Washington, DC. September.
5. SEPA. 1995. Integrated Risk Information System (IRIS). National Library of Medicine online
(TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental
Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. June.
6. Saleh, M.A., and J.E. Casida. 1978. Reductive dechlorination of the toxaphene component 2,2,5-
endo,6-exo,8,9,10-heptachlorobornane in various chemical, photochemical, and metabolic
systems. /. Agric. Food Chem. 26:583-590.
7. Eisler, R., and J. Jacknow. 1985. Toxaphene hazards to fish, wildlife, and invertebrates: A
synoptic review. U.S. Fish Wildl. Serv. Biol. Rep. 85(1.4), U.S. Department of the Interior,
Laurel, MD.
8. Cohen, D.B., G.W. Bowes, and S.M. Ali. 1982. Toxaphene. California State Water Research
Control Board Toxic Substances Control Program, Spec. Proj. Rep. pp. 82-143.
9. Niethammer, K.R., T.S. Baskett, and D.H. White. 1984. Organochlorine residues in three heron
species as related to diet and age. Bull. Environ. Contam. Toxicol. 33:491-498.
10. Harder, H.H., T.V. Carter, and T.F. Bidleman. 1983. Acute effects of toxaphene and its
sediment-degraded products on estuarine fish. Can. J. Fish. Aquat. Sci. 40:2119-2125.
11. Isensee, A.R., G.E. Jones, J.A. McCann, and E.G. Pitcher. 1979. Toxicity and fate of nine
toxaphene fractions in an aquatic model ecosystem. /. Agric. Food Chem. 27:1041-1046.
12. Holden, A.V. 1964. The possible effects on fish of chemicals used in agriculture. /. Proc. Inst.
Sewage Purif. 1964:361-368.
799
-------
BIOACCUMULATION SUMMARY TOXAPHENE
13. Johnson, D.W. 1968. Pesticides and fishes: A review of selected literature. Trans. Amer. Fish.
Soc. 97:398-424.
14. Fukano, K.G., and F.F. Hooper. 1958. Toxaphene as a selective fish poison. Prog. Fish-Cult.
20:189-190.
15. White, D.H., C.A. Mitchell, H.D. Kennedy, AJ. Krynitsky, and M.A. Ribick. 1983. Elevated
DDE and toxaphene residues in fishes and birds reflect local contamination in the lower Rio
Grande Valley, Texas. Southwest Natur. 28:325-333.
16. Lockhart, W.L., M.A. Saleh, A.H. El Sebae, N. Doubleday, M. Evans, B. Jansson, V. Jerome,
J.B. Walker, and J. Witteman. 1993. Report of working group on toxicology of chlorinated
bornane compounds. Chemosphere 27:1841-1848.
17. Schimmel, S.C., J.M. Patrick, Jr., and J. Forester. 1977. Uptake and toxicity of toxaphene in
several estuarine organisms. Arch. Environ. Contain. Toxicol. 5:353-367.
18. Schimmel, S.C., J.M. Patrick, and J. Forester. 1976. Heptachlor: Toxicity to and uptake by
several estuarine organisms. /. Toxicol. Environ. Health 1:955-965.
19. Mayer, F.L., P.M. Mehrle, and P.L. Crutcher. 1978. Interactions of toxaphene and vitamin C in
channel catfish. Trans. Amer. Fish. Soc. 107:326-333.
20. Mehrle, P.M., and F.L. Mayer, Jr. 1975. Toxaphene effects on growth and bone composition
of fathead minnows, Pimephales promelas. J. Fish. Res. Ed. Can. 32:593-598.
21. Mehrle, P.M., and F.L. Mayer, Jr. 1975. Toxaphene effects on growth and development of brook
trout (Salvelinusfontinalis). J. Fish. Res. Ed. Can. 32:609-613.
22. Goodman, L.R., D.J. Hansen, J.A. Couch, and J. Forester. 1977. Effects of heptachlor and
toxaphene on laboratory-reared embryos and fry of the sheepshead minnow. Proceedings, 30th
Annual Conference, Southeastern Association of Fish and Wildlife Agencies, pp. 192-202.
800
-------
BIOACCUMULATION SUMMARY ZINC
Chemical Category: METAL
Chemical Name (Common Synonyms): ZINC CASRN: 7440-66-6
Chemical Characteristics
Solubility in Water: Insoluble [1] Half-Life: Not applicable, stable [1]
LogKow: — LogKoc: —
Human Health
Oral RfD: 3 x 10"1 mg/kg/day [2] Confidence: Medium, uncertainty factor = 3
Critical Effect: 47 percent decrease in erythrocyte superoxide dismutase concentration, also decreased
serum ferritin and hematocrit values, in adult human females after 10 weeks of zinc exposure; lowered
HDL-cholesterol values in human males after several weeks of zinc exposure
Oral Slope Factor: No data [2] Carcinogenic Classification: D [2]
Wildlife
Partitioning Factors: Partitioning factors for zinc in wildlife were not found in the literature.
Food Chain Multipliers: Food chain multipliers for zinc in wildlife were not found in the literature.
Aquatic Organisms
Partitioning Factors: Zinc in the water column can partition to dissolved and particulate organic carbon.
Water hardness (i.e., calcium concentration), pH, and metal speciation are important factors in controlling
the water column concentrations of zinc since the divalent zinc ion is believed to be responsible for
observed biological effects [17]. Bioavailability of zinc in sediments is controlled by the AVS
concentration [18].
Food Chain Multipliers: Most studies reviewed contained data which suggest that zinc is not a highly
mobile element in aquatic food webs, and there appears to be little evidence to support the general
occurrence of biomagnification of zinc within marine or freshwater food webs [3]. A log
biomagnification factor of 2.90 was determined for the midge Chironomus riparius [3].
801
-------
BIOACCUMULATION SUMMARY ZINC
Toxicity/Bioaccumulation Assessment Profile
Zinc does not appear to be a highly mobile element under typical conditions in most aquatic habitats.
Tissue residue-toxicity relationships can also be variable because organisms sequester metals in different
forms that are measurable as tissue residue but can actually be stored in unavailable forms within the
organism as a form of detoxification [4,5]. Whole-body residues also might not be indicative of effects
concentrations at the organ level because concentrations in target organs, such as the kidneys and liver,
can be 20 times greater than whole body residues [6]. The application of "clean" chemical analytical and
sample preparation techniques is also critical in the measurement of metal tissue residues. After
evaluating the effects of sample preparation techniques on measured concentrations of metals in the edible
tissue of fish, Schmitt and Finger [7] concluded that there was little direct value in measuring copper,
zinc, iron, or manganese tissue residues in fish because they do not bioaccumulate to any appreciable
extent. It has also been suggested that there is no compelling evidence to support inordinate concern
about zinc as a putative toxic agent in the environment, and in fact there is considerable evidence that zinc
deficiency is a serious, worldwide human health problem that outweighs the potential problems associated
with accidental, self-imposed, or environmental exposure to zinc excess [8].
802
-------
Summary of Biological Effects Tissue Concentrations for Zinc
Species:
Taxa
Invertebrates
Invertebrates,
field-collected
Tubificidae,
Oligochaete worm
Nereis diversicolor,
Polychaete worm
Concentration, Units in1:
Sediment Water
Total SEM
Hg/g ng/g
10,100 8,873 18900 |ig/L
911 700 1180|ig/L
631 408 187|ig/L
734 562 189 |ig/L
365 294 132 |ig/L
29 <15 <70 |ig/L
2,560 |ig/g
UlOjig/g
3,180|ig/g
3,210 |ig/g
2,550 ng/g
339 |ig/g
140 ng/g
99 |ig/g
122 |ig/g
518 |ig/g
532 |ig/g
2,237 |ig/g
Toxicity: Ability to Accumulate2: Source:
Log Log
Tissue (Sample Type) Effects BCF BAF BSAF Reference Comments3
[9] F
1665 ng/g
304 |ig/g
293 |ig/g
453 |ig/g
359 ng/g
212 ng/g
203.1 mg/g [10] F
113.9mg/g
264.1 mg/g
393.4 mg/g
256.6 mg/g
199|ig/g [11] F
163 |ig/g
176 |ig/g
155 ng/g
185 ng/g
194 ng/g
00
o
-------
Summary of Biological Effects Tissue Concentrations for Zinc
Species: Concentration, Units in1:
Taxa Sediment Water
Elliptic complanata, 1.5-78.4 jj.g/g
Freshwater mussel
19.1 -342 |ig/g
16-433 ng/g
Mytilus edulis,
Mussel
Mytilus
galloprovincialis,
Mussel
Toxicity: Ability to Accumulate2: Source:
Log Log
Tissue (Sample Type) Effects BCF BAF BSAF Reference Comments3
127 |ig/g (foot) [12] F
83 |ig/g (muscle)
78 (j.g/g (visceral)
123 |ig/g, (hepato-
pancreas)
265 ng/g (gills)
173 |ig/g (mantle)
144 |ig/g (foot) [12] F
88 |ig/g (muscle)
90 |ig/g (visceral)
119 |ig/g (hepato-
pancreas)
790 |ig/g (gills)
275 |ig/g (mantle)
148 |ig/g (foot) [12] F
119 |ig/g (visceral)
208 |ig/g (hepato-
pancreas)
1360 |ig/g (gills)
11 90 |ig/g (mantle)
130 mg/kg Mortality, [21] L; 100% mortality
(whole body)4 ED100 in 14 days
14-20 mg/kg 0.145 [19] F
-------
Summary of Biological Effects Tissue Concentrations for Zinc
oo
o
Species:
Taxa
Dreissena
polymorpha,
Zebra mussel
Concentration, Units in1:
Sediment Water Tissue (Sample Type)
21.6mg/kg
(whole body)4
600 mg/kg
(whole body)4
130 mg/kg
(whole body)4
600 mg/kg
(whole body)4
22 mg/kg
(whole body)4
40 mg/kg
(whole body)4
46 mg/kg
(whole body)4
130 mg/kg
(whole body)4
600 mg/kg
(whole body)4
22 mg/kg
(whole body)4
Toxicity: Ability to Accumulate2:
Log Log
Effects BCF BAF BSAF
Physiological,
NOED
Mortality,
LOED
Physiological,
LOED
Physiological,
NA
Growth,
NOED
Growth,
NOED
Growth,
NOED
Growth,
NOED
Growth,
NOED
Mortality,
NOED
Source:
Reference
[25]
[26]
[26]
[26]
[26]
[26]
[26]
[26]
[26]
[26]
Comments3
L; no effect on
internal zinc
regulatory process
L; increased
mortality
L; reduced
filtration rate
L; reduced
filtration rate
L; no effect on
weight gain of
surviving mussels
L; no effect on
weight gain of
surviving mussels
L; no effect on
weight gain of
surviving mussels
L; no effect on
weight gain of
surviving mussels
L; no effect on
weight gain of
surviving mussels
L; no effect on
mortality
-------
o Summary of Biological Effects Tissue Concentrations for Zinc
Species: Concentration, Units in1:
Taxa Sediment Water Tissue (Sample Type)
40 mg/kg
(whole body)4
46 mg/kg
(whole body)4
130 mg/kg
(whole body)4
22 mg/kg
(whole body)4
40 mg/kg
(whole body)4
46 mg/kg
(whole body)4
Toxicity: Ability to Accumulate2:
Log Log
Effects BCF BAF BSAF
Mortality,
NOED
Mortality,
NOED
Mortality,
NOED
Physiological,
NOED
Physiological,
NOED
Physiological,
NOED
Source:
Reference
[26]
[26]
[26]
[26]
[26]
[26]
Comments3
L; no effect on
mortality
L; no effect on
mortality
L; no effect on
mortality
L; no effect on
filtration rate
L; no effect on
filtration rate
L; no effect on
filtration rate
Daphnia magna,
Cladoceran
1340 mg/kg
(whole body)4
2690 mg/kg
(whole body)4
Reproduction,
ED10
Mortality, ED50
[13]
[13]
L; 10% reduction
in number of
offspring
L; lethal body
burden after 21-
day exposure
Hyallella azteca,
Amphipod
13.0 |ig/L
21.2|ig/L
42.3 |ig/L
185 |ig/L
316 |ig/L
66 |ig/g
85 |ig/g
126 |ig/g
136 |ig/g
167 |ig/g
167 |ig/g
50% survival
56% survival
51% survival
35% survival
6% survival
3% survival
[14]
-------
Summary of Biological Effects Tissue Concentrations for Zinc
Species:
Taxa
Balanus crenatus,
Barnacle
Concentration
Sediment
Total SEM
|ig/g |ig/g
10100 8873
911 700
631 408
734 562
365 294
29 <15
, Units in1: Toxicity: Ability to Accumulate2: Source:
Log Log
Water Tissue (Sample Type) Effects BCF BAF BSAF Reference Comments3
[9] F
18900 |ig/L 259 |ig/g
1180|ig/L 106|ig/g
187ng/L 80ng/g
189|ig/L 79|ig/g
132|ig/L 74|ig/g
<70|ig/L 56|ig/g
71.4mg/kg Mortality, NA [21] L; 7.5% mortality
(whole body)4 in 14 days
3200mg/kg Behavior, [28] L; regulation of
(whole body)4 NOED metals endpoint -
winter experiment
Chironomus
riparius,
Midge
0.9 mg/L 710 |ig/g
[3]
L
Chironomus gr.
thummi,
Midge
42.89 mg/kg
16.22mg/kg
61.6 mg/kg
(whole body)4
Normal larvae
Deformed larvae
Morphology,
NOED
[15]
[24]
L; 4th instar larvae
00
o
-J
-------
oo
o
oo
Summary of Biological Effects Tissue Concentrations for Zinc
Species: Concentration, Units in1:
Taxa Sediment Water
Fishes
Oncorhynchus
mykiss, Rainbow
trout
Salvelinusfontinalis,
Brook trout
Tissue (Sample Type)
40 mg/kg
(whole body)4
22.6 mg/kg
(whole body)4
30 mg/kg (gill)4
30 mg/kg (gill)4
30 mg/kg (gill)4
50 mg/kg (liver)4
50 mg/kg (liver)4
50 mg/kg (liver)4
7 mg/kg (kidney)4
Toxicity: Ability to Accumulate2:
Log Log
Effects BCF BAF BSAF
Physiological,
LOED
Reproduction,
LOED
Growth,
NOED
Growth,
NOED
Growth,
NOED
Mortality,
NOED
Mortality,
NOED
Mortality,
NOED
Reproduction,
NOED
Source:
Reference
[20]
[23]
[23]
[23]
[23]
[23]
[23]
[23]
[23]
Comments3
L; induction of
metallothionein
L; reduction in
percentage of eggs
hatching in second
generation trout
L; no effect on
growth
L; no effect on
growth
L; no effect on
growth
L; no effect on
survival
L; no effect on
survival
L; no effect on
survival
L; no effect on
number of eggs
produced
-------
Summary of Biological Effects Tissue Concentrations for Zinc
Species: Concentration, Units in1:
Taxa Sediment Water Tissue (Sample Type)
7 mg/kg (kidney)4
7 mg/kg (kidney)4
19.3 mg/kg
(whole body)4
15.3 mg/kg
(whole body)4
6.7 mg/kg
(whole body)4
Toxicity: Ability to Accumulate2:
Log Log
Effects BCF BAF BSAF
Reproduction,
NOED
Reproduction,
NOED
Reproduction,
NOED
Reproduction,
NOED
Reproduction,
NOED
Source:
Reference
[23]
[23]
[23]
[23]
[23]
Comments3
L; no effect on
number of eggs
produced
L; no effect on
number of eggs
produced
L; no reduction in
percentage of eggs
hatching in second
generation trout
L; no reduction in
percentage of eggs
hatching in second
generation trout
L; no reduction in
percentage of eggs
hatching in second
generation trout
Salvelinus
namaycush,
Lake trout
oo
o
6 cpm/g (whole)
17 cpm/g (spleen)
30 cpm/g (liver)
21 cpm/g (kidney)
9 cpm/g (brain)
32 cpm/g (gonad)
4 cpm/g (muscle)
8 cpm/g (blood)
11 cpm/g (gill)
80 cpm/g (gut)
[16]
-------
22 Summary of Biological Effects Tissue Concentrations for Zinc
Species: Concentration, Units in1:
Taxa Sediment Water Tissue (Sample Type)
Salmo salar, 60 mg/kg
Atlantic Salmon (whole body)4
60 mg/kg
(whole body)4
42 mg/kg
(whole body)4
37 mg/kg
(whole body)4
60 mg/kg
(whole body)4
42 mg/kg
(whole body)4
37 mg/kg
(whole body)4
42 mg/kg
(whole body)4
37 mg/kg
(whole body)4
Toxicity: Ability to Accumulate2:
Log Log
Effects BCF BAF BSAF
Physiological,
LOED
Growth, NOED
Growth,
NOED
Growth,
NOED
Mortality,
NOED
Mortality,
NOED
Mortality,
NOED
Physiological,
NOED
Physiological,
NOED
Source:
Reference
[22]
[22]
[22]
[22]
[22]
[22]
[22]
[22]
[22]
Comments3
L; reduced caloric
content of fish
L; no effect on
growth
L; no effect on
growth
L; no effect on
survivorship
L; no effect on
survivorship
L; no effect on
survivorship
L; no effect on
survivorship
L; no effect on
caloric content of
fish
L; no effect on
caloric content of
fish
-------
Summary of Biological Effects Tissue Concentrations for Zinc
Species:
Taxa
Pimephales
promelas,
Fathead minnow
Concentration, Units in1:
Sediment Water
770 ng/g
2560 |ig/g
HlOjig/g
2180 |ig/g
3180ng/g
3210 |ig/g
3120ng/g
2550 |ig/g
2050 iig/g
Toxicity: Ability to Accumulate2: Source:
Log Log
Tissue (Sample Type) Effects BCF BAF BSAF Reference Comments3
320.0 mg/g [10] F
25 1.5 mg/g
300.2 mg/g
268.3 mg/g
402.0 mg/g
264.6 mg/g
378.8 mg/g
366.8 mg/g
333.0 mg/g
3 14. 7 mg/g
Jordanella floridae,
American flagfish
50 mg/kg
(whole body)4
58 mg/kg
(whole body)4
50 mg/kg
(whole body)4
58 mg/kg
(whole body)4
220 mg/kg
(whole body)4
Mortality,
LOED
Growth,
NOED
Mortality,
NOED
Reproduction,
NOED
Growth,
LOED
[29]
[29]
[29]
[29]
[30]
L; body burden
estimated from
graph
L; body burden
estimated from
graph
L; body burden
estimated from
graph
L; body burden
estimated from
graph
L; body burden
estimated from
graph, total length
of females
-------
Summary of Biological Effects Tissue Concentrations for Zinc
Species:
Taxa
Poecilia reticulata,
Guppy
Concentration, Units in1:
Sediment Water Tissue (Sample Type)
300 mg/kg
(whole body)4
220 mg/kg
(whole body)4
230 mg/kg
(whole body)4
190 mg/kg
(whole body)4
300 mg/kg
(whole body)4
220 mg/kg
(whole body)4
0.284 mg/kg
(whole body)4
Toxicity:
Effects
Growth,
LOED
Mortality,
LOED
Growth,
NOED
Growth,
NOED
Mortality,
NOED
Mortality,
NOED
Mortality,
NOED
Ability to Accumulate2: Source:
Log Log
BCF BAF BSAF Reference
[30]
[30]
[30]
[30]
[30]
[30]
[27]
Comments3
L; body burden
estimated from
graph, total length
of males
L; body burden
estimated from
graph
L; body burden
estimated from
graph, total length
of males
L; body burden
estimated from
graph, total length
of females
L; body burden
estimated from
graph
L; body burden
estimated from
graph
L
1 Concentration units based on wet weight unless otherwise noted.
2 BCF = bioconcentration factor, BAF = bioaccumulation factor, BSAF = biota-sediment accumulation factor.
-------
3 L = laboratory study, spiked sediment, single chemical; F = field study, multiple chemical exposure; other unusual study conditions or observations noted.
4 This entry was excerpted directly from the Environmental Residue-Effects Database (ERED, www.wes.army.mil/el/ered, U.S. Army Corps of Engineers and U.S.
Environmental Protection Agency). The original publication was not reviewed, and the reader is strongly urged to consult the publication to confirm the information
presented here.
-------
BIOACCUMULATION SUMMARY ZINC
References
1. Weast handbook of chemistry and physics, 68th edition, 1987-1988, B-143. (Cited in: USEPA.
1995. Hazardous Substances Data Bank (HSDB). National Library of Medicine online (TOXNET).
U.S. Environmental Protection Agency, Office of Health and Environmental Assessment,
Environmental Criteria and Assessment Office, Cincinnati, OH. September.)
2. USEPA. 1995. Integrated Risk Information System (IRIS). National Library of Medicine online
(TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental
Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. September.
3. Timmermans, K.R., W. Peelers, and M. Tonkes. 1992. Cadmium, zinc, lead, and copper in
Chironomus riparius (Meigen) larvae (Diptera, Chironomidae): Uptake and effects. Hydrobiologia.
241:119-134.
4. Klerks, P.L., and P.R. Bartholomew. 1991. Cadmium accumulation and detoxification in a Cd-
resistant population of the oligochaete Limnodrilus hoffmeisteri. Aquatic Toxicol. 19:97-112.
5. Kraak, M.H.S., D. Lavy, W.H.M. Peelers, and C. Davids. 1992. Chronic ecotoxicily of copper and
cadmium lo the zebra mussel Dreissenapolymorpha. Arch. Environ. Contam. Toxicol. 23:363-369.
6. McKinney, J. 1993. Melals bioavailabilily and disposition kinetics research needs workshop. July
18-19, 1990. Environ-Toxicol Chem. 38:1-71.
7. Schmill, C.J., and S.E. Finger. 1987. The effecls of sample preparation on measured concentrations
of eighl elemenls in edible tissues of fish from slreams contaminated by lead mining. Arch. Environ.
Contam. Toxicol. 16:185-207.
8. Walsh, C.T., H.H. Sandslead, A.S. Prasad, P.M. Newberne, and P.J. Fraker. 1994. Zinc: Health
effecls and research priorities for Ihe 1990s. Environ. Health Perspect. 102:5-46.
9. Ingersoll, C.G., W.G. Brumbaugh, FJ. Dwuer, andN. E. Kemble. 1994. Bioaccumulalion of melals
by Hyalella azteca exposed lo conlaminaled sedimenls from the Upper Clark Fork River, Montana.
Environ. Toxicol. Chem. 13:2013-2020.
10. Kranlzberg, G. 1994. Spatial and temporal variability in melal bioavailabilily and loxicily of
sedimenl from Hamilton Harbour, Lake Ontario. Toxicol. Environ. Chem. 13:1685-1698.
11. Bryan, G.W., and WJ. Langslon. 1992. Bioavailabilily, accumulation and effecls of heavy melals
in sedimenls with special reference lo United Kingdom esluaries: A review. Environ. Pollut. 76:89-
131.
12. Tessier, A., P.G.C. Campbell, J.C. Auclair, and M. Bisson. 1984. Relationships belween the
partitioning of Irace melals in sedimenls and Iheir accumulation in the tissues of the freshwater
mollusc Elliptio complanata in a mining area. Can. J. Fish. Aquat. Sci. 41:1463-1472.
814
-------
BIOACCUMULATION SUMMARY ZINC
13. Enserink, E.L., J.L. Mass-Diepeveen, and CJ. Van Leeuwen. 1991. Combined effects of metals:
An ecotoxicological evaluation. Water Res. 25:679-687.
14. Borgmann, U., W.P. Norwood, and C. Clarke. 1993. Accumulation, regulation and toxicity of
copper, zinc, lead and mercury in Hyalella azteca. Hydrobiologia 259:79-89.
15. Bisthoven, J., K.R.Timmermans, and F. Ollevier. 1992. The concentration of cadmium, lead,
copper, and zinc in Chironomus gr. thummi larvae (Diptera, Chironomidae) with deformed versus
normal antennae. Hydrobiologia 239:141-149.
16. Harrison, S.E., J.F. Klaverkamp, and R.H. Hesslein. 1990. Fates of metal radiotracers added to a
whole lake: Accumulation in fathead minnow (Pimephales promelas) and lake trout (Salvelinus
namaycush). Water Air Soil Pollut. 52:277-293.
17. Di Toro, D.M., J.D. Mahony, DJ. Hansen, K.J. Scott, M.B. Hicks, S.M. Mayr, and M.S. Redmond.
1990. Toxicity of cadmium in sediments: The role of acid volatile sulfide. Environ. Toxicol. Chem.
9:1487-1502.
18. Schubauer-Berigan, M.K., J.R. Dierkes, P.D. Monson, and G.T. Ankley. 1993. pH-dependent
toxicity of Cd, Cu, Ni, Pb, and Zn to Ceriodaphnia dubia, Pimephales promelas, Hyalella azteca,
and Lumbriculus variegatus. Environ. Toxicol. Chem. 12:1261-1266.
19. Houkal, D., B. Rummel, and B. Shephard. 1996. results of an in situ mussel bioassay in the Puget
Sound. Abstract, 17th Annual Meeting, Society of Environmental Toxicology and Chemistry,
Washington, DC, November 17-21, 1996.
20. Bonham, K., M. Zararullah, and L. Gedamu. 1987. The rainbow trout metailothioneins: Molecular
cloning and characterization of two distinct cDNA sequences. DNA 6:519-528.
21. Burbidge, F.J., DJ. Macey, J. Webb, and V. Talbot. 1994. A comparison between particulate
(elemental) zinc and soluble zinc (ZnCl2) uptake and effects in the mussel, Mytilus edulis. Arch.
Environ. Contam. Toxicol. 26:466-472.
22. Farmer, G.J., D. Ashfield, and H.S. Samont. 1979. Effect of zinc on juvenile Atlantic salmon Salmo
Solar. Acute toxicity, food intake, growth and bioaccumulation. Environ. Pollut. 19:103-117.
23. Holcombe, G.W., D.A.Benoit, and E.N. Leonard. 1979. Long-term effects of zinc exposures on
brook trout (Salvelinus fontinalis). Trans. Amer. Fish. Soc. 108:76-87.
24. Janssens De Bisthoven, L.G., K.R. Timmermans, and F. Ollevier. 1992. The concentration of
cadmium, lead, copper, and zinc in Chironomus gr. thummi larvae. Hydrobiologia 239:141-149.
25. Kraak, M.H.S., M. Toussaint, E.A.J. and D. Lavy. 1992. Metal regulation in two species of
freshwater bivalves. In Ecotoxicology of metals in invertebrates, R. Dallinger and P.S. Rainbow,
pp. 175-186. Lewis Publishers, Boca Raton, FL.
26. Kraak, M.H.S., Y.A. Wink, S.C. Stuijfzand, M.C. Buckert-de Jong, CJ. De Groot, and W.
Admiraal. 1994. Chronic ecotoxicity of Zn and Pb to the zebra mussel Dreissena polymorpha.
Aquat. Toxicol. 30:77-89.
815
-------
BIOACCUMULATION SUMMARY ZINC
27. Pierson, K.B. 1981. Effects of chronic zinc exposure on the growth, sexual maturity, reproduction,
and bioaccumulation of the guppy, Poecilia reticulata. Can. J. Fish. Aquat. Sci. Vol. 38.
28. Powell, M.I., White, K.N.. 1990. Heavy metal accumulation by barnacles and its implications for
their use as biological monitors. Mar. Environ. Res. 30: 91-118.
29. Spehar, R.L., E.N. Leonard, and D.L. Defoe. 1978. Chronic effects of cadmium and zinc mixtures
on flagfish (Jordanella floridae). Trans. Am. Fish. Soc. 107(2): 354-360.
30. Spehar, R.L. 1976. Cadmium and zinc toxicity to flagfish, Jordanella Floridae. J. Fish. Res. Board
Can. Vol. 33.
816
------- |