U.S. DEPARTMENT OF COMMERCE
National Technical Information Service
PB-253 677
Criteria Document
for Toxaphene
Environmental Protection Agency
June 1, 1976
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EPA-440/9-76-014
CRITERIA DOCUMENT
TCKAPHENE
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BIBLIOGRAPHIC DATA
SHEET
1. Report No.
EPA-440/9-76-014
3. Recipient's Accession No.
Title and Subtitle
5. Report Date
Jtme 1. 1976
Criteria Document for Toxaphene
6.
7. Authors)
8. Performing Organization Kept.
No.
?. Performing Organization Name and Address
U..JL.-Environmental Protection Agency
Office of Water Planning and Standards
401 M Street,, S.W.
n.C*. 20460
10. Project/Task/Work Unit No.
11. Contract/Grant No.
12. Sponsoring Organization Name and Address
Office of Water Planning and Standards
U. S. Environmental Protection Agency
401 M Street, S.W.
Washington, D.C. 20460
13. Type of Report & Period
Covered
Interim
14.
15. Supplementary Notes
16. Abstracts
This document summarizes the physical/chemical properties, toxicological
information and environmental fate and effects of Toxaphene, with
emphasis on aquatic behavior. From these data a criterion for the
protection of aquatic life and human health is developed.
17. Key Words and Document Analysis. 17o. Descriptors
Criteria
Toxicity
Aquatic animals
Aquatic biology
Human ecology
Safety factor
17b. Identifiers/Open-Ended Terms
Toxic Pollutant Effluent Standards
Federal Water Pollution Control Act
17c. COSATI Field/Group
18. Availability Statement
Release Unlimited
19.. Security Class (This
Report)
UNCLASSIFI
121.'No. of Paxes
IINTI -AfS
urity Clas
20. Security
Page
UNCLASSIFIED
FORM NTIS-SS (*cv. 10-781 ENDORSED BY ANSI AND UNESCO.
THIS FORM MAY BE REPRODUCED
U1COMM-DC S2ซซ-P74
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INTRODUCTION
CRITERIA DOCUMENTS FOR TOXIC POLLUTANTS
Scientific rationale and criteria developed pursuant to Section 307(a)
of tin; Kutteral Water Pollution Control Act, P. I,. ป2-!ป00, 3:i tl.S.C. $ง 1251
et acq. 0 (1972). for the development and establishment of effluent limitations
for toxic substances are set forth in the following chapters.
Section 307(a)(2) states inter alia that a proposed effluent standard
".. o shall take into account the toxicity of the pollutant, its persistence,
degradability. the usual or potential presence of the affected organisms in
any water, the importance of the affected organisms and the nature and extent
of the effect of the toxic pollutant on such organisms..." Thereafter, having
considered these factors, the Administrator is to set an effluent standard
for toxic pollutants which provides an ample margin of safety.
In the development of criteria which serve as both the basis and the goal '
for the establishment of effluent limits, reliance was placed on the toxicity
data derived from laboratory studies on a range of organisms including
invertebrate, vertebrate, and mammalian test species. These studies
provided extensive acute and chronic toxicity data based on feeding experi-
ments for a wide range of aquatic organisms and consumers of aquatic
organisms. Environmental studies documenting bioaccumulation in the food
wob of the toxic material by the food chain organisms and bioconcentration
uj organisms directly from water provided an important component data
base upon which criteria were derived. Appropriate human toxicity data
and mammalian carcinogenic studies, where available, were used also in
developing criteria.
ii
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Aquatic ioxicity data generally are obtained by one of two basic
methods, the static and flow-through bioassay. The more traditional
static bioassay employs a tank in which the test organisms are living
and to which a given concentration of toxicant is added. Any water
loss due to evaporation is made up by the addition of fresh water. The
flow-through bioassay. which is a more recent development, reflects
more nearly the natural conditions. Concentrations of toxic substances
are constantly maintained and provide a more accurate test of sensitivity
of aquatic species. Water in a flow-through test is replenished constantly
through flushing. Comparative results using the static and flow-through
bioassay s demonstrate that flow-through data yield lower toxicity values
for a pollutant than a static bioassay. This fact is demonstrated by
comparative-studies as discussed in the endrin document. However*
most of the data available were developed using static bioassays.
Some toxic pollutants are extremely stable and degrade only slowly
or form persistent degradation products. Those pollutants which degrade
rapidly pose a less severe long-term hazard unless their entry to
the environment is continuous. A parent compound, e.g.. aldrin, may
rapidly degrade or be altered to a more toxic form. i. e., dieldrin.
Bioconcentration of toxic pollutants is a significant consideration in
the development of criterion. The rate and degree of accumulation in
an animal and the rate of loss from the animal are factors that help .
define the potential magnitude of the pollution load problem. As an i
HI
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example, & pollutant which bioaccumulates presents a hazard both to
aquatic systems and potentially to man or other carnivores associated
with the iMroHystem. To satisfactorily manage a persistunt or
non-degradable pollutant requires the maintenance of a ceiling for
ambient levels in water which will affo'rd protection to the food chain
and the consumers of aquatic life (animals including humans). The
body burden of toxic pollutants in fish or food chain organisms may
have no outward effect on the species but will affect consumers of that food
- . I
level. As an example, the brown pelican, when feeding on endrin-contaminated'
.. .'.. . !
fish may die or suffer species depletion through reproductive impairment. j
Data on toxic effects of pollutants are not available for all species
that may be exposed to the toxic pollutant in these complex societies.
Such data would be necessary to ensure protection of the most sensitive
species. It is desirable to know the relative sensitivity of a wide
variety of species in order to have a better estimate of the sensitivity
of the untested, most sensitive species. Because such data are not
available on all species, the range in sensitivity of a small number of
tested species is used to provide a measure of the range of sensitivity
of all species.
The natural aquatic environment includes many kinds and life stages
of plants and animals that are intricately interrelated to form communities.
Criteria are developed to protect these interrelationships and incorporate
aquatic toxicity data for a phylogenetic cross section of organisms as well as
Iv
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species representative of wide geographic distribution. Chronic
studies are an important consideration in establishing criteria and require
Htudius of at leaat one generation, i.e., one reproductive cycld. llso of
an application factor for persistent and bioaccumulatcd toxic pollutants
represents consideration of a safety factor. As discussed in the
National Academy of Science publication on water quality (p. 185 of
the NAS/NAE Water Quality Criteria 1972. GPO-5501-00520), the
use of ah application factor of 0.01 when applied to acute toxic values
is thought to provide an ample margin of safety for certain chlorinated -
hydrocarbon pesticides. .
Ecological importance of an organism is dependent on the
role the organism plays within the ecosystem and upon its relationship
to the food chain within the aquatic community and to consumers of
aquatic life, including man. Thus, toxicity data for the top.carnivores
in a given ecosystem* as well as economically important species such
as trout, salmon, menhaden and shrimp are needed for the development
of a protective criteria level. Toxicity data for organisms such as the
stonefly and Daphnia are of equivalent importance since these organisms
are a food base for higher consumers and are representative.of invertebrate
species found in most waters of the United States.
Invertebrate species, such as the stonefly and the Daphnia, are an
indication of the integrity of the aquatic food chain and their presence
may be the controlling factor for the abundance of economically and
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recreationally important predators such as trout, bass or pike. While
these fish may not directly consume the Daphnia or stonefly or, in i
fact, even inhabit the same waters, these lower order organisms are
representative of the food chain base supporting predators.
i
t
Criteria levels, by their nature, are developed to protect aquatic
organisms and consumers of aquatic life from direct toxic effect when
placed on contact with the toxic pollutants; and, to protect from a
more insidious and even greater danger, e.g., chronic effects.
Chronic effects take the form of reproductive failures or the poisoning
of predators consuming food organisms which have bioaccumulated levels
of toxic pollutants as in the case of the brown pelican and consuming
endrin loaded fish (see Attachment D, Endrin), and a variety of other
physiological effects as discussed in the various documents. Decreases
in aquatic organisms or consumers of aquatic life not always are coupled
to point source discharges of toxic pollutants at concentrations below
acute toxic levels; however, the addition of toxic levels which are not
acutely toxic can achieve the destruction or at least disruption of aquatic
systems by causing reproduction of failure. Hence, the need for application
factors. The relationships between discharges of toxic pollutants and
effects on important organisms of economic and environmental importance .
and consumers of these organisms are well documented in the criteria
documents,
vi
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An approach to criteria development is to provide ample protection .
of the test species on the assumption that the response of these species
wilt hซ characteristic of other UHtiori&tetl orj;uni.:4ms in the
environment. A number of nperieH have been ronsideretl in
a Criteria
Use of mammalian systems to determine the carcinogenic potential
of toxicants found in water follows the same principle as use of aquatic
organisms to determine toxicity to fish and other organisms. Carcinogenic
substances pose a special hazard to man through environmental exposure.
Cancer producing substances may reach man by several distinct pathways.
The following four criteria documents for aldrin/dieldrin. DDT and its
metabolites, endrin and toxaphene, represent a survey of the scientific
literature documenting the effects of these toxic pollutants to aquatic
life and consumers of aquatic life including man. A glossary of terms is
*
provided to define the terms used throughout the documents and will be
expanded as necessary when additional documents are added.
vii
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TOXAPHENE
TABLE OF CONTENTS
I. Preambl e. .... 1
fl. Chemical -Physical Properties 2
III. Toxicological Data 5
a. General Toxicological Information 5
b. Microscopic Life 7
c. Aquatic Invertebrates ...-....7
1. Freshwater 7
2. Marine .9
d. Fish 9
1. Freshwater 9
2. Marine 16
e. Birds 16
f. Mammal s- 17
g. Hunan Toxicity ....23
IV. Environmental Fate and Effects 23
V. Criteria Formulation....... 32
VI. References .36
vui
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I. Preamble
Toxaphene (Chlorinated caraphene) behaves much like other
chlorinated hydrocarbon pesticides 1n the aquatic environment.
That 1s, 1t degrades slowly, adsorbs on partlculate matter and
i .-' '
'' concentrates In living, tissues, especially lipids. At one time
:' ' ' - ...._:.-. .--..' ' ซ
& ':.'' 1t was widely used as a pisctdde for the elimination of "rough11
j. fl.sh from lakes prior to selective restocking, but Its persistence
-;f , made 1t unsuitable for such applications. .
;.{ .: . . ' . .'..... ' . '. ''....
; . Toxaphene 1s highly toxic to both vertebrates and Inverte-
*f: brates. It accumulates in plants and animals and persists for
:jr;' ' - ' . .-;.'.
| long periods 1n the aquatic environment. At extremely low levels
1t has been shown to cause the "broken back syndrome11 1n fish
] fry (15). Toxaphene has been associated with the death of birds
; that feed on fish living 1n contaminated waters (1).
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The purpose of this document Is to review available data
concerning the properties, tori city and environmental fate and
effects of toxaphene. Based upon the data, a concentration In
-water of-jjj.oos ug/1 (ppb) Is recommended as a criterion,. ;
IK Chemical and Physical Properties :> ' ": "
"'\', /Toxaphene Is defined as chlorinated 'camphene (67-69 percent
chlorine) and has the empirical formula C10H10C18 w-i1tn ปn-' average
molecular weight of 414. .
: Toxaphene (U.S. Patents 2,565,471 and 2 ,6.57,1 64* Hercules)
.: Is commercially produced by reacting camphene and chlorine in
..'the presence of ultraviolet radiation and certain catalysts to
. yield chlorinated camphene with a chlorine content of 67 to.
69 percent. The final product is a relatively stable mixture
of related, compounds and isomers with a mild terpene odor.
A large number of chlorinated compounds Is present in
toxuphene. A typical gas chroma togram suggests that 30 or 40
N principal constituents may exist. The chlorine content In the
. commercial product is limited to 67 to 69 percent since insecti-
, .
ddal activity peaks sharply in that range.
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i'
Infrared absorptivity at 7.2u helps distinguish toxaphene
from other chlorinated terpene products such as Strobane. Some
trlcydene may accompany the camphene, but less than 5 percent
of other terpenes 1s. present (1).
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Table 1
Physical form:
Melting point:
Solubility:
Vapor pressure:
Physical Properties (1)
Amber, waxy solid.
70ฐ-90ฐC.
High solubility 1n most organic solvents, but
greater 1n aromatic solvents; water solubility
1s about 0.5 ppm.
0.2-.4 mm/250; 3-4mm/90ฐC.
Product Specifications
Total organic chlorine, % by weight
Acidity, % by weight as HC1
Drop softening point, ฐC
Infrared absorptivity at 7.2u
Specific gravity at 100ฐC/15.6ฐC
67.0-69.0
0.05% max.
70 min.
0.0177 max.
1.600 minimum
When dispersed 1n a natural water toxaphene tends to be
adsorbed by the participates present or to be taken up by
living organisms 1n which 1t may be bloaccumulated. Thus,
1t Is seldom found at high levels as a soluble component 1n
receiving waters but can persist 1n sediments and on suspended
sol Ids for prolonged periods.
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III. lexicological Aspects
Toxic effects resulting from the presence of toxaphene 1n
water have been documented for aquatic organisms representing
a wide phylogenetlc cross section and a wide geographic distribu-
tion. While all test organisms used may not be universally
distributed In the waters of the United States, they do represent
types of organisms present in fresh, marine, and estuarine systems.
Extrapolation from the effects found in laboratory and field tests
is the only means for predicting effects of toxaphene on Individ-
ual organisms and their food chains.
It should be noted that the LC50 values reported for static
bioassays are likely to be substantially higher that LC50 values
found using flow-through bioassays. Because of a paucity of flow-
through data, comparisons of flow-through and static results with
toxaphene are not feasible. However, with endrin Earnest in 1970
(76) found a 96-hour TL50 (LC50) of 4.7 ug/1 of endrin for Korean
shrimp, Palaemon macrodacty 1 us, using a static bioassay and a
TL50 (LC50) of 0.30 ug/1 using an intermittent-flow bioassay.
This may explain why Katz 1n 1961 (22) reported a 96-hour static
j
TLm (LC50) for endrin of 1.2 ug/1 1n fresh water for Chinook
salmon, Oncorhynchus klsutch, while Earnest in 1970 (76) calcu-
lated a value of 0.14 ug/1, about one-tenth of the static bioassay
value, from freshwater Intermittent-flow bioassay data. These
data suggest loss of toxicant in static bioassays. Static
tests in which dissolved oxygen and toxicant concentrations are
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measured periodically are more reliable than those in which
these parameters are not monitored. The flow-through bioassays
more accurately reflect nature, where "container wall" effects
are likely to be negligible and where the volume of water per
fish is much greater.
A review .of published toxciity values shows that toxaphene
is extremely toxic to many fish (16, 20, 21, 22) and to inverte-
brate species such as the stoneflies (9).
In humans acutely toxic doses of toxaphene produce symptoms
that include salivation, spasms of the leg and back muscles,
nausea, vomiting, hyperexcitability, tremors, chronic convulsions
and tetanic contractions of all skeletal muscles. Most of these
effects are the results of diffuse stimulation of the cerebrospinal
axis. After lethal doses the convulsions continue until death
occurs. Respiration is arrested due to tetanic muscular contrac-
tions (5).
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A. Microscopic Life
The effects of 17 toxicants on 5 pure cultures of marine
phytopUnkton were reported by Ukeles in 1962 (8). Toxaphene
was the most potent of the chlorinated hydrocarbons tested.*
At a concentration of 10 ug/1 no appreciable effect was seen
with four species; however, a concentration of 150 ug/1 was
lethal to all organisms. One organism, Mpnochrysis 1utheri,
was killed by a concentration of 0.15 ug/1 toxaphene but not
by a concentration of .015 ug/1 (8).
*0ther tested substances were: TEPP, Depterex, carbolic acid,
Oowacide A, o-dichlorobenzene, Niagara compound 3514, PVP, DOT,
Lindane, Nabam, Sevin, Lignasan, Fenuron, Monuron, Oiuron, and
Neburon.
B., Aquatic Invertebrates
1. Freshwater
Toxaphene LC50 data for several species of freshwater
invertebrates commonly found in U.S. waters exposed to
toxaphsne are found in Table Z,
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ft
TABLE 2
LC50 Values for Various Freshwater Invertebrates (Static Bfoassaysj
LC50 (ug/1)
Species 24-hr. 48-hr, 96-hr. Ref.
Stonefly
Claassenla sabulosa
Pteronarcella badla
Pteronarcys callfornica
6
9.2
18
3.2
5.6
7
1.3
3.0
2.3
. - 9-
9
Anphipod
Gammarus lacustrls 180 70 ' 26 - 10
Waterflea
Daphnia pulex 15 .11
Sanders and Cope (11) conducted laboratory bloassays with
toxaphene to determine Immobilization values for two species
of amphlpods, Daphnia pulex and Slmocephalus serrulatus.
Estimated 48-hr. EC50 Immobilization values for S. serrulatus
were 19 ug/1 at 60ฐF and 10 ug/1 at 70ฐF. For D. pulex the
value was 15 ug/1 at 60ฐF.
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It has been demonstrated that the stoneflles, Pteronarcys
call forn lea, Pteronarcella badla. and
extremely sensitive to toxaphene, with 96-hr. LCSO values of
1.3 to 3 ug/1 (9).
2. Marine
Schlmmel In 1975 (13) found a 96-hous? EC50 of
1.4 ug/1 for the pink shrimp, Penaeuf duprarums, 4.4 ug/1 for
the grass shrimp, Palaemonetes pug1q9 and 4.9 ug/T for the
American oyster, Crassostrea vlrglnlca. Aetual toxicant
concentrations were measured during exposures Although
few data are available, it is reasonable to ex pact further
testing to uncover more sensitive species*
D. Fish
. 1. Freshwater
Considerable work has been done on the effects of
toxaphene on freshwater fish. The data in Tab]ฉ 38 obtained
under various exposure conditions. Illustrate Its high
toxlclty to many species widely distributed 1rn fresh waters
of the United States.
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10
TABLE 3
Toxldty to Various Freshwater Fishes
(Static Bloassays)
96-hour
Fish Species LC50 fug/1) Reference
Largemouth bass 2 20
(Mlcropterus salmoldes)
Brown trout 3 20
(Salmo trutta)
BluegHI 3.5 21
(Leponris macrochlrus)
Carp * 20
(Cyprlnus carpio)
Black Bullhead . 5 20
(Ictalurus melas)
Goldfish"5.6 21
(Carasslus auratus)
Coho salmon8 zo
(Oncorhynchus Msutch)
Rainbow trout 11 20
(Salmo galrdneri)
Yellow perch12 20
(Perca flavescens)
Channel catfish13 20
(Ictalurus punctatus)
Redear sunflsh13 20
(Lepomis micro!ophus)
Goldfish 14 20
(Carasslus auratus)
Fathead minnow (hard water) 5.1 21
(Plmephales prpmelas)
Fathead minnow (soft water) 7.5 21
(Plmephales promelas)
Gupples (soft water) 20 21
(Poecilla retlculata)
Chinook salmon2.5 22
(Oncorhynchus tshawytscha)
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11
Fish Species
Coho salmon
(OncorhynchuS klsutch)
Rainbow trout
(Sal mo galrdnerp
Rainbow trout (53ฐF.)
Stonerollers (53ฐF.)
(Camoostoma anomalum)
(73ฐF.J
Goldfish (53ฐF.)
(Carassius auratus)
. . ^.p }
Golden shiner (73ฐF.)
(Notemigonus crysoleucas)
Bluntnose minnow (53"F.)
(Plmephales notatus)
(73ฐF.).
Black bullhead (53ฐF.)
(Ictalurus melas)
: (73ฐF.)
96-hour
LC50(ug/l)
9.4
8.4
8.4
< 5
94
50
6
30
6,3
25
1.8
Referen
22
22
16
16
16
16
16
16
16
16
16
16
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12
Mayer and co-workers (14, 15) In 1974 and 1975 demon-
strated the chronic effects of toxaphene on two species of
freshwater fish. In one series of tests* young fathead
minnows, Plmephales promelas. were exposed for 150 days to
concentrations of toxaphene as low as 0.055 ug/1 In a flow-
through system. At the end of the exposure period the growth
of alI fish exposed to all levels of the toxicant was signifi-
cantly reduced, indicating the no-effect level of toxaphene
to be less than 0.055 ug/1 (14).
in the other series of experiments year-old brook trout,
Salvelinus fontlnails, were continuously exposed for as long
as 180 days to water concentrations of toxaphene ranging from
0.502 to 0.039 ug/1 In a flow-through system. Water temperature
and duration of light exposure were altered to correspond to
natural conditions. The results of the experiment may be
summarized as follows: growth of yearling brook trout was
reduced through continuous exposure to 0.288 and 0.502 ug/1 for
180 days; concentrations of 0.068 ug/1 and higher reduced egg
viability; the composition (i.e., the ratio of calcium plus
phosphorus to collagen) of the vertebral column of fry was
significantly altered during a 90-day exposure; there were
marked liver, pancreatic, and kidney pathologies; and finally,
the mortality of fish at every concentration tested was signifi-
cantly greater than In the controls, indicating a no-effect
level of less than 0.039 ug/1 (15).
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13
Mahdi In 1966 (16) determined lethal concentrations of
toxaphene for the stoneroller, Campostoma anomalumi golden
shiner, Notemigonus crysoleucas; goldfish, Carasslus auratus;
i .
black bullhead, Ictalurus me!as; and bluntnosฉ minnow,
Plmephales notatus 1n water at 53ฐF and 73ฐFs rainbow trout,
Salmo galrdnerl were tested at 53ฐF. These tests Indicated
that the potency of toxaphene Increased with temperature.
The 96-hr. TLm (LC50) values were below 100 ug/1 of toxaphene
for all species tested and for fish other than goldf1sh9
ranged from 1.8 to 30 ug/1.
Macek, et a]_., In 1969 (18) studied the effects of
temperature on the susceptibility of bluegills to toxaphene.
Their data are presented 1n Table 4.
Ferguson, et_ al_., 1n 1965 (17) reported the tolerances
of black bullheads, Ictalurus melas, and mosqultefish,
Gambusia affinis, from a transect of the lower Mississippi
River. The approximate 36-hour TLm (LC50) value for mosquito-
fish from five main river sites ranged from 10 to 30 ug/1,
while a resistant population of mosquitofish yielded a TLm
(LC50) of 480 ug/1. Mississippi River data on black bullheads
from four sites gave 36-hr. TLm (LC50) values of 3.J5, 12.5
50, and 22.5 ug/1. Obviously the more resistant fish could
transfer more toxaphene to predators, including man.
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14
Predatlon by sunfish on toxaphene-contamlna'ted mosquito-
fish caused mortality to the sunfish (68).
In ethological studies using the Comet strain of
goldfish, Carassius auratus, Warner and associates In 1966 (19)
showed that behavioral pathology occurred when the fish were
exposed to sublethal doses of toxaphene. Effects were observed
at levels as low as 0.44 ug/1, which 1s approximately 1/25 of
the 96-hour TLm (LC50) reported by Macek and McAllister in
1970 (20). Behavioral pathology was scored using a complicated
system based on a number of parameters, including responses to
light stimulus, total movement and habituation to light stimulus.
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15
TABLE 4
24 and 96-hr. TL50 (LC50) Values for Bluegnis
at Various Temperatures (18)
Exposure
Time 12.7"C 18.3ฐC 23.8"C R.I.3.*
TL50 (ug/1)
24 hours 9.7 6.8 6.6 1.46
96 hours 3.2 2.6 2.4 1.71
*R.I.S. a Relative Increase in susceptibility: The ratio
of the TL50 value at the lowest temperature to
that at the highest temperature.
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2. Marine
The plnffsh, Laqodon rhomboldes. 1s an omnlvore (73).
It ranges from Cape Cod to the Yucatan Peninsula and 1n many
areas .Is the most abundant species of nonpelagic fish (74, 75).
It serves as a link in the food chain supporting such commer-
cially Important species as the spotted sea trout, Cynoscion
' nebuTosin; the sailffsh, Istophosus americanus; and the gulf
flounder, Para11chthys a1biguttas. It is also of some
.. * -
importance as bait and as human food (74). .
'" . . .- ' f ~ ' . ' .
In 1975 Schimmel (13) reported a 96-hour EC50 value for
the pinflsh, Lagodon rhomboides, to be 0.5 ug/1 (measured
concentration) 1n a flow-through bioassay. Chronic exposure
. -of spot, Leiostomus xanthurus, to sublethal concentrations
. (0.1 ug/1) of toxaphene In seawater for five months under
flow-through conditions yielded evidence suggestive of histo-
pathological changes (23). Korn and Earnest in 1974 (69)
reported a TL50 (LC50) of 4.4 ug/1 for the striped bass,
Morone saxatilis. ,
E. Birds
Keith 1n 1966 (24) studied groups of five white pelicans
maintained on sardines contaminated with each of the following
toxicant concentrations: 10 ppm toxaphene, 50 ppm toxaphene,
50 ppm DDT or a combination of 10 ppm toxaphene and 150 ppm DOT.
Death occured earlier in those pelicans fed toxaphene at the 50 ppm
level than 1n all other groups.
T
!
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17
Toxaphene LDSO's have been reported for a variety of birds:
young mallards (less than six months of age). 70.7 mg/kg; young
pheasants, 40.0 rag/kg; young bobwhite quail, 85.4 mg/kg; sharp-
tailed grouse, 10 to 20 mg/kg; fulvous treeducks, 99 mg/kg; and
lesser sandhill cranes, 100 to 316 mg/kg (25).
In 1958 a study was conducted on pheasants fed 100 and 300
ppm of toxaphene 1n their diets for two to three months (27).
The 300 ppm level caused a decrease 1n egg laying and hatchab111ty
and 1n the food Intake and weight gain. Both dose levels caused
greater mortality 1n young pheasants during the first 2 weeks
after hatching than was observed in the controls.
F. Mammals
Acute toxldty
, The acute toxldty of toxaphene has been determined for a
number of mammalian species. A comparison of the oral and dermal
toxlcities of several chlorinated hydrocarbon Insecticides in rats
under standardized conditions was published by Gaines in 1960 (28),
Table 6 presents data from that report. For oral administration,
the compounds were dissolved or suspended in peanut oil. For
dermal application xylene solutions were used.
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18
TABLE 5
Acute Oral and Dermal Toxicitv of Several Chlorinated
Hydrocarbons to Rats (28)
Compound
Toxaphene
DDT
Chlordan
AldHn
Dieldrin
Endrln
Oral LD50 (mg/kg)
Males Females
90
113
335
39
46
18
80
118
430
60
46
8
Dermal LD50 (mg/kg)
Males Females
1075
840
98
90
780
2510
690
98
60
15
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19
The data in Table 5 show that toxaphene resembles DOT 1n
acute oral toxldty to rats. A number of factors influence
the toxicity of toxaphene. The route of administration, the
solvent used for the tests, and the species must be considered
in evaluating the potential hazard.
The data in Table 6 show the variation in toxicity of
toxaphene given orally and dermally to several common species
by means of different vehicles.
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20
TABLE 6
LD50 Values of Toxaphene to Several Manmals (1)
Species
Rat
Rat
Rat
Mouse
Dog
Dog
Guinea pig
Guinea pig
Cat
Rabbit
Rabbit
Cattle
Goat
Sheep
Rat
Rabbit
Rabbit
Route
Oral
Oral
Oral
Oral
Oral
Oral
Oral
Oral
Oral
Oral
Oral
Oral
Oral
Oral
Dermal
Dermal
Dermal
1050
(mg/kg)
90
60
120
112
49
>250
270
365
25-40
75-100
250-500
144
200
200
930
>4000
< 250
Vehicle*
Peanut oil
Corn ซo11
Kerosene
Corn oil
Corn oil
Kerosene
Corn oil
Kerosene
Peanut oil
Peanut oil
Kerosene
Grain
Xylene
Xylene
Xylene
Dust
Peanut oil
*The vehicle used to apply a toxicant may Influence the rate
and extent of toxicant absorption by the animal, whether by
oral or dermal or other mode of application. Furthermore,
some vehicles may themselves be significantly toxic.
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21
Assuming for the sake of safety that man resembles the
most sensitive experimental species (the cat), the lethal
dose for a 70 kg adult would be about 2 to 3.5 g. The
lethal dose for man has been estimated by others to be from
2 to 7 g (3, 29).
Chronic toxldty
The chronic toxlclty of toxaphene was studied by Ortega
et al_., In 1951 (31) In small groups of rats fed 50 and 200
ppm 1n the diet. These dietary levels'produced no clinical
signs of toxlclty, Inhibition of food consumption or growth
rate. Only the livers, spleens, and kidneys were examined
h1stolog1ca1ly. There was no damage to the kidney or spleen
but the livers of 3 of the 12 rats that received 50 ppm
showed slight changes. Six of the 12 rats fed 200 ppm showed
distinct liver changes.
In lifetime feeding studies with rats, dosages of 25, 100,
and 400 ppm of toxaphene 1n the diet were Investigated (32).
Liver enlargement was noted at all levels.
The kidneys and livers of 2 dogs fed toxaphene at a rate
of 4 mg/kg of body weight per day for 106 days showed degenera-
tive changes (33).
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22
Innes et al_., in 1969 (34) attempted to cause tumors In
mice by stomach tube administration of maximum tolerated doses
of pesticides starting at 7 days of age and continuing to 4 weeks
of age. Front 4 weeks of age until 18 months of age, the
chemicals were fed 1n the diet at levels near the maximum
tolerated dose. Toxaphene was not Included 1n that study but
the-closely related material, Strobane, given at a dally dose
of 4.64 mg/kg between ages 7-28 days and at 11 ppm 1n the diet
thereafter caused a higher Incidence of lymphomas and hepatomas
than was seen In controls.
Toxaphene can change the toxicity of drugs and other
chemicals detoxified by hepatic microsomal enzymes and alter
steroid metabolism because 1t induces synthesis of hepatic
microsomal enzymes. Dose-response relationships for enzyme
induction by toxaphene were measured by feeding various dietary
levels to rats for as long as 13 weeks. The lowest dietary
level of toxaphene that caused induction of the synthesis
of one or more of the three microsomal enzymes studied was
5 ppm. Maximum induction occurred within the first 3 weeks
of the feeding period at all levels of toxaphene that caused
enzyme Induction. After this time the activity was maintained
at a constant, elevated level until feeding of the pesticide
was discontinued (35).
These results show that dietary levels of 5 ppm and higher
could alter the rate at which other chemicals are metabolized.
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23
Similar enzyme Induction was obtained with DDT at a dietary level
of 1 ppm.
G. Humans
Acute toxaphene poisoning In humans 1s rare. When toxaphene
was first used, four cases of poisoning by Ingestion 1n children
under 4 years of age were reported (5). The same report contained
a description of severe toxaphene poisoning in adults from acci-
dents or Injudicious use of the pesticide. The dosage of toxaphene
estimated to have been Ingested by three of the people ranged from
9.5 to 47 mg/kg.
Inhalation of toxaphene can cause irritation of the respiratory
tract. Warraki In 1968 (47) has described acute bronchiolitis with
Hilary lung shadows in two men with an occupational history of
heavy and prolonged exposure to toxaphene sprays. The threshold
limit value for atmospheric levels of toxaphene has been established
by the Conference of Government Industrial Hyg1en1sts at 0.5 mg
per cubic meter of air (48).
IV. Environmental Fate and Effects
Toxaphene may persist in soil from several months to more than
10 years (62). It has been shown to persist for up to 9 years in
lakes and ponds (49, 50, 52).
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24 f
The fate and movement of a pesticide in and from the soil
depend on the following broadly categorized factors: (a) the
pesticide characteristics; (b) edaphic considerations;, (c) climate-;
(d) topography; and (e) land use and management. Any of these
factors that tend to promote the pesticide's persistence will tend
to increase its potential for environmental dispersion (2). :
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25
Pesticide movement through or across soil 1s facilitated by
the movement of water. Overland flow Is generally more Important
1n pesticide transport than passage through soil. Two processes
fcre Involved: (a) pesticide movement while dissolved In water
and (b) pesticide movement while adsorbed on soil. Reports of
the water solubility of toxaphene have ranged from 0.4 mg/1 to 3 mg/1 (56).
j Bailey and White 1n 1970 (57) stated that the principal means
'i
] of pesticide transport within soils are: (a) diffusion In the
:l
;! airspaces of soil; (b) diffusion In soil water; (c) downward
1) . . . '
I flowing water; and (d) upward moving water.
; A report by Hermanson et a1_., In 1971 (58) gives half-life
i figures on a number of chlorinated pesticides, Including toxaphene,
-1
1 In Holtvllle sandy clay. The half-lives of toxaphene and DOT were
; calculated to be 4 years.
Johnston, et aj_. (59), studied pesticide concentrations In tile
drainage and open drains In the San Joaquln Valley of California
between 1963 and 1965. Toxaphene was detected In 13 of 66 analyses
of tile drainage effluents In concentrations varying from 0.13 ug/1
to 0.95 ug/1 and averaging 0.53 ug/1. Water from surface drains
that collected surface and subsurface water was positive for toxaphene
In 60 out of 61 samples. Concentrations varied from 0.10 ug/1 to
7.90 ug/1 and averaged 2.01 ug/1. The predominant residues found
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26
in surface waters were DOT/DOT and toxapheneo The average concen-
tration of toxaphene was higher than that of any other chlorinated
hydrocarbon Insecticide and It was found most frequently.
Velth and Lee In 1971 (60) Investigated the sorptlon of
toxaphene to lake sediments and concluded that within the limits
of their analytical system, detectable concentrations of toxaphene
could not be leached from sediments by lake water. However, their
limit of detection was about 1 ug/1 and they carefully concluded,
\
"Also, the laboratory study does not rule out lake waters that may
contain ng/liter concentrations of toxaphene due to desorptlon
from the sediments." They also explicitly did not rule out the
possibility of the transport of toxaphene from lake sediments
through the migration of bottom fauna.
Nicholson et aJL, 1n 1966 (61) showed the relative Importance
of sediment versus solution 1n the transport of toxaphen@9 DDT and
BHC in Flint Creek, Alabama. Suspended sediment seemed Ttss
important to toxaphene and BHC transport than to DDT transport. This
suggests a lesser affinity of toxaphene for solid substrates than
that possessed by DDT, which 1s strongly hydrophobic. Support
for this contention comes from the fact that toxaphent was frequently
recovered in clarified and treated municipal drinking water while
DDT was found less often.
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27
Johnson, et al_., 1n 1966 (49) used gas chromatography to
I
study the mechanisms of detoxification. This study shows that
toxaphene may persist 1n a lake for several years after applica-
tion for fishery management even when detoxification Is rapid.
All of the lakes studied were shallow and eutrophlc. The authors
point out that detoxification 1s accomplished, In part, by
sorptlon reactions rather than degradation, but Indicate some
evidence based on the gas chromatographlc "fingerprint" that
toxaphene may be chemically modified.
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28
Johnson and Lew 1n 1970 (64) determined chlorinated hydro-
carbon Insecticide residues In fish of.the Lower Colorado River
system which drains an Irrigated agricultural area where Insecti-
cides are often used. The following residues of DDT and Its
congeners, DDT and IDE, and toxaphene were reported In the fat
and/or viscera of these fish.
Carp : DDT, etc., 2.0 - 185.0 mg/kg
Cyprtnus carpio toxaphene, 50.0 mg/kg
Channel Catfish : DDT, etc., 0.7 - 77.0 mg/kg
Ictalurus punctatus toxaphene, 8.2 - 11.4 mg/kg
Sonoran Sucker : DDT, etc., 7.3 - 46.3 mg/kg
Catostomus.insignis toxaphene, 2.8 - 172.9 mg/kg
611a Sucker : "DDT, etc., 36.2 - 39.5 mg/kg
Pantosteus clarkl toxaphene, 25.2 .- 42.9 mg/kg
Although the practice of applying toxaphene to lakes for
fisheries management has been discouraged, one study of that usaye
revealed Information on bioaccumulation in the hydrosphere under
conditions of gross contamination. Terrlere, et ajL (65), applied
toxaphene in Davis Lake, Oregon at 88 ug/1 in 1961 and found in
1962 and 1963 that toxaphene was present 1n water at average
levels of 2.1 ug/1 and 1.2 ug/1, respectively. They reported a
concentration factor of about 500 for aquatic plants, 1000 to 2000
for aquatic Invertebrates, 10,000 to 20,000 for rainbow trout,
4000 to 8000 for Atlantic salmon and 1000 to 2000 for lake bottom
and mud.
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29
Hughes 1n 1970 (66) studied biological accumulation and
persistence of toxaphene In Wisconsin lakes. When applied to
the lakes 1n fisheries management, toxaphene In the lake water
declined to less than the detection limit (1 ug/liter) within
9 to 12 months. However, aquatic fauna, particularly fish
stocked 1n the lakes following treatment, accumulated as much
as 19 ug of toxaphene residues per gram of body weight. In
general, prey fish accumulated higher concentrations of toxa-
phene than did predators. Bluegllls stocked in Fox Lake about
eight months following the last of 3 treatments accumulated
9.4 ug/g in 176 days, after which toxaphene residues began
declining until, after 787 days, 0.8 ug/g remained. Two months
after fish were stocked, plankton contained 34 ug/g.
Schimmel, eฃ aj_. (72), studied the bioaccumulation of
toxaphene in the ova of the longnose klllifish, Fundulus similus,
and found that at a measured water concentration of 0.2 ug/1,
the concentration of toxaphene in the eggs rose to 0.3 mg/kg in
fourteen days (a factor of. 1500) and 1n thirty-two days to
1.1 mg/kg (a factor of 5500).
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30
Lowe e_t aJL, 1n 1971 (67) demonstrated an accumulation of
as much as 30 ppm in oysters exposed for 24 weeks to 1 ppb of
toxaphene a concentration factor fo 30,000. In the ensuing
16 weeks 1n clean sea water the oysters excreted 90 percent of
this toad, but retained 3.0 ppm In their tissues still 3.000
times the water concentration they had been exposed to originally.
Mayer et aU, In 1975 (15) reported that brook trout concen-
trated toxaphene by factors as high as 76,000 and that the more
highly chlorinated isomers were preferentially stored.
Until recently there was no evidence of the existence of
toxaphene conversion products, or metabolites in crops that had been
\
exposed to toxaphene or in adipose tissues of animals fed toxaphene
diets. When toxaphene was extracted either from alfalfa that had
been exposed to toxaphene, or from adipose tissue of steers that had
been fed toxaphene-treated alfalfa, it had insecticidal activity
Identical to that of unaltered toxaphene (1). New studies reported
in 1974 and 1975 by Casida's groups, however, produced evidence that
toxaphene is degraded in vivo (36). They have shown substantial
dechlorination In 14 days or less in tissues of rats given toxaphene
orally. Although they consider dechlorination essentially equiva-
lent to detoxification, they have not tested the recovered metabolites
on Insects.
The effects of toxaphene on plankton in treated lakes were
studied by Hoffman and Olive in 1961 (7) using a concentration of
100 ug/1. The groups tested were Rotatoria, Protozoa, and Entomostraca.
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31
The first two of these exhibited decreased growth rates, while the
population of Entomostraca disappeared 1n the treated lakes.
Hllsenhoff 1n 1965 (12) studied the effects of toxaphene on
macroscopic bottom fauna 1n a reservoir and found that an applica-
tion level of 100 ug/1 markedly affected the Chlronomldae and
Chaoborus populations. Living Chlronomldae were absent from samples
taken three days after treatment and population recovery was not
complete until nine months later. Chaoborus larvae exhibited no
Immediate effects, but were absent six months later and had not
reappeared when the study ended. 01igochaetes showed no adverse
effects from toxaphene; their populations actually increased during
the eleven-month study period. Chaoborus larvae were the only
profundal organisms adversely affected by treatment of the top
30 feet with 100 ug/1 of toxaphene. They were eliminated and had
not become reestablished two years after treatment. However, these
organisms are not strictly profundal and appear to have been killed
during sorties into the epilimnion.
Unusually high mortalities were observed in fish-eating birds
at the Tule Lake and Lower Klamath.Refuges in 1960, 1961, and 1962.
The mortalities were reportedly and apparently due to application
of large quantities of toxaphene for several years, beginning in
1956, to the agricultural lands immediately surrounding the
refuges. Water from the farmlands drains into the marshes.
Toxaphene was found in the fish from the marshes at levels of
about 8 ppm and 1n the fat of fish-eating birds at levels as
high as 31.5 ppm (51).
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32
Criteria Formulation
The data presented, above establish that toxaphene Is a powerful
Insecticide capable of persisting 1n the aquatic environment, tha
soil or animal tissues for long periods* capable of b1oaccumu1at1rig
by factors of as much as 30,000, and capable of producing deleterious
effects on fish at levels as low as 0.039 ug/1. Since at least some
aquatic organisms can readily bioaccumulate toxaphene, formulation
of criteria for this pesticide 1n natural Waterways must take Into
account the potential danger to terrestrial predators, Including man,
which consume that aquatic life. However, many Important aquatic
organisms are exquisitely sensitive to direct poisoning by toxaphene
and must themselves be protected.
Sanders and Cope 1n 1968 (9) demonstrated 96-hour LC50 values
from 1.3 to 3.0 ug/1 for several species of freshwater stonefHes.
The 96-hour LC50 values for largemouth bass and brown trout have
been reported as 2.0 and 3.0 ug/1, respectively. Katz in 1961 (22)
demonstrated the 96-hour TLm (LC50) for Chinook salmon to be 2.5 ug/1.
ScMmmel (13) reported a 96-hour EC50 of 1.1 ug/1 for the sheepshead
minnow.
Mayer, et al_., 1n 1974 (IS) experimenting on brook trout, found -
the no-effect level for a six-month exposure to toxaphene to be less
than 0.039 ug/1. Similar studies on the fathead minnow (14) showed that
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33
the no-effect level for this species was less than 0.055 ug/1. It
Is Important to emphasize that In neither series of experiments was
a toxaphene concentration used which was low enough to have no effect.
Work by Schlmmel 1n 1975 (13) demonstrated the 96-hour EC50
(death) for adult pink shrimp to be 1.4 ug/1. Lowe (23) demonstrated
the 48-hour EC50 for spot to be 1.0 ug/1. The 144-hour EC50 for the
same species was 0.5 ug/1. Additional work by Schlmnel (13) demonstrated
96-hour EC50 values for plnflsh to be 0.5 ug/1.
Lowe et aj_., 1n 1971 (67) reported that oysters exposed to 1 ug/1
of toxaphene concentrated It about 30,000 times in their tissues. Upon
transfer to clean water the oysters excreted the toxaphene slowly;
excretion was not complete after 16 weeks.
The data set forth above establish the following facts:
(a) Toxaphene 1n concentrations clustered around 1 ug/1 1s
acutely toxic to fish and to the lower organisms on which
they feed;
(b) Toxaphene can be bioaccumulated by factors as high as
30,000 in aquatic organisms, thereby posing a potential
threat to other aquatic organisms, to birds, and to
mammals (Including man) which feed on them.
(c) Toxaphene can be quite persistent In aquatic systems, on
soil, and 1n animal tissues.
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34
(d) Toxaphene can have serious adverse effects on aquatic life
exposed to concentrations as low as 0.039 ug/1 and perhaps
even lover. At higher concentrations these effects become
pore pronounced, to the point of death.
Acute toxicity has been reported at levels as low as 0.5 ug/1
of -toxaphene (13). Thus, some damage to aquatic life could be expected
at higher levels. At levels of 1.0 to 2.0 ug/1 a large number of
species are known to be affected. These include stoneflies (9), the
sheepshead minnow (13), the black bullhead (16), the pinfish (13), the
pink shrimp (13) and the spot (23). An LC50 is the concentration at
which half the population dies and can be lowered by other environmental
stresses, for instance, by low dissolved oxygen concentration or
elevated temperature.
Chronic Criterion: 0.005 ug/1
Several common aquatic species have LC50 or EC50 values in the
neighborhood of 1 ug/1; among these are the Stonefly, Claassenia
sabulosa. 1.3 ug/1 LC50 (9); the sheepshead minnow, 1.1 ug/1 EC50 (13);
the black bullhead, 1.8 ug/1 LC50 (16); the marine pinfish, 0.5 ug/1
LC50 (13); and the pink shrimp, 1.4 ug/1 EC50 (16). In addition, Lowe
(23) reported a 48-hour LC50 of 1.0 ug/1 and a 144-hour LC50 of
0.5 ug/1 for the spot.
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35
The 96-hour LC50 for the pinfish, Lagodon rhomboides. an organism
of vide geographic distribution and of ecological importance in the
food chain, has been reported as 0.5 ug/1 (13>. While the use of an
application factor of 0.01 has been recommended by the NAS-NAE (77), its
.*-'.,
use is especially appropriate in the case of toxaphene because long-term
studies with fathead minnows, Pimephales promelas (14), and brook trout,
Salvelinus fontinalis (15), have failed to establish a no-effect level.
Application of this factor to the 96-hour pinfish LC50 value yields a
criterion of 0.005 ug/1.
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36
REFERENCES
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the Hazardous Materials Advisory Committee. EPA.
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5. McGee, L. C., H. L. Reed and J. P. Fleming, 1952.
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6. Negherbon, W. 0., 1959. Toxaphene. Handbook of
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Umnolo Oceanegr., 6:219-222.
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37
'f 8. Ukeles* R., 1962. Growth of pure cultures of marine
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* . V
10. Sanders, H. 0., 1969. Toxicity of pesticides to the
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Bur. Sport Fish, and Wildlife, U.S.D.I., 18 pp.,
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11. Sanders, H. 0. and 0. B. Cope, 1966. Toxicities of
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t'
! benthos in a thermally-stratified lake. Trans. Amer.
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38
15. Mayer, F. L., P. M. Mehrle. and W. P. Dwyer, 1975.
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17. Ferguson, 0. E., W. D. Cotton, 0. 0. Culley, 1965.
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39
20. Macek, K. J. and W. U. McAllister, 1970. Insecticide
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22. Katz, M., 1961. Acute toxlclty of some organic
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40
26. Genelly, R. E. and R. C. Rudd, 1956. Chronic toxlclty of
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41
J'
Kฎ
3?.~ Fitzhugh, 0. G., and A. A. Nelson, 1951.- Comparison of
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L. Fishbein, E. R. Hart, A. J. Pallotta, R. R. Bates,
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36* Casida, J. E., R. L. Holmstead, and S. Khamfa, 1974.
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-
mixture. Science, 183:520-521.
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42
i
37. Schlndler, U., 1955. Allge Forstzeltsh 33/34. p. 384.
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; mice.In orchards. Farm Research. N.Y. State Agrlc.
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40. Marsh, H., L. H. Johnson, R. S. Clark and J. H. Pepper,
1951. Toxlclty to cattle of toxaphene and chlordane
grasshopper baits. Montana State Coll. Agr. Exp.
Sta. Bull. 477:11.
41. Marsh, H., 1949. Toxaphene residues III. Experimental
feeding of toxaphene treated alfalfa to cattle and
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43. Radeleff, R. D. and R. C.-Bushland, 1950. Acute toxlclty
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44. Eubank, N. H., 1964. Toxaphene Intoxication from home
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43
j 45- Choudbury, B. and V. Robinson, 1950. Clinical and
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: Ingestion of toxic amounts of chlordane and
! ' "
i .
'. toxaphene. Amer. J. Vet. Res. 11:50-56.
r I 46. Bushland, R. C., R. W. Wells, and R. D. Radeleff, 1948.
'?',!'
r | Effect on livestock of sprays and dips containing
^ I new chlorinated Insecticides. J. Econ. Ent.
i
41:642-645.
TTBfc,
$);
''||! 47. Warrakl, S., 1963. Respiratory hazards of chlorinated
;ป! : caniphene. Arch. Environ. Health 7:253-256.
u^'tt- >
;*' ! 48. Gafafer, W. M., 1964. Occupational diseases, A guide to
" ' their recognition. U.S. Public Health Service
;*.; ''I Publication 1097, 244 pp.
A ! 49. Johnson, W. D., G. F. Lee and D. Spyrldakls., 1966.
; Persistence of toxaphene 1n treated lakes. A1r and
Water Pollut. Int. J. 10;555-560.
50. Keith, J. 0., 1966. The effect of pesticides on white
pelicans. 4th Conf. Use of Agr. Chem. In Calif.,
Feb. 8, 1966, Davis, Calif., 8 pp.
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44
51. Keith, J. 0., 1966. Insecticide contaminations In
wetland habitats and their effects on fish-eating
birds. Pesticides in the environment and their
effects on wfldl1 f e. J. Appl. Ecol., 3(Suppl.) 71-85.
,52. Rucker, R. R., 1967. Ground water toxic to fish. Proc.
N.W. F1sh Culture Conf., 87 p.
53. U.S. Department-of Agriculture, ARS, 1936. Monitoring
agricultural pesticide, residues. A Preliminary
Report of Studies on Soil, Sediment and Mater in
Mississippi River Delta. U.S.D.A., A.R.S. 13-81.
54. H111en, R. H., 1967. Special Report pesticide
surveillance program range caterpillar control
project. Colfax and Union Cols, New Mexico, Bur.
Spt. Fish. Wildlife* Div. Wildlife Services, Fort
Collins, Colorado, 31 pp.
56. Gunther, F. A., W. E. Westlake, and P. S. Jaglan, 1968.
Reported solubilities of 738 pesticide chemicals In
water. Residue Reviews. 20, 1-145.
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45
57. Bailey, G. W.and J. L. White, 1970. Factors :
Influencing the adsorption, desorption* and
movement of pesticides 1n soil. Residue Reviews
32, 29-92.
58. Hermanson, H. P., F. A. Gunther, L. D. Anderson, and
M. J. Garber, 1971. Installment application effects
upon Insecticide residue content of a California
soil. J. Agr. Food Chem. 19:722.
* ' ' '
W. Johnston, W. R., F. T. Itt1had1eh, and K. R. Craig, 1967.
Insecticides In the tile drainage effluent. Water
Resources Research, 3(2):525-537.
60. Veith, E. D. and G. F. Lee, 1971. Water chemistry of
toxaphene Role of lake sediments. Environmental
Science and Technology, 5(3):230-234.
61. Nicholson, H. P., A. R. Grzenda, and J. I. Tensley, 1966.
Water pollution by Insecticides: a six and one-half
year study of a watershed. Proc. Symposium on
Agricultural Waste Waters, Univ. of Calif., Davis. .
132-141 pp.
62. Nash, R. G.and E. A. Woolson, 1968. Distribution of j
chlorinated Insecticides 1n cultivated soil. Soil '
Scl. Soc. Amer. Proc. 32:525-527. !
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64. Johnson, 0. W. and S. Lew* 1970. Chlorinated hydrocarbon
9.
pesticides In representative fishes of Southern
**
Arizona. J4stป Monlt. Jour. 4(2):57-61. See also
Ertvfron; Nealth Abst. 1(7):2765. 1971.
65. Terrle^e, L., C., |L KHgemagi, A. R. Gerlach and R. L.
Borovlcka** 1966. The persistence of toxaphene In
lake water a$id Its uptake by aquatic plants and
animals. J.fAgr. Food Chem. 14:66-69.
56. Hughes, R. A., 1970. Studies on the persistence of
toxaphene 1n treated lakes. Ph.D. thesis,
University of Wisconsin (Water Chemistry).
57., Lowe, J,* I., Pป 0. WHson, A. J. Rick and A. J. WHson
Jr., )'971. Proceedings, of the Nat. ShellflsheHes
Association. Vol. 61:71-79.
68. Ferguson, D. E., 1975. The ecological consequences of
pesticide resistance 1n fishes. Transactions of the
32nd North American Wi-ldllfe and Natural Resources
Conference, pp. 103-107.
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69. torn, S. and R. Earnest, 1974. Acute Toxlclty of Twenty
Insecticides to Striped Bass, Morone saxatnis.
Calif. Fish and Game. 60(3):128-131o
70. Crockett, A. B., (5. B. Wlersma, H. Ta1, and W, Mitchell,
1975. Residues in F1sh, Wildlife, and Estuaries.
Pesticides Monitoring Journal 8(4):235-240,
71 . Hawthorne, J. C., J. H. Ford, and G. P. Morkln, 1974.
Residues of M1rex and other Pesticides 1n Commercially
Raised Catfish. Bulletin of Environmental Contamination
and Toxicology ll(3):258-264.
72. Schlmmel, S. C., J. M. Patrick, Jr., and J. Forester, 1975.
Uptake and Toxlclty of Toxaphene 1n Several EstuaHne
Organisms. Unpublished Date. Gulf Breeze Envlr.
Research Lab.
73. Hansen, D. J. 1969. Food, growth, migration,
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48
7f* Daugherty, F. M. Jr. 1951. A proposed toxldty test for
Industrial wastes to be discharged to marine, waters.
Sewage and Indus. Wastes, 23(8)-.1029-1031.
f . . . . ' :'
^Earnest, R. 1970. Effects of pesticides on aquatic
animals in the estuarine and marine environment. .
, Unpublished data. In: Annual Progress Report,
Bureau of Sport Fisheries and Wildlife. U.S. Dept. .
of the Interior.
77. MAS -NAE, 1973* Water Quality Criteria, 1972, EPA-R3-73-033
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49
GLOSSARY
Acutely toxic: Causing death or severe damage to an organism by
. poisoning during a brief exposure period, normally ninety-six.
hours or less.
Anadromous fishes: Fishes that spend a part of their lives in seas
or lakes, but ascend rivers and streams at certain intervals to
spawn. Examples are sturgeon, shad, salmon, trout, and
striped bass.
Application factor: The ratio of the safe concentration to the lethal
concentration as determined for potential aquatic pollutants
administered to species of interest.
Bioaccumulation (Bioconcentration): The phenomenon wherein elements
or compounds are stored in living organisms because elimination
fails to match intake.
Carcinogenic: Producing Cancer.
Catadromous fished: Fishes that feed and grow in fresh water, but
return to the sea to spawn. The best example is the American
eel.
Chronically toxic: Causing death or damage to an organism by
poisoning during prolonged exposure, which, depending on the
organism tested and the test conditions and purposes, may range
from several days, to weeks, months, or years, or through a
reproductive cycle.
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50
EC50: The concentration at which a specified effect is observed
under the test conditions in a specified time in fifty percent of
the organisms tested. Examples of specified
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LC35:. The eoncentr^on of a toxicant that is lethal (fatal) 'to twenty-
five percent of the organisms tested under toฉ test conditions in
a specified time.
LC50? The concentration of a toxicant which is lethal (fatal) to
fifty percent of the organisms tested under the test conditions
in a specified time. It is virtually identical with TLm and TL50.
LDSOs The dose of a toxicant that is lethal (fatal) tฉ fifty percent
of the organisms tested under the test coaditLoas in a specified
time. A dose is the quantity actually administered to the
organism and is not identical with a concentration, which is the
amount of toxicant in- a unit of test medium rather than the
amount ingested by or administered to the organism.,
Liter fl):. The volume occupied by one kilogram of water at a pressure
,. . o
of 760 mm of mercury and a temperature of 4 Co A liter is
1.05-7 quart.
Methylmercury: Mercury which has been methylated,, usually through
gome biological agent, such as bacteria,,
Microgram per liter (ug/1); The concentration at which one millionth
of a gram (one microgram) is contained in a Wtame of one liter.
Where the density of solvent is equal to one, one ug/1 is equiva-
lent to one part per billion (ppb) or one microgram per kilogram
(ug/kg).
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52
#Microgram per kilogram (ug/kg): The concentration at which one
- millionth of a gram (one microgram) is contained in a mass of
,, one kilogram. A kilogram is 2. 2046 pounds.
igrahi per kilogram (mg/kg): The concentration at which one
' i .
thousandth of a gram (one milligram) is contained in a mass of
i
one kilogram. A gram contains 1000 milligrams.
per liter (mg/1): The concentration at which one milligram
is contained in a volume of one liter. Where the density of the
,3 * '
solvent is equal to one, one mg/1 is equivalent to one part per .
ป ' ' .
million (ppm) or one milligram per kilogram (mg/kg).
Milliliter (ml): A volume equal to one thousandth of a liter.
ffenogram per liter (ng/1): The concentration at which one billionth
of a gram (one nanogram) is contained in a volume of one liter.
Where the density of the solvent is equal to one, one ng/1 is
equivalent to one part per trillion or one nanogram per kilogram
(ng/kg).
Neoplastic: Describing any new and abnormal growth, such as a tumor.
Part per million (ppm): A concentration in which one unit is contained
in a total of a million units. Any units may be used (e. g. , weight,
volume) but in any given application identical units must be used
(e. g. , grams per million grams or liters per million liters).
Where the density of the solvent is one, one part per million is
equivalent to one milligram per liter.
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53
Parts per thousand (o/oo): A concentration at which one unit is '
contained in a total of a thousand units. The rules for using
this term are the same as those for parts per million. Normally,
this term is used to specify the salinity of eatuarine or sea waters.
Piscicide* A substance used for killing fish.
Static bioassay: A bioassay in which the toxicant is not renewed during
the test.
Thermocline: That layer in a body of water where the temperature
difference is greatest per unit of depth. It is the layer in which
the drop in temperature is 1 t. or greater per meter of depth.
TLm - Median Tolerance Limit: The concentration of a test material
at which fifty percent of the test animals are able to survive
under test conditions for a specified period of exposure. It is
virtually synonymous with LC50 and TL50.
TL50: Synonymous with TLm and virtually synonymous with LC50.
Tumorigenic: Causing or producing tumors.
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