Env'ronmerrai P'otection
Agency
Seg'j.arons arc Stanaarcs
Criteria ar.a Standards Division
Wasnington DC 2O460
vvEPA
Ambient
Water Quality
Criteria for
Copper
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AMBIENT WATER QUALITY CRITERIA FOR
COPPER
Prepared By
U.S. ENVIRONMENTAL PROTECTION AGENCY
Office of Water Regulations and Standards
Criteria and Standards Division
Washington, D.C.
Office of Research and Development
Environmental Criteria and Assessment Office
Cincinnati, Ohio
Carcinogen Assessment Group
Washington, D.C.
Environmental Research Laboratories
Corvalis, Oregon
Duluth, Minnesota
Gulf Breeze, Florida
Narragansett, Rhode Island
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DISCLAIMER
This report has been reviewed by the Environmental Criteria and
Assessment Office, U.S. Environmental Protection Agency, and approved
for publication. Mention of trade names or commercial products does not
constitute endorsement or recommendation for use.
AVAILABILITY NOTICE
This document is available to the public through the National
Technical Information Service, (NTIS), Springfield, Virginia 22161.
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FOREWORD
Section 304 (a)(l) of the Clean Water Act of 1977 (P.L. 95-217),
requires the Administrator of the Environmental Protection Agency to
publish criteria for water quality accurately reflecting the latest
scientific knowledge on the kind and extent of all identifiable effects
on health and welfare which may be expected from the presence of
pollutants in any body of water, including ground water. Proposed water
quality criteria for the 65 toxic pollutants listed under section 307
(a)(l) of the Clean Water Act were developed and a notice of their
availability was published for public comment on March 15, 1979 (44 FR
15926), July 25, 1979 (44 FR 43660), and October 1, 1979 (44 FR 56628).
This document is a revision of those proposed criteria based upon a
consideration of comments received from other Federal Agencies, State
agencies, special interest groups, and individual scientists. The
criteria contained in this document replace any previously published EPA
criteria for the 65 pollutants. This criterion document is also
published in satisi faction of paragraph 11 of the Settlement Agreement
in Natural Resources Defense Counci 1. et. al. vs. Train, 8 ERC 2120
(D.O.C. 19/6], modified, 12 ERC 1833 (D.D.C. 1979).
The term "water quality criteria" is used in two sections of the
Clean Water Act, section 304 (a)(l) and section 303 (c)(2). The term has
a different program impact in each section. In section 304, the term
represents a non-regulatory, scientific assessment of ecological ef-
fects. The criteria presented in this publication are such scientific
assessments. Such water quality criteria associated with specific
stream uses when adopted as State water quality standards under section
303 become enforceable maximum acceptable levels of a pollutant in
ambient waters. The water quality criteria adopted in the State water
quality standards could have the same numerical limits as the criteria
developed under section 304. However, in many situations States may want
to adjust water quality criteria developed under section 304 to reflect
local environmental conditions and human exposure patterns before
incorporation into water quality standards. It is not until their
adoption as part of the State water quality standards that the criteria
become regulatory.
Guidelines to assist the States in the modification of criteria
presented in this document, in the development of water quality
standards, and in other water-related programs of this Agency, are being
developed by EPA.
STEVEN SCHATZOW
Deputy Assistant Administrator
Office of Water Regulations and Standards
111
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ACKNOWLEDGEMENTS
Aquatic Life Toxicology:
Charles E. Stephan, ERL-Duluth
U.S. Environmental Protection Agency
John H. Gentile, ERL-Narragansett
U.S. Environmental Protection Agency
Mammalian Toxicology and Human Health Effects:
George Davis (author)
University of Florida
Christopher T. DeRosa (doc. mgr.)
ECAO-Cin
U.S. Environmental Protection Agency
Jerry F. Stara (doc. mgr.) ECAO-Cin
U.S. Environmental Protection Agency
Minka Fugus
Yugoslav Academy of Science and
Arts for Medical Research and
Occupational Health
Paul B. Hammond
University of Cincinnati
Dinko Kello
Yugoslav Academy of Sciences and
Arts for Medical Research and
Occupational Health
Si Duk Lee, ECAO-Cin
U.S. Environmental Protection Agency
David J. McKee, ECAO-RTP
U.S. Environmental Protection Agency
Magnus Piscator
Karolinska. Institute
William 8. Buck
University of Illinois
Edward Calabrese
University of Massachusetts
Sylvia M. Charbonneau
Health and Welfare, Canada
Patrick Durkin
Syracuse Research Corp.
Earl Frieden
Florida State University
Norman E. Kowal, HERL-Cin
U.S. Environmental Protection Agency
Terri Laird, ECAO-Cin
U.S. Environmental Protection Agency
Steven 0. Lutkennoff, ECAO-Cin
U.S. Environmental Protection Agency
Harold Petering
University of Cincinnati
Marc Saric
Yugoslav Academy of Sciences and
Arts for Medical Research and
Occupational Health
Technical Support Services Staff: D.J. Reisman, M.A. Garlough, B.L. Zwayer,
P.A. Daunt, K.S. Edwards, T.A. Scandura, A.T. Pressley, C.A. Cooper,
M.M. Denessen.
CJerical.Staff: C.A. Haynes, S.J. Faehr, L.A. Wade, D. Jones, B.J. Bordicks,
B.J. Quesnell, C. Russom, B. Gardiner.
IV
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TABLE OF CONTENTS
Page
Criteria Surmary
Introduction A-l
Aquatic Life Toxicology 8-1
Introduction B-l
Effects B-4
Acute Toxicity 8-4
Chronic Toxicity B-8
Plant effects B-I1
Residues 8-11
Miscellaneous 8-12
Summary 8-13
Criteria B-15
References B-67
Mairmalian Toxicology and Human Health Effects C-l
Introduction C-l
Exposure C-l
fngestion from Water C-l
Ingestion from Foods C-6
Inhalation C-18
Dermal C-19
Pharmacokinetics C-20
Absorption C-20
Distribution C-25
Metabolism C-28
Excretion C-31
Effects C-34
Acute, Subacute and Chronic Toxicity C-34
Synergism and Antagonism C-38
Teratogenicity C-39
Mutagenicity C-39
Carcinogenicity C-39
Criteria Formulation C-42
Existing Guidelines and Standards C-42
Current levels of Exposure C-43
Special Groups at Risk C-44
Basis and Derivation of Criterion C-45
References C-47
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CRITERIA DOCUMENT
COPPER
CRITERIA
Aquatic Life
For total recoverable cooper the criterion to protect freshwater aauatic
14
life as derived using the Guidelines is 5.J? ug/1 as a 24-hour average and
the concentration (in ug/1) should not exceed the numerical value given by
e(0.94[ln(hardness)!-1.23) at any time. For example, at hardnesses of 50,
100, and 200 mg/1 as CaCOj the concentration of total recoverable copper
should not exceed 12, 22, and 43 ug/1 at any time.
For total recoverable copper the criterion to protect saltwater aauatic
life as derived using the Guidelines 1s 4.0 ug/1 as a 24-hour average and
the concentration should not exceed 23 ug/1 at any time.
Human Health
Sufficient data are not available for copoer to derive a level which
would protect against the potential toxicity of this compound.
Using available organoleptic data, for controlling undesirable taste and
odor Quality of ambient water, the estimated level 1s 1 mg/1. It should oe
recognized that organoleptic data as a basis for establishing a water aual-
ity criteria have limitations and have no demonstrated relationship to po-
tential adverse human health effects.
V I
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INTRODUCTION
Copper is a soft heavy metal, atomic number 29, with an atomic weight of
63.54, a melting point of 1,083*C, a boiling point of 2,595*C, and a density
in elemental form at 20"C of 8.9 g/cc (Stecner, 1968). Elemental copper is
readily attacked by organic and mineral acids that contain an oxidizing
agent and is slowly soluble in dilute ammonia. The halogens attack copper
slowly at room temperature to yield the corresponding copper halide. Oxides
and sulfides are also reactive with copper.
Copper has two oxidation states: GJ I (cuprous) and Cu II (cupric). Cu-
prous copper is unstable in aerated water over the pH range of most natural
waters (6 to 8) and will oxidize to the cupric state (Garrels and Christ,
1965). Bivalent copper chloride, nitrate, and sulfate are highly soluble in
water, whereas basic copper carbonate, cupric hydroxide, oxide, and sulfide
will precipitate out of solution or form colloidal suspensions in the pres-
ence of excess cupric ion. Cupric ions are also adsorbed by clays, sedi-
ments, and organic participates and form complexes with several inorganic
and organic compounds (Riemer and Toth, 1969; Stiff, 1971). Due to the com-
plex interactions of copper with numerous other chemical species normally
found in natural waters, the amounts of the various copper compounds and
complexes that actually exist in solution will depend on the pH, tempera-
ture, alkalinity, and the concentrations of bicarbonate, sulfide, and organ-
ic ligands. Based on equilibrium constants, Stumm and Morgan (1970) calcu-
lated copper solubility in a carbonate-bearing water. They found that cj-
2+
pric ion (Cu ) would be the dominant copper species up to pH 6, and from
pH 6 to 9.3 the aqueous copper carbonate complex (CuCCu aq) would domi-
nate. The presence of organic ligands such as humic acids, fulvic acids,
amino acids, cyanide, certain polypeptides, and detergents would alter this
equilibrium (Stiff, 1971).
A-l
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Zirino and Yamamoto (1972) developed a model to predict the distribution
of copper species in seawater. Mixed ligand complexes and organic cnelates
were not considered in the model. They predicted that the distribution of
copper species in seawater would vary significantly with pH and that
Cu(OH)-, CuC03, and Cu would be the dominant species over the entire
ambient pH range. The levels of Cu(OH)2 increase from about 18 percent of
the total copper at pH 7 to 90 percent at pH 8.6. CuCCL drops from about
30 percent at pH 7 to less than 0.1 percent at pH 8.6. Field and laboratory
studies by Thomas and Grill (1977) indicate that copper adsorbed to sedi-
ments and partlculates 1n freshwater may be released as soluble copper when
it comes in contact with seawater in estuarine environments.
Copper is ubiquitous 1n the rocks and minerals of the earth's crust. In
nature, copper occurs usually as sulfides and oxides and occasionally as me-
tallic copper. Weathering and solution of these natural copper minerals re-
sults in background levels of copper 1n natural surface waters at concentra-
tions generally well below 20 ug/1. Higher concentrations of copper are us-
ually from anthropogenic sources. These sources include corrosion of brass
and copper pipe by addle waters, industrial effluents and fallout, sewage
treatment plant effluents, and the use of copper compounds as aquatic algi-
cides. Potential industrial copper pollution sources number in the tens of
thousands 1n the United States. However, the major industrial sources in-
clude the smelting and refining industries, copper wire mills, coal burning
industries,, and iron and steel producing industries. Copper may enter nat-
ural water* either directly from these sources or by atmospheric fallout of
air pollutants produced by these industries. Precipitation of atmospheric
fallout may be a significant source of copper to the aquatic environment in
industrial and mining areas.
A-2
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The levels of copper able to <-emain in solution are directly depenaent
on water chemistry. Generally, ionic copper is more soluble in low pH,
acidic waters and less soluble in high pH, alkaline waters.
A-3
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REFERENCES
3arrels, R.M. and C.L. Christ. 1965. Solutions, Minerals and Equilibria.
Harper and Row, New York.
Riemer, O.N. and S.J. Tcth. 1969. Absorption of copper by clay minerals,
humic acid, and bottom 'nutis. Jour. Am. water Works Assoc. 62: 195.
Stecher, P.G. (ed.) 1968. The Merck index. Merck and Co., Inc., Rahway,
Mew Jersey.
Stiff, M.J. 1971. The chemical states of copper 1n polluted fresh water
and a scheme of analysis of differentiating them. Water Res. 5: 585.
Stumm, W. and J.J. Morgan. 1970. Aquatic Chemistry - An Introduction Em-
phasizing Chemical Equilibria in Natural Waters. John Wiley and Sons, Inc.,
New York.
Thomas, D.J. and E.V. Grill. 1977. The effect of exchange reactions be-
tween Fraser River sediment and seawater on dissolved Cu and In concentra-
tions in the Strait of Georgia. Sstuarine Coastal Mar. Sd. 5: 421.
Zirino, A*, and S. Yamamoto. 1972. A pH dependent model for the chemical
speclation of copper, zinc, cadmium, and lead in seawater. Limno. Ocean-
ogr. 17: 661.
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Aquatic Life ""ox-icoloqy*
INTRODUCTION
Acute toxicity tests on copper have been conducted with 45 freshwater
soecies and chronic tests with 15 species. Although the acute toxicity of
copper seems to be related to water hardness, chronic toxicity apparently is
not. Freshwater plants show a wide range of sensitivities to copper, but
few data are available concerning bioconcentration by freshwater organisms.
Four fish and eighteen saltwater invertebrate species have been acutely
exposed to copper. Results of these tests indicate a range of acute sensi-
tivities from 28 ug/1 for the summer flounder to 600 ug/1 for the shore
crab. Most of these tests were conducted using static procedures; however,
seven species were exposed In flow-through tests with measurements of the
concentrations of copper. Chronic data are available for only one species,
but bioconcentration tests have been conducted with a wide variety of
species.
Copper, which occurs in natural waters primarily as the divalent cupric
ion in free and complex forms, is a minor nutrient for both plants and ani-
mals at low concentrations but is toxic to aquatic life at concentrations
not too much higher. Concentrations of 1 to 10 ng/1 are usually reported
for unpolluted surface waters in the United States, but concentrations in
the vicinity of municipal and industrial outfalls, particularly from smelt-
ing, refining, or metal plating industries, may be much higher.
*The reader is referred to the Guidelines for Deriving Water Quality Cri-
teria for the Protection of Aquatic Life and Its Uses in order to better un-
derstand the following discussion and recommendation. The following tables
contain the appropriate data that were found in the literature, and at the
bottom of each table are calculations for deriving various measures of tox-
icjty as described in the Guidelines.
3-1
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The cupric ;on is highly reactive and forms moderate to strong complexes
and precipitates with many inorganic and organic constituents of natural
waters, e.g., carbonate, phosphate, amino acids and humates, and is readily
absorbed on surfaces of suspended solids. The proportion of copper present
as the free cupric ion is generally low and may be less than 1 percent in
eutrophic waters where complexation predominates. Various copper complexes
and precipitates appear to be largely nontoxic and tend to mask and remove
toxicity attributable to copper (Andrew, 1976). This fact greatly compli-
cates the interpretation and application of available toxicity data, because
the proportion of free cupric ion present is highly variable and is diffi-
cult to measure except under special laboratory conditions. Few toxicity
data have been reported using measurements other than total or dissolved
copper.
Of the analytical measurements currently available, a water quality cri-
terion for copper is probably best stated in terms of total recoverable
copper, because of the variety of forms that can exist in natural waters and
the various chemical and toxicological properties of these forms. The com-
monly occurring forms not measured by the total recoverable procedure, e.g.,
copper occluded in suspended mineral particulates, are forms that are less
available to aquatic life and probably will not be converted to the more
toxic forms readily under various natural conditions. The procedure for to-
tal recoverable copper, however, does measure those forms directly toxic to
aquatic lifff*, e.g., the free ion, and those labile forms (hydroxide, carbon-
ate, and some phosphate precipitates) readily converted to more toxic forms
under various natural conditions. Since the criteria are derived on the
B-2
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53S1S o* tests conducted using solub:e inorganic cooper sa^ts, total $r.-~
total recoverable copper concentrations in the tests should be nearly equiv-
alent, and the results are used interchangeably.
Because a majority of the reported test results (Tables 1 and 2} nave
been conducted with oligotrophic waters having relatively low complexing
capacities, the criteria derived herein may be at or below ambient total
copper concentrations in some surface waters of the United States. Season-
ally and locally, toxicity in these waters may be mitigated by the presence
of naturally occurring chelating, complexing, and precipitating agents. In
addition, removal from the water column may be rapid due to normal growth of
the more resistant aquatic organisms and settling of solids. The various
forms of copper are in dynamic equilibrium and any change in chemical condi-
tions, e.g., pH, could rapidly alter the proportion of the various forms
present and, therefore, toxicity.
Since increasing calcium hardness and associated carbonate alkalinity
are both known to reduce the acute toxicity of copper, expression of the
upper limit as a function of water hardness allows adjustment for these
water quality effects. This results in a much better fit with the available
acute toxicity data, because the upper limit is higher at high hardness to
reflect calcium antagonism and carbonate complexation. Some data on the re-
lationship of toxicity to other factors, i.e., temperature, alkalinity, size
of organism, and total organic carbon, are available for a limited number of
species and will be discussed later.
The following data on the effects of copper on aquatic biota (Tables 1
through 6) have been summarized from the literature from 1950 to 1980. Ef-
forts to.obtain residue data, or effects data on algae and other plants,
were not exhaustive, since previous reviews have indicated that these
3-3
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effects are of minor importance relative to toxicity of copper to fish and
invertebrate species.
All concentrations are reported as cooper, not as the compound.
EFFECTS
Acute Toxicity
Acute toxicity tests with copper have been conducted on 18 invertebrate
and 27 fish species (Table 1), with approximately 175 acute values available
for comparison. Most of these tests have been conducted with four salmonid
species, fathead and bluntnose minnows, and bluegills. The acute values
range from a low of 7.24 ug/1 for Daphnla pulicaria in soft water to 10,200
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Lind, et al. (Manuscript) (Table 1) and Brown et al. (Table 6)(1974)
have shown quantitative relationships between the acute toxicity of copper
and naturally occurring organic chelating agents. Although these relation-
ships have been demonstrated for only a few species (Daphnia magna, fathead
minnow, and rainbow trout), the effects shown should be generalizable
through chemical effects on cupric ion activity and bioavailability. Lind
et al. (Manuscript) measured the toxicity of copper in a variety of surface
waters and found that total organic carbon (T.O.C.) is a more important
variable than hardness, with Daphnia magna acute values varying
approximately 30-fold over the range of T.O.C. covered. Similar results
were obtained with fathead minnows. This would Indicate that the criteria
should be adjusted upward for surface waters with T.O.C. significantly above
the 2 to 3 mg/1 usually found in the waters used for toxicity tests.
An exponential equation was used to describe the observed relationship
of toxicity to hardness by performing a least squares regression of the
natural logarithms of the acute values on the natural logarithms of hard-
ness. Sufficient data were available for Daphnia magna, Daphnia pulicaria,
Chinook salmon, cutthroat and rainbow trout, fathead minnows, and bluegills
to show a correlation of acute toxicity and hardness. The slope of the re-
gression equations ranged from 0.67 for chinook salmon to 1.34 for Daphnia
magna with an arithmetic mean of 0.94. The close agreement of the slopes
and the highly significant (p • 0.01) regressions in each case reflect the
quality of the toxlcological data available and confirm the premise that the
effect of hardness on the acute toxicity of copper is similar for various
aquatic animals.
In the absence of the contradictory data, it is assumed that the hard-
ness relationship holds for the acute toxicity of copper to all freshwater
B-5
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aquatic animals. The irean slope (0.94) was fitted through the geometric
Tean toxicity value and hardness for each species to obtain a logarithmic
intercept for each species, "he species mean intercept, calculated as tne
exponential of the logarithmic intercept, was used as a measure of relative
species sensitivity to copper (Table 3).
Daphnia pulicaria was found to be the most sensitive species. Two other
daphnid species and the scud Gammarus pseudolimnaeus were only slightly less
sensitive. Salmonids and the bluntnose minnows were nearly as sensitive as
the daphnids, but fathead minnows and several other cyprinids were approxi-
mately 3 to 11 times more resistant. Bluegills and other centrarchids are
approximately 10 to 100 times more resistant than salmonids.
A freshwater Final Acute Intercept of 0.29 ug/1 was obtained for copper
using the species mean acute intercepts listed in Table 3 and the calcula-
tion procedures described in the Guidelines. Thus the Final Acute Equation
is e(0.94[ln(hardness)]-1.23)e
The saltwater invertebrate data (Table 1) include investigations on
three phyla: annelids, molluscs, and arthropods (crustaceans). The acute
sensitivities of crustaceans ranged from 31 ug/1 for Acartia tonsa (Sosnow-
ski and Gentile, 1978) to 600 ug/1 for shore crab, Carcinus maenus (Connors,
1972). Adult polychaete worm acute values ranged from 77 ug/l (Pesch and
Morgan, 1978) to 480 ug/1 (Jones, et al. 1976). Pesch and Morgan (1978) de-
termined that the 96-hour LCrQ for Neanthes arenaceodentata increased from
77 yg/1 1rr a flowing water system to 200 ug/l in the presence of a sandy
sediment. Jones, et al. (1976) indicated that Nereis diversicolor exhibited
a variable response to salinity over a range of 5 to 34 g/kg with the
greatest toxicity occurring at 5 g/kg. The lowest reported acute value fcr
the bivalve molluscs was 39 ug/1 fsr the soft-shelled clam, My a arenaria
3-6
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fEisler, 1977), and the highest was 560 ug/1 for the adult Pacific oyster,
Oassostrea gigas (Okazaki, 1976). Eisler (1977) indicated that trie sensi-
tivity of Mya arenaria to copper varied according to the seasonal tempera-
tu^e, with copper being at least 100 times more toxic at 22*C than at 4*C.
The arthropods (crustaceans) were both the most sensitive invertebrate spe-
cies tasted, with an acute valua of 31 ug/1 for Acartia tonsa (Sosnowski and
Gentile, 1578), and the least sensitive of all animals tested, with an acute
value of 600 ug/1 for larvae of the shore crab, Carcinus maenus (Connor,
1972). Sosnowski, et al. (1979) showed that the sensitivity of field popu-
lations of Acartia tonsa to copper was strongly correlated with population
density and food ration (Table 6), whereas cultured A_. tonsa manifested a
reproducible toxicologlcal response to copper (Table 1) through six genera-
tions (Sosnowski and Gentile, 1978), Johnson and Gentile (1979) reported
that lobster larvae appear to be twice as sensitive to copper as the adults.
The acute values for saltwater fishes include data for four species and
two different life history stages (Table 1). Acute toxicity ranged from 28
ug/1 for summer flounder embryos, Paralichthys dentatus (U.S. EPA, 1980) to
510 ug/1 for the Florida pompano, Trachinotus carolinus (Birdsong and Ava-
vit, 1971). The results of the acute tests on the embryos of summer and
winter flounder were used in Table 1 because embryos of these species ap-
parently are not resistant to copper and because other acute values are not
available for these species.
Studies air- the effect of salinity on the toxicity of copper indicate
that it is more toxic to adult pompano at 10 g/kg than at 30 g/kg (Birdsong
and Avavit 1971). Other species of saltwater fish were tested for sensitiv-
ity to copper, but the experimental conditions were not suitable for inclu-
3-7
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sion in either the acute or chronic tables; consequently, these data were
placed in Table 6. Also, a number of scientists exposed anadromous species
such as Atlantic and coho salmon to copper in freshwater. These data were
utilized in deriving the freshwater criterion, but not the saltwater
criterion.
A Saltwater Final Acute Value of 22.9 ug/1 was obtained for copper using
the species mean acute values in Table 3 and the calculation procedures
described in the Guidelines.
Chronic Toxicity
The data base for chronic toxicity of copper to freshwater aquatic ani-
mals (Table 2) includes chronic values for four invertebrate and eleven fish
species. Life cycle test results are available for two snails, Daphnia mag-
n_a at three hardnesses, an amphipod, brook trout, bluntnose minnow, fathead
minnow at four hardnesses, and the bluegill. Early life stage tests have
been conducted with several additional fish species, including channel cat-
fish at two hardnesses. The chronic values range from a low of 3.9 ug/l for
early life stage tests with brook trout in soft water to 60.4 ug/l for a
similar test with northern pike. Values for invertebrate species nearly
overlap those for fish with a range of 6.1 to 29.0 ug/1. A series of tests
with Oapnnla magna in a hard pond water (Table 6) with unmeasured copper
concentrations resulted in chronic values of about 49 ug/l.
The data available concerning the effect of hardness on the chronic tox-
icity of copper 1s somewhat nebulous. The total range of chronic values is
3.9 to 60.4 ug/1 (Table 2), which is much less than the range of 0.23 to 260
ug/l for species mean acute intercepts (Table 3). This may be due to
differences in the kinds and numbers of species and waters used in the two
kinds of tests, but it may also indicate that hardness affects chronic tox-
B-8
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icity of copper differently tnan it affects acute toxic:ty. Indeed, in
chronic tests with Daphnla nagna, Chapman, et al. (Manuscript) found that
copper was less toxic at a medium hardness than at a low hardness but was
most toxic at a high hardness (Table 2). They indicated that in the nigh
hardness tests the daphnids probably ingested some precipitated copper.
Also, some copper probably sorbed onto suspended food particles. These fac-
tors were not expected to impact chronic toxicity to species whicn are not
filter feeders, however.
Sauter, et al. (1975) found that hardness affected the chronic toxicity
of copper to channel catfish very little, if at all, and the four results
available for brook trout do not show any consistent relationship. The four
chronic tests with the fathead minnow also showed a consistent but small ef-
fect of hardness on chronic toxicity. The slope of 0.26 is not statistical-
ly significant and is much less than the acute mean slope of 0.94. A
chronic value (Table 6) from a test conducted with the fathead minnow in a
hard stream water contaminated with sewage effluent (Srungs, et al. 1976)
was more than twice other values for this species. This probably indicates
that the high levels of hardness, phosphate, and organic material reduced
the chronic toxicity of- copper in this stream. On the other hand, a factor
of two reduction in toxicity is rather small considering the much greater
reductions that occur in acute toxicity of copper.
Acute-chronic ratios for copper (Table 3) vary widely, even for tests
with the same-species. The highest ratios (38 and 156) are for two of the
more acutely resistant species, bluegills and Campeloma decisum (a snail).
Ratios for three tests with 0_._ magna ranged from 1.2 to 7.3, and for four
tests with fathead minnows from 5.4 to 20. The more sensitive species have
ratios below 4, whereas the less sensitive species have ratios above 4.
Also, the ratio seems to increase with hardness.
B-9
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"he available evidence seems to indicate that hardness affects the
acute-chronic ratio but not the chronic toxicity of coooer. Chronic tests
have been conducted with auite a variety of aauatic animals and sresent a
good indication of the range of chronic sensitivity to cooper. The
Freshwater Final Chronic Value for copper, derived from the species mean
chronic values listed in Table 2 using the calculation procedures described
in the Guidelines, is 5.6 ug/1.
The only chronic value reported (Table 2) for a saltwater species was
that for the mysid shrimp, Mysidopsis bahia (U.S. EPA, 1980). The chronic
toxicity of copper to this saltwater invertebrate was determined in a flow-
through life cycle exposure in which the concentrations of copper were
measured by atomic absorption spectroscopy. Groups of 20 individuals were
reared in each of five copper concentrations (control - 2.9 ^.0.5 ug/1, 24.2
+ 7.0 ug/1, 33.5 * 6.3 ug/1, 77.4 + 7.4 wg/l, 140.2 + 11.8 ug/1) for 46 days
at 2Q*C and 30 g/kg salinity. The biological responses examined included
time of appearance of first brood, the number of spawns, mean brood size,
and growth. The appearance of embryos 1n the brood sac was delayed for 6
and 3 days at 77 ug/1 and 140 ug/1, respectively. The number of spawns re-
corded at 77 ug/1 was significantly (p < 0.05) fewer than at 38.5 ug/1. The
number of spawns at 24 and 38 ug/1 was not significantly different from the
control. Brood size was significantly (p < 0.05) reduced at 77 ug/l but not
at lower-concentrations, and no effects on growth were detected at any of
the copp«r concentrations. Based upon reproductive data, adverse effects
were observed at 38 ug/1, but not at 77 ug/1, resulting in a chronic value
of 54' ug/1. Using the acute value of 181 ug/1, the acute-chronic ratio for
this species is 3.4.
The species mean acute-chronic ratios of 38 and 156 appear to be nigh
(Table 3), but the other seven are all within a factor af 10. The geometric
3-10
-------
mean of these seven is 5.73. If the Saltwater Final Acute Value o* 22.9
ug/I is divided by the acute-chronic ratio of 5.78, a Saltwater Final
Chrome Value of 4.Q ug/i is obtained.
°1ant Effects
Copper has been widely used as an algicide and herbicide for nuisance
aouatic plants. Although it is known as an inhibitor of photosynthesis and
plant growth, toxicity data on individual species (Table 4) are not numer-
ous. The relationship of toxicity to water chemistry and the importance of
the culture medium on toxicity has only recently been recognized (Gachter,
et al. 1973).
Copper concentrations from 1 to 8,000 ug/1 have been shown to inhibit
growth of various plant species. Several of the values are near or below
the chronic values for fish and invertebrate species, but most are much
higher. No Final Plant Value can be obtained because none of the plant val-
ues were based on measured concentrations.
For saltwater algae the concentrations of copper which cause a 50 per-
cent reduction in photosynthesis or growth are tabulated in Table 4 for one
species of macro-algae and eight species of micro-algae. The most sensitive
species were Thalassiosira pseudonana and Scrippsiella faeroense which were
inhibited by 5 ug/1.
Residues
Bioconcentratlon factors (Table 5} ranged from zero for the bluegill to
2,000 for the alga Chlorella regularis. Because copper is a required ele-
ment for animal nutrition, the significance of copper residues has never
been established, and few tests have been run for the purpose of determining
bioconcentration factors.
3-11
-------
Copper is an essential element in the respiratory pigments of sere salt-
water invertebrates, especially crustaceans, and plants have enzymes which
contain copper and are necessary for photosynthesis. However, copper is
also bioconcentrated in excess of any known needs by several saltwater spe-
cies (Table 5). The polychaete worm, Neanthes arenaceodentata, bioconcen-
trated copper 2,550 times {Pesch and Morgan, 1978), whereas in a series of
measurements witn algae by Riley and Roth (1971) the highest reported con-
centration factor was 617 for Heteromastlx Longifi His.
The highest bioconcentration factors for copper are those for the bi-
valve molluscs. Shuster and Pringle (1969) found that the American oyster
could concentrate copper 28,200 times after a 140-day continuous exposure to
50 ug/1. Even though the tissue of the oyster became bluish-green in color,
mortalities at this level were only slightly higher than the controls. This
amount of copper is not known to be harmful to man, but there have been in-
stances recorded that oysters have been unmarketable because of their green-
appearance due to high copper content.
Because no maximum permissible tissue concentration exists, neither a
freshwater nor a saltwater Final Residue Value can be calculated.
Mi seellaneous
The results of many additional tests of the effects of copper on fresh-
water aauatic organisms are listed in Table 6. Many of these are acute
tests with non-standard durations for the organisms used. Many of the other
acute tests-1r» Table 6 were conducted in dilution waters which were known to
contain materials which would significantly reduce the toxicity of copper.
These reductions were different from those caused by hardness, and not
enough data exist to account for these in the derivation of the criteria.
For example, Lind, et al. (Manuscript) conducted tests with Daphnia pulicar-
3-12
-------
j_a and fathead minnow in waters with concentrations of T.O.C. ranging up to
34 mg/1. Similarly, Geclcler, et al. (1976) and Brungs, et al. (1976) con-
ducted tests with many species in stream water which contained a large
amount of effluent from a sewage treatment plant. Also, Wallen, et al.
(1957) tested mosquitofish in a turbid pond water. Until chemical measure-
ments which correlate well with the toxicity of copper in a wide variety of
waters are identified and widely used, results of tests in unusual dilution
waters, such as those in Table 6, will not be very useful for deriving water
quality criteria.
Longer exposures than the standard acute studies have been recorded in
Table 6. Most noteworthy are the values reported for the bay scallop Ar_-
gopecten irradiens (U.S. EPA, 1980), which suffered mortality and reduced
growth at concentrations of 5 and 5.8 ug/1, respectively. Even though
several studies have been reported on the sublethal effects on survival,
growth, and reproduction, the significance of these effects has yet to be
evaluated. However, these studies do indicate existence of demonstrable
lethal effects due to chronic exposure at very low concentrations of copper.
Summary
Acute toxicity data are available for 45 species of freshwater animals.
The approximately 175 acute values range from 7.2 ug/1 for Daphnia pulicaria
in soft water to 10,200 Hg/1 for the blueglll in hard water. Statistically
significant regressions of acute toxicity on water hardness are available
for seven species, with toxicity decreasing as hardness increases. Addi-
tional data for several species indicate that toxicity also decreases with
increases in alkalinity and total organic carbon.
The range of acute values indicates that some of the more resistant spe-
cies could survive in copper concentrations over 100 times that which would
B-13
-------
be readily lethal to the Tiore sensitive species. Among the more sensitive
species are daphnids, scuds, midges, and snails which form the major food-
webs for both warm- and cold-water fishes. Concentrations of copper lethal
to these sensitive organisms in soft water are only slightly above those
chronically toxic to most fish and invertebrate species.
Chronic values are available for 15 freshwater species, ranging from a
low of 3.9 ug/1 for brook trout to 60.4 ug/1 for northern pike. Hardness
does not appear to affect the chronic toxicity of copper. Fish and inverte-
brate species seem to be about equally sensitive to the chronic toxicity of
copper. The two most sensitive species, bluntnose minnow and 13. pseudo-
limnea, are both important food organisms.
Copper toxicity has been tested on a wide range of plant species, with
results approximating those for animals. Complexing effects of the test
media and a lack of good analytical data make interpretation and application
of these results difficult. Protection of animal species, however, appears
to offer adequate protection of plants as well. Cooper does not appear to
bioconcentrate very much in the edible portion of freshwater aauatic species.
The acute toxicity of copper to saltwater animals ranges from 17 ug/1
for a calonoid cupepod to 600 ug/1 for the shore crab. A chronic lifecycle
test has been conducted with the mysid shrimp, and adverse effects were
observed at 77 ug/1 but not at 38 ug/1 which resulted in an acute-chronic
ratio of 3.4. Several saltwater algal species have been tested, and effects
were observed between 5 and 100 ug/1. Oysters can bioaccumulate copper up
to 28,200 times, and become blirsh-green, apparently without significant
mortality. In long-term exposures, the bay scallop was killed at 5 ug/1.
C3ITE3IA
For total recoverable copper the criterion to protect freshwater aauatic
life as derived using the Guidelines is 5.6 ug/1 as a 24-hour average, and
3-14
-------
the concentration (in ug/1) should not exceed the numerical value given by
e(0.94[ln(hardness)l-1.23) at any time> For exampie, at hardnesses of 50,
100, and 200 mg/1 as CaCO^ the concentration of total recoverable copper
should not exceed 12, 22, and 43 ug/1 at any time.
For total recoverable cooper the criterion to protect saltwater aauatic
life as derived using the Guidelines is 4.0 ug/1 as a 24-hour average, and
the concentration should not exceed 23 ug/1 at any time.
B-15
-------
Table I. Acute values for copper
Spec let
Metl
hod*
Ch~lc.l
(•0/1 M
C*CO,>
LC50/EC50
tuft/H"
Specie* Me**
Acute Value
(ufl/D** Reference
FRESHMATER SPECIES
Mora,
Llmnodrllus hoff met start
Worm.
Malt »p.
Snail (adult).
Awtl col a sp.
Snail,
Campeloma dec 1 sum
Snail,
Gyraulus clrcumstrlatus
bnal 1,
Khysa l>olm ostropha
Ptiyia Integra
Ctadoceran,
Udphla magna
Cladoceran,
Daphnla maqna
Cladoceran,
Oaphnla magna
Cladooaran,
Oaphnla magna
Cladoceran,
Daphn 1 a magna
Cladoceran,
Daphnla magna
Clddocaran,
Oaphnla magna
s,
s.
s.
FT.
s.
s.
FT,
s.
R.
s,
s.
s.
s.
s.
U
H
M
M
U
U
M
U
U
U
U
U
U
M
Copper
-------
TabU I.
Species
Clddoceran,
Daphnla «agna
Cladoceran,
Daphnla wtgna
Cladoceran,
Uaphnla «agna
Cladoceran,
Dophnlo *agna
Cladoceran,
Oaphn la pul ex
Cladoceran,
Oaphn la pu Hear I a
Cladoceran,
Oaphn 1 a pu 1 1 car 1 a
Clddoceran,
Daphnla pull car la
Cladoceran,
Daphn 1 a pull carlo
Cladoceran,
Daphnla pul (carlo
Cladoceran,
Daphnla pul (car la
Cladoceran,
Daphn la pu 1 1 car 1 a
Cladoceran,
tidphnla pul 1 car la
Scud,
Gamarus pseudol Innaeub
Method*
S, 14
S. M
S, M
S. U
S. U
R. M
R, M
R. M
R, M
R. M
R, M
R. M
R, M
FT, M
CtMBlcal
Copper
ch lor I de
Copper
chloride
Copper
chloride
Copper
Copper
«i If at*
-
-
-
Copper
sul fate
Hard****
(•g/l M
w
106
207
45
45
48
48
48
44
45
95
145
245
35-55
Species Mean
LC50/EC50 AcMt* Vain*
Cua/l)""
-------
TabI* I. (Continued)
Species
Scud,
Gammarus sp.
Crayfish,
Orconectes rustlcus
Stonefly,
Acroneurla ly cor las
Damsel fly.
Unidentified
Midge,
Chlronomus sp.
Caddlsf ly.
Unidentified
Hotl fur.
I'lil tociknd acultcornls
Rotifer,
Phltodlna acutlcornls
Rotifer,
Phllodlna acutlcornls
American eel.
Angullla rostrata
American eel.
Angullla rostrata
Cono salmon (adult).
Oncorhynchus Msutch
Cono salmon (year ling).
Oncorhynchus Msutch
Cono salmon (yedrllng).
Oncorhynchus klsutch
Method*
S.
FT,
s.
s.
s.
s.
s.
R,
R.
s.
s.
FT,
S.
S.
M
M
M
M
H
M
M
U
U
M
M
M
M
M
Chemical
_
Copper
sul fate
Copper
sul fate
-
-
_
Copper
sut tate
Copper
sul fate
Copper
sul tate
Copper
nitrate
_
Copper
chloride
Copper
chloride
Copper
ch lor 1 do
Hardness
-------
Tab I* I. (Co»tlmu«4)
Specie*
Cotto salmon (smolt).
Oncorhynchus kliutch
Chinook salmon (•levin).
Oncorhynchxt tthattyttch*
Chinook salmon (swim-up).
Oncorhynchus tsha*ytscha
Chinook salmon (parr).
Oncorhnychus tshaaytscha
Chinook salaon (saoin.
Oncorhynchus tshawyttcha
Chinook salmon.
Oncorhynchus tshawytscha
Chinook salaon.
Oncorhynchus tshawytsctia
Chinook salmon.
Oncorhynchus tshaaytscha
Chinook salmon.
Oncorhynchus tshawytscha
Cutthroat trout.
Salno clarkl
Cutthroat trout.
Sal«o clarkl
Cutthroat trout,
Sal no clarkl
Cutthroat trout.
Salao clarkl
Cutthroat trout.
Salno clarkl
Method*
5,
nr.
FT.
FT.
FT.
FT.
FT,
FT,
FT.
FT.
FI.
n.
FT.
FT.
M
M
H
M
M
M
M
M
H
M
H
M
M
H
ChwBlca!
Copper
chloride
-
-
-
-
_
-
-.
-
Copper
chloride
Coppar
chloride
Copper
chloride
Copper
chloride
Copper
chlorite
Hortfn***
(•0/1 M
c£o\}
89-99
25
25
25
25
11
46
162
3W
205
70
18
204
83
Sp*ct*s Neaa
LC50/EC50 Acute Valu*
(Mfl/l)'"
60
26
19
M
26
10
22
65
130
367
186
36. tt
232
162
-------
Table I. (Continued)
Species
Cutthroat trout,
Sal»o clarkl
Cutthroat trout.
Salao clarkl
Cutthroat trout,
Saleo clarkl
Cutthroat trout,
Sat mo clarkl
Rainbow trout.
Salao galrdnerl
Rainbow 1rout.
Sal »o galrdnar I
Rainbow trout.
Sal»o t}a I f dnur I
Rainbow trout,
Rainbow trout,
Sal«o qalrdnerl
Rainbow trout,
Sal mo galrdnerl
HdlnboM trout,
Salnto galrdnerl
Ra I nbow trout ,
Rainbow trout,
Rainbow trout,
Saliao galrdnarl
Method*
FT, H
FT,
FT,
FT,
FT.
".
FT.
FT.
FT,
FT,
FT,
FT,
FT,
FT,
M
M
M
M
M
H
M
M
M
H
H
H
M
Chealcal
Copper
chloride
Copper
chloride
Copper
chloride
Copper
chloride
Copper
Sulfate
Copper
sul fate
Copper
sulfate
Copper
sulfate
Copper
sulfate
Copper
sulfate
Copper
sul fate
Copper
sulfatu
Copper
sulfate
Copper
su 1 f a te
Hardness
(•y/l M
C«C03>
31
160
74
26
30
32
31
31
30
101
101
99
102
101
Species MeM
U50/ECSO Acute Value
(ua/l)" "
73.6
91
44.4
15.7
19.9
22.4
28.9
30
30
176
40
33.1
30.7
46.3
Reference
Ctiakou«aki
19/9
C.'kikoueaXi
H79
Chakouaaki
Cnakou«aki
Howarth &
U78
Huwarth 4
I-J78
howarth A
1978
Huwarth &
1978
Huwaith &
1978
Howarth &
1978
Ikjwarth &
1978
huwarth &
1978
Itowarth &
1978
licwarth &
I97U
& Spraguo,
4 Sprague,
& Sprague,
& Sprague,
& Sprayue,
& Sprague,
& Sprague,
& Spraguu,
& Spraguu,
& Sprague,
B-20
-------
Table I. (Coat lftit*d>
Ra I nbcw trout ,
Sa I go oa I rdn»r I
Rainbow trout,
Salao oalrdnarl
RalnboM trout,
Salt«o Qalrdnerl
Rainbow trout,
Salad oalrdnerl
Rainbow trout,
SalfK> oalrdnerl
Rainbow trout,
Salao galrdnerl
Rainbow trout.
jg I mo qa 1 1 dnef I
Kalnbow trout,
balmo
Kalntxjw trout,
Sal mo (jalrdnerl
Rainbow trout,
Sal»o
Rainbow trout,
Sat»o qalrdnarl
Rainbow trout,
Sal»o golrdnorl
Rainbow trout,
Sal»o oalrdnarl
Rainbow trout,
Salno
Method'
FT, M
FT, M
FT, M
FT, N
FT, N
FT, M
fT, M
FT, M
FT, M
FT. N
FT, M
FT, H
FT, M
FT, M
Chaailcal
Copper
sulfate
Copper
sulfate
Copper
tuI fata
Coppar
sulfate
Copper
sultate
Copper
&ul tatu
Copper
sulfate
Copper
sulfate
Copper
chloride
Copper
chloride
Copper
chloride
Copper
chloride
Copper
chloride
Copper
ctilorlde
Hardness
(•9/1 M
CaCO,)
99
KM)
100
9fi
370
366
371
361
194
194
194
194
194
194
LC50/EC50
(Mfl/l)"
47.9
48.1
81.1
85.9
232
70
82.2
298
169
85.3
81.3
103
274
128
Species Mean
Acute Value
(t«o/l)" Reference
How art h i Sprayue,
1978
- Huwarth I Sp rogue,
1978
Howarth & Spratjua,
1978
Howarth & Sprayue,
1978
Howarth & Sprayue,
1978
Mowarth & Sprague,
1978
Howarth & Sprague,
1978
Howarth & Sprague,
1978
ChakouMakos , et a I
1979
Chakouaakos, at al
1979
Chakou»akc6, ut al
1979
Chakouaakos , ut al
1979
Chakouiiakos, ut al
1979
Chakou«akos, et al
1979
B-2i
-------
T*bU I. (Continued)
Spec let
Rainbow trout,
Salmo galrdnwl
Rainbow trout,
Salmo galrdnwl
Rainbow trout,
Salmo galrdnerl
Rainbow trout.
Salmo galrdnmrl
Rainbow trout,
Sal no galrdnerl
Rainbow trout (a lev In),
Sal MO galrdnerl
Rainbow trout (swim-up).
Sal no qalrdnerl
Rainbow trout (parr).
Sal MO galrdnerl
Rainbow trout (smolt),
Salmo galrdnerl
Rainbow trout (adult).
Sal «o galrdnerl
Rainbow trout.
Sal no galrdnerl
Rainbow trout.
Sal BO galrdnerl
Rainbow trout.
Sal no galrdnerl
Rainbow trout,
Salmo galrdnerl
tUthod"
FT,
FT,
FT.
FT.
FT,
FT.
FT,
FT.
FT.
FT.
FT.
FT.
FT.
FT.
M
M
M
N
H
M
M
M
M
H
M
N
M
H
Chmmtcml
Coppor
chlorldw
Copper
chloride
Copper
dtlorld*
Copper
dilorlde
Copper
chloride
Copper
chloride
Copper
su 1 fate
Copper
su 1 fate
Copper
sulfate
Copper
sul fate
Hardness
(•a/I M
C-COxJ
194
194
194
194
194
25
25
25
25
42
350
125
125
125
LC50/EC50
(uo/»**
221
165
197
514
243
28
17
18
29
57
102
200
190
210
Specie* H**N
Acut* Value
(|ia/O** Reference
Chakouaakos, et al.
1979
Chakouaakos , et a 1 .
1979
Chakouaakos, at al.
1979
ChakouMkos, et al.
1979
ChakoiMtakos, et al.
1979
Chapman, 1978
Chapman, 1978
Chapman, 1978
Chapman. 1978
Chapman t Stovens,
1978
fogels & Sprayue, 19/7
Spear, 1977
Spear, 1977
Spear, 1977
3-22
-------
TabU I. (Continued)
Species
ftalnbOM trout.
Sal BO qalrdnerl
Atlantic salMon,
Salmo salar
Atlantic salaon,
Salno salar
Atlantic salaon,
Salao salar
Brook trout,
Salvellnus fontlnalls
S toner ol ler,
Ca«posto*a anonalu*
Goldfish,
Carasslus auratus
Goldfish,
Car ass 1 us nuratus
Carp.
Cyprlnus carplo
Carp.
Cyprlnus carplo
Longfln dace,
Agosta chrysogaster
Striped shiner.
Notropls cftrysocephalus
Striped shiner,
Ho tf op Is chrysocephalus
Bluntnose eilnnoM,
Plaephales notatus
Method*
•^•^••Avm^k
S, M
FT, M
S. M
FT, M
FT, M
n, M
S, U
FT, M
S. M
S. H
Ru
• "
FT, M
FT, M
FT, M
Chealcal
Copper
suttate
Copper
sulfata
Copper
sulfate
Copper
su 1 fate
Copper
su| fate
Copper
sul fate
Copper
nitrate
-
Copper
sulfate
Copper
sultate
Copper
sulfate
Copper
*u 1 fate
Hardness
(«g/l as
CaCOx)
290
20
8- JO
14
200
20
52
53
55
221
200
200
200
LC50AC5O
890
48
125
32
100
290
36
300
810
800
060
790
1,900
290
Species Mean
Acute Value
(MO/I)" Reference
Calomarl & Mdrchettl,
1973
Spragoe, 1964
Wilson. 1972
Sprague & Ramsey, |96ti
McKI» i bonolt. 1971
Guckler, et al. 197b
Pickering & Henderson,
1966
Tsal & McKee, I960
Keh-Gldt, et al. 1971
RehKoldt, et al. 1972
Lewis. 1978
Geckler, et al. 1976
Gecklar, et al. 1976
Geckler. et al . 1976
B-23
-------
Tab la I. (CoAtlMMd)
Spaclas
Uluntnose Minnow,
PlMephales notatus
Uluntnosa Minnow,
PlMephales notatus
Uluntnosa Minnow.
PlMephales notatus
Uluntnosa Minnow.
PlMephales notatus
Uluntnosa Minnow,
PlMaphales notatus
Uluntnose Minnow,
PlMephales notatus
Uluntnose Minnow,
PlMuphales notatus
Fathead Minnow,
Plnaphales proaelas
Fathead Minnow,
PlMQphales prOMelas
Fathead Minnow,
PlMephalas pronelas
Fathaad Minnow,
PlMephales pr OMB las
Fathead Minnow,
PlMephales proMelas
Fathaad Minnow,
PlMephales proaelas
Fathead Minnow,
PlMephales pronalas
Matl
FT.
n.
FT.
FT.
FT.
FT.
FT.
FT.
FT.
FT.
FT.
s.
s.
s.
**•
M
M
M
M
M
M
M
M
M
M
M
U
U
U
ChaMlcal
Copper
sulfate
Copper
sul fata
Copper
su 1 (ate
Copper
sulfate
Copper
sul (ate
Copper
sul fate
Copper
su 1 fata
Copper
sul fata
Coppar
su If ate
Copper
sulfate
Copper
sul fate
Coppar
sul fate
Hard****
(tM/l M
CaCOj)
200
200
200
200
194
194
194
202
202
200
45
360
20
200
Spacla* Maan
IOO/EC50 Aoita Value
260
260
280
340
210
220
270
460
490
790
200
1.450 (2)»"
23 U)""
430
Reference
Geckler. et al. 1976
GecKler. et al. 1976
Geckler. et al. 1970
Geckler, et at. 1976
Horning 4 Nelhelsel,
1979
Horning & Heine lie),
1979
Hurnlng I Nalhelsel.
1979
Pickering, et al. 1977
Pickering, et al. 1977
Andrew, 1976
Andrew, 1976
Pickering & Henderson,
1966
Pickering & Henderson,
1966
Mount, 196tt
B-24
-------
T«bU I. (Continued)
Species
Fathead Minnow,
Plaepnales propel as
Fathead Minnow,
PlMephales proMlas
fathead Minnow,
Plaephales proMeles
Fathead Minnow.
PlMephales proaelas
fathead minnow,
Pl*ephales grata las
Fathead Minnow,
PlMephales proMelas
Fathead Minnow,
PlMephales proaelas
Fathead Minnow,
PlMephales proMalas
Blacknose dace.
Rttlnlchthys atratulus
Creek chub,
SeMOtllus atroaaculatus
Brown bullhead.
Ictalurus nebulo»us
Brown bul Inead,
Ictalurus nebwlo&us
Banded klllUlsh,
Fundulus dlaphanus
Banded klllltlsh.
Fundulus dlaphanus
Method*
FT.
s.
FT.
fT.
FT.
FT.
FT.
FT.
".
FT.
n.
FT.
s.
s.
H
U
H
N
H
M
H
M
M
H
H
M
M
M
Chemical
Copper
su 1 fa te
Copper
sulfate
Copper
sulfate
Copper
su 1 fate
Copper
sulfate
-
Copper
su 1 fate
Copper
sulfate
Copper
sulfate
Copper
su 1 fate
Copper
nitrate
-
HardM**»
(MO/I M
CaCGy
200
31
31
200
200
48
45
46
200
200
202
200
53
55
Species ItaAA
IOO/EC50 Acwte Value
(pa/I)'* (Ma/l>'* Reference
470
B4
75
440
490
114
121
68.5
320
3)0
160 <2)«"
540
660
640
Mount & STttptan,
Mount & Stephan,
Mount & Stephan,
Cockier, at al.
Geckler. et al.
Llnd, et al.
Manuscript
Llnd, et al.
Manuscript
1969
1969
1969
1976
1976
Llnd, et al.
Manuscript
Geckler, et al. 1976
Geckler, «t al. 1976
Brungs, et al. 1973
Geckler, et al. 1976
Rehwoldt. et al. 1971
Kehwoldt, et al.
197*
B-25
-------
Tabl* I. (CoatlM***1)
Spacla*
Flagflsh.
Jordanalla florldaa
Guppy,
Poacllla ratlculata
Guppy,
Poacllla ratlculata
Guppy.
Poacllla ratlculata
Mhlta porch.
HOT one a*ar Icanus
White parch.
Hot one Amur Icanus
Sir (pad U>ii,
Hoi one Sdxatllls
Striped bass,
HOT one &axatl 1 Is
Strlpad bass.
Moron* saxatl 1 Is
Strlpad bass (larva).
Moron* saxat 1 1 1 ft
Strlpad bass (larva).
Moron* saxat Ills
Striped bass (f Ingarl Ing),
Mor one saxatills
Rainbow darter,
Ctheostoa* caaruleua)
Orongethrodt dorter,
Etheostoaia spectabl le
M»tl
FT.
s,
fT.
FT.
S.
S.
s.
s.
s.
s.
s.
s.
FT.
FT,
to*"
M
U
M
M
M
H
M
M
U
U
U
U
M
M
"— leal
Copper
sul fat*
Copper
nl trata
Copper
nl trata
Copper
su 1 fata
Copper
sulfate
Copper
sul fate
(»
-------
Table I. (Continued)
Species
PuMpklnseed,
L spool s ' g I bbosus
Pu*pklnseed,
L spools glbbotus
PiMpklnseed,
Lepo»ls fllbtootus
Puapklnseed,
Lepomls gl bbosus
Puwpklnseed,
lepoals gl bbosus
Punpkln&eed,
Lepoals gl bbosus
PuMpklnseed,
lepouls gl bbosus
Punpk Inseed,
lepo»ls gl bbosus
Pu«pk Inseed.
Lepcmls gl bbosus
Bluegl 1 1,
Lepomls «acrochlrus
B 1 ueg III,
Lepomls Mcrochlrus
Bluegl II.
Lepoals nacrochlrus
Bluegl II,
Lepo»ls aacrochlrus
61 ueg II 1,
Lepo»ls aocrochlrus
Method* Cheaical
S. M Copper
nitrate
S. M
FT. M Copper
so 1 fate
rT, M Copper
sultate
FT, M Copper
MI If ate
FT, M Copper
su 1 fate
FT, M Copper
sulfate
FT, M Copper
sulfate
FT, M Copper
sulfate
FT, M Copper
sulfate
FT, M Copper
tultate
n, M Copper
sulfate
S, U Copper
chloride
S. U Copper
sulfate
Hard«esc
(•9/1 M
53
55
125
125
125
125
125
125
125
45
200
200
43
20
LC50/EC50
2.400
2,700
1,240
1,300
1,670
1,940
1.240
1,660
1,740
1,100
8.300
10,000
1,250
660
Species. Mea»
Acute Value
(yg/|)*« Reference
Hflhiroldt, et al.
KehMoldt, et al.
Spear, 1977
Spear, 1977
Spear. 1977
Spear, 1977
Spear, 1977
Spear, 1977
Spear, 1977
Uenolt, 1975
Geckler, et al.
Geckler, et al.
1971
1972
1976
1976
Patrick, et al. 1968
Pickering t Henderson
1966
B-27
-------
Table I. (ContlMMd)
Blueglll,
Lepoals Mcrochlrus
Blueglll,
Lepo»U MBcrochlrus
Largenouth toss,
Mlcropterus salitoldes
Polychaete MOT*,
Neanthes arenaceodentata
Polychaete norm,
Noanthes arenaceodentata
Polychaete worm.
Nereis dlverslcolor
Polychaete wor«,
Nereis dlverslcolor
Polychaete worm,
Nereis dlverslcolor
Polychaete worm,
Karat* dlver&tcolor
Polychaete warm,
Phyllodoc* aaculata
pacific oyster,
Crassostrea qlgas
American oyster,
Crassostrea vlrglnlca
black aba lone.
Ho Mot Is cracherodll
Hud db*i loflu.
Ml***
S, U
FT, N
R, U
FT, M
FT, M
S. U
s, u
S, U
s. u
S, U
FT, M
S. U
S, U
S, U
CIM.IC.I ££!)**
Copper 360
MI! fat*
Copper 35
sul fate
100
SALTWATER SPECIES
Copper
nitrate
nitrate
Copper
sulfat*
Copper
su 1 fate
Copper
cul fat*
Copper
suilate
Copper
su 1 tat*
Copper
su 1 fate
Copper
chloride
Copper
MJ! fate
Copper
sul loto
LC30/BCSO
iHfl/D11*
10,200
2,400
6,970
77
200
200
44)
460
410
120
560
128
50
65
Acute Velu*
(HO/I)** Reference
Pickering i Henderso
1966
O'Hora, 1971
Uli g« i BUck. 1979
Pesch I Morgan, 1970
124 Pescii i Morgan, 1970
Jones, et al. 1976
Jones, et al. 1976
Jones, et al. 1976
364 Jones, at al. 1976
120 McLuiky i Phillips,
1975
560 Gkazakl. 1976
120 Calabrase, et al. 19]
50 Martin, at al. 1977
Martin, at al. 1977
B-28
-------
T«t>l» I. (Continued)
Species
Red abalone (larva).
Ha Hot Is rutescens
Soft shelled claw.
My a aranarla
Calanold copepod,
Acartla clausl
Calanold copepod,
Acartla tonsa
Calanold copepod.
Acartla tonsa
Calanold copepod,
Acartla tonsa
Copepod ,
turylewora dt finis
Uopepod,
Pbeudodlaptomus corooatus
Copepod,
Tlylopus Japonlcus
Hysld shrliip,
Hysldopsls bah la
Hysld shrlqp,
Mysldopsls blgelowl
Aaerlcan lobster (larva),
Homarus aaerlcanus
Aaer 1 can lobster ( adu It).
Huaarus aiter Icanus
Brown shrl«j> (larva),
Crangon crangon
Method*
S, U
s, u
s. u
s, u
s. u
s, u
s, u
s. u
s. u
H, M
H, M
s, u
s, u
s, u
Hardn***
(•9/1 BS
Ch*alcal CaCO^)
Copper
su 1 fate
Copper
ch lor 1 de
Copper
chloride
Copper
chloride
Copper
chloride
Copper
chloride
Copper
chloride
Copper
ch lor 1 de
Copper
chloride
Copper
nitrate
Copper
nitrate
Copper
nitrate
Copper
sul fate
Copper
sul fate
Spec 1 •« Mean
LC30/EC5O Acute Value
(pg/O** (fig/I)** Reference
114 86
39 39
52 52
17
55
31 31
526 526
136 138
487 487
181 181
141 141
48
100 69
330 330
Martin, et al. |977
Elsler, 1977
U.S. EPA. 1900
ScsnowsKI & Gentl lo.
19/8
I9?8
So.nowsKI & Genii lu,
19/8
U.>. EPA, 1980
U.j. EPA, 1980
U.S. fcPA, I960
U.S. tPA, 1980
U.S. kPA. 1980
Junnson & Gentile,
1979
Connor. 1972
3-29
-------
Table I. (CootlMMd)
Specie*
Shore crab (larva),
Carclnus motnu*
F lor 1 da pompano,
Trachlnotus carol lnu»
Florida ponpano,
Trachlnotus carol Inus
Florida po*pano,
Trachlnotus carol Inus
Atlantic cllverslde
(larva).
Men Id la aenldla
SuB»er flounder (enbryo)-,
Paral Ichthys dentatus
M Inter flounder (eabryo).
P seudop 1 euronectes
aaerlcanus
Method"
*•«••••*•»
S, u
s. u
s. u
s, u
FT, M
FT, M
FT, M
ClMalcal
Coppor
su 1 fat*
Coppw
sullat*
Copp~-
wlfat*
Coppw
sulfat*
Copper
nitrate
Copper
ch lor 1 de
Copper
nltrata
HarAMCC
(•0/1 M LC50/BC50
C*CO^) (Hfl/l)"«
600
360
360
510
136 (7)
28 (3)
129 (9)
Sf»«Cl«* M*M
Aoit* Valw
(Pfl/l)"
600
412
••• 136
»»» 28
»*» ,29
R«f*T4HtC*
Connor, 1972
Hlrdsong & Avavlt,
I'J7I
BJrdsoMg i Avav;r,
1971
Blrdioog & Avavlt,
1971
U.S. EPA, I960
U.S. tPA, I960
U.S. tPA, I9HU
* S • static, FT • Hod-through, R » ronawal, U * un«aa^urod, M * Measured
•" Results are expressed as copper, not as the compound.
• "Arithmetic «ean of (N) results.
frashnator;
Acute toxic Ity vb. hardness
Cladoceran, Daphnla »dgna: slope - 1.34. Intercept = -2.64, r • 0.80, p - 0.01, N = 10
Cladoceran. Daphnla pul Icarln; slope » 0.70, Intercept - -0.40, r " 0.94, p * 0.01, N « 8
Chinook saloon, Oticorhynchus tshaxytscha: slope * 0.67, Intercept = 0.93, r » 0.93, p • 0.01, N = 8
Cutthroat trout, Saloo clarkl: slope « O.B8, Intercept = 0.79, r » 0.78, p = C.01. N - 9
B-30
-------
TabU t.
Ralnbov trouf, S«lao galrdnerl: slope - 0.87, Intercept » 0.33, r = 0.76, p » 0.01, N - 39
fathead •IniKM, Plaaphales pr coal as: slope » 1.12. Intercept * 0.38, r = 0.96. p « 0.01, N = 15
|, l«pt»U •ttcrocMru*: »lop* » 1.00, Intercept « 3.60, r • 0.95, p - 0.01, N • 7
ArlthMtic aAon acut* slop* * 0.94
B-31
-------
Tebl* 2. Chronic v*ln*» for
SpecUt
Snail,
Ca«peloMa declsua
Snail,
Physa Integra
Cladoceran,
Daphnla •agna
Cladocerarn,
Ddphnla raagna
Cladoceran,
Ddphnla macfna
Scud.
Camnaius pseudol Imnaeub
KalnbuM trout,
Salmo galrdnerl
Brown trout ,
Salno trutta
Brook trout.
Salvellnus font (nails
Brook trout.
Salvellnus fontlnalls
Brook trout,
Salvellnus tontlnalls
Brook trout.
Salvellnus tontlnalls
Lake trout.
T«t«
Cl>«»lc*l
HardMts
(•0/1 •*
CaOH)
Halts Chronic Value
Refer enc*
FRESHWATER SPECItS
LC
LC
LC
LC
LC
LC
ELS
ELS
LC
ELS
ELS
as
ELS
Copper
sul fate
Copper
sul fata
Copper
chloride
Copper
chloride
Copper
ch lor Ida
Copper
sul tate
Copper
sul fate
Copper
sul tate
Copper
sul fate
Copper
sul fate
Copper
sul fate
Copper
sul tate
Copper
sul fate
45
45
51
104
211
45
45.4
45.4
45
45.4
37.5
187
45.4
8-14.8
8-14.8
II. 4-16.3
20-43
7.2-12.6
4.6-8
II. 4-31. 7
22.0-43.2
9.5-17.4
22.3-43.5
3-5
5-8
22.0-42.3
10.9
10.9
13.6
29.0
9.5
6.1
19
30.8
12.9
31.1
3.9
6.3
30.5
Arthur t Leonard.
1970
Arthur & Leonard.
1970
Chapaan, et al.
Manuscript
Chapman, et al.
Manuscript
Chapaan, et al.
Manuscript
Arthur & Leonard,
1970
HcKla. et al. 1978
McKIm, et al. 1978
McKIm i Uonojr, 1971
McKIn, et al. 19/8
Sauter. et al. 1976
Sauter. et al. 1976
McMu, et al. 1978
3-32
-------
Tab I* 2.
Specie*
Northern pike,
Esox luclus
Bluntnosa Minnow,
Plaephalas notatus
Fathead •IniKM,
PlMephale* jkroewlM
Fathead •Innott,
Plewpttales proMela*
Fathead •Innow,
PlMepnaleS prOMlaS
Fathead alnncw,
Plnephales proatelas
While sucfcar.
CatostoMus coamrsoni
Channet catfish,
Ictalurus punctatus
ChaniMl cattish,
Ictalurus punctatus
Bluaglll,
L«po«ls aacrochlrus
Hal ley*.
Stlzostadlon v I trend
Mysld shrlap,
Hysldopsls ball la
T^t"
ELS
LC
LC
1C
LC
ELS
as
ELS
ELS
LC
as
LC
ChMlcal
Copper
sulfata
Coppar
sulfat«
Copp«r
sulfata
CoppM-
tultat*
Coppw
sultat*
Copper
Mil fat*
Copp*r
sulfat*
Copper
su 1 fat*
Copper
sul fata
Copper
sul fat*
Copper
nitrate
Heron***
(•g/l •*
CaCO,)
45.4
194
198
30
200
45
45.4
36
166
45
35
SALTWATER SPECIES
54
Llaltc Chronic Value
" the compound.
B-33
-------
Tabl* 2. (Continued)
Acute-Chronic Ratios
Sf«cl««
Snail,
CMMM|CMM& (toclsiMi
Snail.
Phyta Integra
Cladocaran,
Oaphnla •agna
Cladocwan,
Daphnla *agna
Cladocvran,
Oaphnla aagna
Scud,
Caaaarus pseudol Iwtaaus
Brook trout,
Salv«llnu$ fontlnalls
Bluntnota Minnow,
Plaaphalas ootatut
Fathaad aliuMM,
Fattoad •lnoo«,
Pl»«phal*s proa* las
Fathaad •IDIKM,
Pla*phal«s proavlas
Fattwad •InnoM,
Pla*phal«s pro** la*
L«go«lt *acrochlrus
Mysld shrlap,
Mysldopsls bah In
(•9/1 as
CaCOO
45
45
57
104
211
45
45
194
198
30
200
45
45
Acut« Valua
1.700
26
34
69
20
100
233
430
75
475
K>8
1,100
181
Chronic Valua
10.9
10.9
13.6
29.0
9.5
6.1
12.9
8.8
21.9
14.0
27.7
18.5
29.0
54
Ratio
156
3.6
1.9
1.2
7.3
3.3
7.8
26
20
5.4
17
5.8
38
3.4
B-34
-------
Table 2.
Freshwater Species Mean Chronic Values
Species Mean
Chronic Value
Rank* Specie*
15 Morthern pike, 60.4
Esox luclut
14 Brown trout. 30.8
Salaa trutta
13 Lake trout 30.5
Satvailnu» naaaycush
12 SluegllJ, 29.0
II
10
White sucker,
Cato&toMis c caper son t
Fathead Minnow,
Rainbow trout.
Sal BO galrdnwl
Wa Maya,
Stlzostedlon vltraua
Cladoceran,
Oaphnla Magna
Channel cattish,
Ictalurus punctatus
Snail,
Physa Integra
Snail,
CaopefcMa doc 1 sum
Brook trout ,
Salvellnus fontlnalls
20.9
19.9
19.0
16.5
15.5
15.2
10.9
10.0
B-35
-------
Tab I* 2.
Speclas Mean
Chronic Value
Rank* Species (UQ/|)
2 Blunt nose Minnow, 8.8
Pl«*pt>al»fc notatus
I Scud, 6.1
psaudoll«na«us
fr«cl«6 «»an chronic value.
Fr«shwat*r Final Chronic Valu* - 5.96 |ig/l
B-36
-------
Table 3. (Continued)
Species M»ar> Species Mean
Acwte Intercept Acute-Chronic
tonfc* Species (ug/l) Ratio
30
29
26
27
26
25
24
23
22
21
20
19
18
Rotifer.
Phllodlna acutlcornls
Striped bass,
Morone saxat Ills
Striped shiner.
Mo tr op Is chrysocephalus
Orongethroot darter,
Eth«osto»a spectabl la
Longfln dac«,
Agosla chrysogaster
flogflsh.
J or d anal la florldae
Atlantic saloon,
Salno sal or
Goldfish.
Car ass 1 us ourotus
fathead •Inno*.
Pl«aptiales proaalas
Brook trout,
Salvellnus fontl nails
Worn,
Nals sp.
Rainbow darter,
EtheostoM caeruleu*
Blocknose dace,
Khlnlchthys atratulus
brovn bul (head,
lctaluru!> nubulosus
14.4
10. 1
8.41
5.61
5.37
5.00
4.95
3.97
3.29 10. 1
2. BO 7.8
2.28
2.20
2.20
2.13
3-38
-------
Table 3. Specie* mean acute Intercept* MM! values and acute-chronic ratios for copper
Specie* Mean Specie* Mean
Acute Intercept Acute-Chroalc
.Rank* SpOCla* lde&
Blueglll,
Lopoals Mcrochirus
Snail,
CoopeloMB daclsu*
Crayfish,
Orconect«s rustlcu&
Scud,
GaMMrus sp.
Snail.
Ann 1 co la sp.
PumpK I nseed,
LupOMlK glbbosus
Banded kll llflsh,
Fundulus dlaphanus
Carp,
Cyprlnus carplo
SPECIES
260
ttO
148
145
117
91. B
47.9
46.5
35.2
23.1
22.9
21. B
20.1
18.9
38
156
3-37
-------
(able 3. (Continued)
Species Mean Species Mean
Acute Intercept Acute-Chronic
Rank'
17
16
15
14
13
12
II
10
9
8
1
6
5
4
Species
Creek chub,
Seootilus atromaculatus
Guppy.
Poocllla retlculata
Stonero! ler,
CampostoM anomaliw)
Blunt nose minnow,
Plmaphales notatus
Cutthroat trout,
Salno clarkl
Snail.
Gyraulus clrcumstrlatus
Worm.
Llnnodrllus hotfmalsterl
Coho salmon,
Oncorhynchus Klsutch
Snail,
Phy&a Integra
Ha Inbox trout,
Salmo ^alrdnttrl
Chinook saloon,
Oncorhynchus tshawytscha
Snail,
Physa heterostropha
Midge,
Unidentified
Scud,
Gammarus psuudol Innaeus
-------
Tabl* 3. (Continued)
Acwte Intercept
Rent* Specie* (ufl/l) Ratio
3 Cladoceran. 0.43 2.6
Daphnla eogna
2 Cladoceran. 0.28
Oaphnla pulex
I Cladoceran, 0.23
Oaphnla pullcarla
Acvte Value
(ua/l) Ratio
SALTWATER SPECIES
22 Shore carb, 600
Conlnus Menus
21 Pacific oyster, 560
Crassostrea glgas
20 Copepod. 526
Euryteeora off In Is
19 Copepod, 487
Tlgrlopus Japonlcus
18 Florida poepano, 412
Trachlnotus carolInus
17 Polycnaete wore, 364
Nereis dlverslcolor
16 Brown shrlep, 330
Crangon crangon
15 Hysld shrlep, 181 3.4
Mysldopsls bah Ia
14 Hysld shrlep, 141
Mysldopsls
B-40
-------
Table 3. (Continued)
Rank*
13
12
II
10
9
8
7
6
5
3
2
1
Sp«cla*
Copapod,
P&eudodl apt onus coronatus
Atlantic silvers! de,
Menldla aenldla
Winter flounder,
Pseudop 1 auronactes
Marlcanul
AMarlcan oyster,
Crassostrea virgin lea
Polychaete Morn,
Nediithes arenaceodontata
Polycnaeta worn,
Hhyllodoce waculatd
Had abalone,
Ha Hot Is rufescens
A«er 1 can lobster ,
Hooarus amrlcanus
Calanold oopapod,
Acartla clausl
Black abalona.
Ha II otls crachurodll
Soft shelled claa,
Mya aronarla
Ca 1 anol d coptipod ,
Acartla tonsa
Summer flounder,
Paral Ichthys dentatus
Sp«clac M«an Specie* Maan
Acut* Valu* Acut*-Chronlc
(M9/D Ratio
138
136
129
128
124
120
86
69
52
50
39
31
28
B-41
-------
Table 3. (Continued)
* Ranked fro* least sensitive to «ost sensitive based on species *ean
acute value or lnt«rc*pt.
Final Acute Intercept > 0.29 119/1
Natural logarltta of 0.29 •> -1.23
Acute slope • 0.94 (see Table I)
Final Acute Equation - e<0-9«"'><'»ar 1-1.23)
Flnal Acute Value - 22.9 |ig/l
Acute-Chronic Ratio - 5.76 (see text)
Final Chronic Value - (22.9 ng/M/5.76 • 4.0 M9/I
B-42
-------
Tab I a 4» Plant valua* for
Spacla*
Alga,
Anabaana flos-aqua
Alfla,
Anabaana varlabllls
Alga.
Anacystls nldulans
Alga,
Ch 1 aaydoaona* sp.
Alga,
Chloral la pyranoldosa
Alga,
Chloral la pyrenoldosa
Alga,
Chloral la regular Is
Alga.
Chloral la sp.
Alga.
Chloral la vulgar Is
Alga.
Chloral la vulgar Is
Alga.
Chloral la vulgar Is
Alga.
Cyclotella Meneghlnlana
Alga.
Eudorlna callfornlca
Alga,
Scanedesiius acunlnatus
EHact
H&SHWATER SPtCIES
751 growth
Inhibition
Growth
Inhibition
Growth
Inhlblton
Growth
reduct loo
Lag In growth
Growth
Inhibition
Lag In growth
Photosynthesis
Inhlbltad
Growth
Inhibition
EC50 growth,
13 days
50J growth
raduct Ion
Growth
raduct Ion
Growth
Inhibition
40} growth
raduct Ion
Result
tMfl/ll
200
100
100
8,000
1
100
20
6.3
200
IBO
100-200
8.000
5,000
300
R«far«AC«
Young i LlsK, 1972
Young 4 LIsK, 1972
Young i Llsk, 1972
Cairns, at al. 1978
Staeoan-fllalsan &
MluM-Anderson. 1970
StaaMn-Nlalseti &
Ka^>-Nlalser>, 1970
Sakaguchl, at al.
1977
Gachtar, at al.
1973
Young & LIsK, 1972
RosKo 1 ftachlln,
1977
Stokes &
Hutch Inson, 19/6
Cairns, at al. 1978
Young & Llsk. 1972
Stokes &
Hutch Inson, 1976
B-43
-------
TabU 4. (Continued)
Alga.
Sc«o»d«s»tis quadrlcauda
Alga.
Scenedes»us quadrlcauda
Alga*.
Mixed culture
tff«ct
threshold
toxlclty
Growth
reduct Ion
Significant
reduction In
photos y nt hes 1 &
Result
l«te growth 5
Inhibition
tC50, 7 day 119
50]( reduction In
photosynthetlc 02
product Ion
50J root weloht 250
reduct Ion
Growth 50
reduct Ion
l son &
Bruun-Laur&en, IS76
Patrick, et al.
I960
Stee»an-NIel sen &
Wlua-Anderscn. 1970
Wai bridge. 1977
150 brown A Rattlgan.
1979
Stanley. 1974
Bartlett. et al.
1974
Alga, giant kelp,
Macrocystls pyrlfera
Alga,
SALTWATfcR SPECIES
96 hr EC50
photosynthesis
InactlvatIon
72 hr EC50
growth ratu
100 Clendennlng &
North, 1959
trlckson, 1972
3-44
-------
Tab I* 4. (Continued)
Specie*
Alga.
Aaphldlnlu* carter!
Alga,
Qllsthodlscus luleus
Alga,
SKeletoneMa costatuw
Alga.
Nltichla closterlu*
Alga.
Scrlppslella foeroense
Alga.
HICM ocentrua alcans
Alga.
Gyjnodlnlua splendens
fctt«ct
M day EC 50
grovth rate
M day fC50
growth rate
14 day ECM
growth rate
96 hr EC 50
growth rale
5 day EC 50
growth rate
5 day EC 50
growth rate
5 day EC 50
growth rate
Result
Uifl/l>
<50
<50
50
33
5
10
20
Reference
trlck&on, ot al.
S970
fcrlckion, et al.
1970
Crlck&on, et al.
1970
Ko&ko A ftachlin.
1975
Salfullah, 1976
Salfullah. 1978
Salfullah, 1978
3-45
-------
Alga.
Chloral la regular Is
Stonafly,
Ptaronarcys call torn lea
Fathaad •Innow (larva),
Plaaphalas prcpalat
Blueglll,
aacroctilrus
Tab I* 5. R**ldu*» for copp»r
Blc
Tl**u*
itratlo*
Factor
FRESHWATER SPECIES
Muse la
2.000
203
290
Duration
(day*)
20 hrs
14
30
660
Safcaguchl. at al.
1977
Nehrlng. 1976
Llnd. et al.
Manuscript
Benolt. 1975
SALTWATER SPECIES
Polychdotu HUTU,
Ctri Itormla splrabracha
Holychaete wora,
Noanthas aranacaodentata
Polychaete wor«,
Nereis dlverslcolor
Polychaeta worm,
Phyllodoca »aculata
Bay sea I lop,
Argopecten Irradlans
Bay scallop,
Argopactan Irradlgns
Avar I can oyster,
Crassostraa virgin lea
A*arlcan oyster,
Crassostraa vlrglnlca
Northern quahdug,
warcanarla
250*
2,550«
203*
1,750"
3,310
4,160
28,200
20,700
BS
24
28
24
21
1 12
112
140
140
70
Ml lanovlch, et al.
1976
P«sch & Morgan. 1978
Jones, et al. 1976
McLusky & Phil lips,
1975
Zarooglan, 1978
Zarooglan, 1978
Shuster & Hrlngle,
1969
Snustor & Pi Ingle,
1969
Shuster & Pr Ingle,
1968
3-46
-------
TabU 5. (Continual)
SpocUs
Soft shall ad cla».
My A weoarla
Mytltut »<>">'*.
Mytl luc «
-------
Table 5. (ContlMMd)
Bloconceatratlon Duration
T Issue Factor (days) Reference
Alga,
Monochry*!* 1 utherl
Alga.
Psfeudopedlnel la pyrltor»ls
Alga,
Heteromastlx long! til Us
Alga,
Mlcrononas sguaaata
Alga.
Tetraselals tetrathele
136" 25 Rlley & Roth,
65* 25 Rlley & Roth,
617* 25 Rlley & Roth,
279* 25 Rlley & Roth,
265* 25 Rl ley & Roth,
1971
1971
1971
1971
1971
•Dry weight to wet weight conversion
3-43
-------
T*bl« 6. Other d»t« for copp«r
Spacla* Duration
E»f«ct
Ra*ult
(Kfl/l)
R*f*r*
nca
FRESHMATER SPECIES
An**lltf norm.
Aax>jc*oaa Kaadlayl
A MM II 4 VOTM,
AaolotQM fcaftdtayl
Annalld uora.
Aaolosoaa haadtayl
Annalld worm.
AaolosoM hMdtayl
Anna! Id MOTB,
Aaolo&OBa haadlayl
Snail (aobryo).
Aanlcol* sp.
Snail.
Gonlobasls llvescans
Snail,
Lyanaa anorglnata
Sna 1 1 ,
Nltrocrls sp.
Snail,
Nltrocrts sp.
Snail.
Nltrocrls sp.
Snail.
Nltrocrls sp.
Snail.
Nltrocrls sp.
Clodocardn,
48
48
48
48
48
96
48
48
48
48
48
48
48
72
hrs
hrs
hrs
hrs
hrs
hrs
hrs
hrs
hrs
hrs
hrs
hrs
hrs
hrs
LCSO
LCSO
LCSO
LCSO
LCSO
LCSO
LCSO
LCSO
LCSO
LCSO
LCSO
LCSO
LCSO
LCSO
2,600
2,300
2,000
1,650
1,000
9.300
860
300
3.000
2.400
1,000
300
2)0
67.7
Cairns
Cairns
Cairns
C«lrn$
Cairn*
. »t
. *t
. «t
. •*
. «t
Rahwoldt,
Cairns
Cairns
Cairns
Cairns
Cairns
Cairns
Cairns
Winner
. at
. *t
. «t
. «t
, «t
. «t
. «t
al.
al.
al.
al.
al.
ot al
al.
al.
al.
al.
al.
al.
al.
& farrel
1978
1978
1978
1978
»978
. 1973
1976
1976
1978
1978
1978
J978
1978
t.
Daphnla aablgua
1976
B-49
-------
Tabl» 6. (Continued)
Re&ult
Cladocwttn,
Daphnla aagna
Cladoc«ran,
Daphnla magno
Cladoceran.
Daphnla aogna
Cladoceran,
Daphnla nagna
Cladoceran,
Daphnla aagna
C. I ddut-ur an ,
Uaphn I a wduna
Cladoceran,
Uaphnla aagna
Cladoceran,
Uaphnla aagna
Cladoceran,
Daphnla »agna
Cladoceran,
Uaphnla aagna
Cladoceran,
Daphnla aagna
Cladoceran.
Daphnla aagna
CIadocaran,
Daphnla
Cladoceran.
Odphnla
Durattoo
48 hrs
40 hrs
46 hrs
48 hrs
48 hrs
lite cycle
Lite cycle
Lite cycle
72 Irs
Eftact
LC50
LCiO (5 C)
LC50 (10 C)
LC50 (15 C)
LC50 (23 C)
90
40
Reduced number ul
young produced
Reduced number of
young produced
Reduced productivity 21.}
60 Ble&lnger &
Chrlstensen, 1972
Cairns, ut a>\. I97U
70 Cairns, et ol. 1978
.)). I97B
Calrni, ut .it.
10 Wlnnor, et ,)!. 1977
10 Winner, ot ol. 1977
Lite cycle Reduced productivity
Chris ten ben, 1972
28.2 Winner, el til. 1977
lite cycle Reduced productivity 2i).2 Winner, ot ul. 1977
Life cycle Reduced productivity
Life cycle Reduced productivity
Lite cycle Reduced number of
young produced
LC50
Winner, et ^1. 1977
49 Winner & t
-------
Table 6. (Continued)
SpecIas
Duration
Effect
Result
(ug/l) Reference
•k^M«M»-
Cladoceran,
Daphnla aagna
Clauocaran,
Daphfll* Mgna
Cladocaran,
Daphnla wigna
Cladoceran,
Daphnla aagna
Cladoceran,
Daphnla MKjna
Cladoceran,
Daphnla •agna
C 1 adoceran ,
Daphnla maqna
Cladooeron,
Daphnla parvula
Cladocuran,
Daphnla parvula
Cladoceran,
Daphnla parvula
Cladoceran,
Daphnla put ex
Cladoceran,
Daphnla pulex
Cladoceran,
Oaphnla pulex
72 hrs
72 hrs
72 hrs
72 hrs
72 hrs
29 hrs
24 liTi
72 hrs
72 hrs
Life cycle
72 hrs
72 hrs
Life cycle
LC50
LC50
LC50
IC50
LC50
Mud Ian survival tine
LC50
LC50
LC50
Reduced productivity
LC50
LC50
Reduced productivity
88.8
85
81.5
81.4
85.3
12.7
60
57
72
49
54
86
49
Winner & Parrel 1,
1976
Winner & Parrel 1,
1976
Winner & Parrot I,
1976
Winner & Parrot i,
1976
Winner & Parrel 1,
1976
Andrew, et a). 1977
Brlmynan & Kutin, 1977
Winner & Parrel 1,
1976
Winner & Parrel),
1976
Winner & Parrel 1 ,
1976
Winner & Parrel 1,
1976
Winner & Parrel 1,
1976
Winner & Parrel I,
1976
B-5I
-------
TafcU 6. (Continued)
Specie*
Duration
DaplMla put ex
Cledooeran,
Dophnle jtulex
Cladoceran,
Daphnla gulex
Cladoceran,
Daphnla gulex
Cladoceran,
Daphn 1 a pu 1 1 car 1 a
Cladoceran.
Daphnla pul (car la
Cladoceran,
Daphnla pul Icarla
Cladoceran,
Daphnla pul Icarla
Cladoceran,
Daphnla pul Icarla
Cladoceran,
Daphnla pul Icarla
Cladoceran,
Daphn la pu 1 1 car 1 a
Cladoceran,
Daphnla pul tear la
Cladoceran,
Daphnla pul Icarla
Cladoceran,
Daphnla pul (car la
46 hrs
46 hrs
46 hrs
46 hrs
46 hrs
46 hrs
46 hrs
46 hrs
48 Irs
48 hrs
48 hrs
48 hrs
48 hrs
48 hrs
LCX) (5 C)
LCX) (10 C)
LC50 (15 C)
LC50 (25 C)
LCX) (TOC 14 «9/l)
LC50 (TOC 13 «9/l)
LCX) (TOC 13 «g/l)
LC50 (TOC 28 ng/l)
LCX) (TOC 34 "9/D
LC50 (TOC 34 »3/l)
LCX) (TOC 32 eg/1)
LC50 (TOC 32 pg/l)
LC50 (TOC 12 M9/I)
LC50 (TOC 13
70 Cairns, et al. 1978
60 Cairns, et al. 1978
20 Cairns, et al. 1976
5.6 Cairns, «t al. 1978
55.5 Llnd, et al.
Manuscript
55.3 Llnd. et al.
Manuscript
53.3 Llnd. et al.
Manuscript
97.2 Llnd, et al.
Manuscript
199
627
215
165
Llnd, et al.
ManuscrIpt
Llnd. et al.
Manuscript
Llnd, et al.
Manuscript
Llnd. et al.
Manuscript
35.5 Llnd. *t al.
Manuscript
78.6 Llnd. et al.
Manuscript
B-52
-------
TabU 6. (Continued)
Cladoceran.
Oaphnla pullcarla
Oaphnla pyllcarla
Cladocaran,
Daphnla pullcarla
Cladoceran,
Daphnla pullcarla
C 1 odocaran,
Daphnla pullcarla
Cladoceran,
Uaphnla amblgua
Scud,
Gdamarus lacustrls
Mayfly.
tpheiBerella subvarla
Mayfly.
tphenerella grand Is
Stonef ly,
Pteronarcys callfornlca
Caddlsf ly,
Hydropsyche batten 1
Midge,
Tanytarsus dlsslMllls
Crayfish,
Orconectes rustlcus
Rotifer,
Phllodlno acuttcornls
Duration
48 hr^
48 hrs
48 hrs
48 hrs
48 hrs
Life cycle
96 hrs
48 hrs
14 days
14 days
14 days
10 days
17 days
48 hrs
EM«ct
LC50 (TOC 28 «g/l)
LC50 (TOC 25 «g/l)
LC50 (TOC 13 «Q/|)
LC50 (TOC 21 .9/1)
LC50 (TOC 34 mg/l)
Reduced productivity
LC50
LC50
LC50
LC50
501 survival
LC50
Survival of
newly hatched young
LC50
R*sult
113
76.4
84.7
184
240
49
1,500
320
100-200
10.100-
13,900
32.000
16.3
125
1,300
R«f*renc«
Llnd. et al.
Manuscript
Llnd, et al.
Manuscript
Llnd, et al.
Manuscript
Llnd, et al.
Manuscript
Llnd. et al.
Manuscript
Winner t Farrel 1
1976
•
Nebeker & i^utin,
1964
Warnlck & Bell. 1969
Nahring. 1976
Nahrlng, 1976
Warnlck & Boll, 1969
Anderson, et al. I9BO
Hub&hman, I96/
Cairns, et al. 1978
B-53
-------
TabU 6. (Continued)
Rot 1 far.
Phllodlna acutlcornls
Rot 1 far,
Phllodlna acutlcornls
Rotifer,
Phllodlna acutlcornls
Rotifer,
Phllodlna acutlcornls
Coho salmon,
Oncorhynchus klsutch
Coho saloon,
Oncorhynchus klsutch
Coho salmon,
Oncorhynchus klsutch
Coho salmon,
Oncorhynchus klsutch
Coho salmon.
Oncorhynchus klsutch
Coho salmon,
Oncorhynchus klsutch
Coho salmon,
Oncorhynchus klsutch
Coho salmon,
Oncorhynchus klsutch
Coho salmon,
Oncorhynchus klsutch
Coho salmon,
Oncorhynchus klsutch
Duration Effact
48 hrs LC50
48 hrs LC50
48 hrs LC50
48 hrs LC50
96 hrs Reduced survival
on transfer to
30 days LC50
72 hrs LC50
72 hrs LC50
72 hrs LC50
72 hrs LC50
72 hrs LC50
72 hrs LC50
72 hrs LC50
R*Mllt
(pa/I) Rafaranc*
1,200 Cairns, at al. 19/8
1,130 Cairns, et al. 1978
1,000 Cairns, at al. 1976
950 Cairns, et al. 19/8
30 Lorz 1 HcPherson,
1976
360 Holland, et al. I960
280 Holland, et al. I960
370 Hoi land, et al. I960
190 Holland, et al. I960
480 Holland, et al. I960
440 Holland, et al. I960
460 Hoi land, et al. I960
480 Holland, et al. I960
560 Ha| land, et al. I960
B-54
-------
T«b|* 6. (Continued)
Sp«l**
Coho salmon.
Oitcorhynchus klsutch
Coho witMM!.
OncorhvftcMis klsutch
Coho salmon,
Oftcorhynchus klsutch
Coho salmon,
Oncorhynchus klsutch
Soclujy* salmon,
Oncorhynchus n«rk«
Chinook salmon,
Oncorhynchus tshawytscha
Chinook salmon,
Oncorhynchus tshayytscha
Chinook salmon (alftvln),
Oncorhynchus tshaxytscha
Chinook salmon (al*vln),
Oncorhynchus tshawytscha
Chinook salmon
-------
T«bU 6.
Spaclat
CftlMX* salmon (smolt),
Oncorhynchu* tshawytscha
Chinook salmon,
Oncorhynchus tshawytscha
Rainbow trout,
Salmo galrdnerl
Rainbow trout,
Salmo galrdnarl
Rainbow trout,
Salmo galrdnerl
Kalnbow ti out,
Salmo galrdnerl
Kalnbow trout,
Salmo gairdnerl
Rainbow trout,
Salmo galrdnarl
Rainbow trout.
Rainbow trout,
Salmo galrdnerl
Rainbow trout (alevln),
Salmo galrdnerl
Rainbow trout (alevln),
Salmo galrdnerl
Rainbow trout (swim-up),
Salmo galrdner 1
Rainbow trout (swim-up).
Duration
200 hrs
72 hrs
96 hrs
96 hrs
96 hrs
2 hrs
7 days
21 days
10 days
7 days
186 hrs
166 hrs
200 hrs
200 hrs
Effect
LCIO
LC50
LC50
LC50
LC50
Depressed olfactory
rasp on sa
LC50
Median period of
survival
Depressed feeding
rate and growth
Median period of
survival
LC50
LCIO
LC50
LCIO
R*sult
18
190
516*
III*
a
44
40
75
44
26
19
17
9
Rataranca
Chapman, 1976
Holland, I960
Huwarth & Sprayue,
1978
Howarth & Sprague
1978
Howarth J> Sprayuu
1978
Hara, et al. 1976
Lloyd, 1961
Grande, 1966
Lett, et al. 1976
Lloyd, 1961
Chapman, In press
Chapman, In press
Chapman, In press
Chapman, In prtt.b
Saloo gali
a- DO
-------
Table 6. (Continued)
Species
Rainbow trout (parr),
Sal«o galrdnerl
Rainbow trout (parr),
Salap galrdnerl
Rainbow trout (saolt).
Sal go aalrdnerl
Rainbow trout (s*olt>,
Salap flalrdnerI
Rainbow trout U«olt),
Salao galrdnerl
Rainbow trout (s»olt),
Sal«o galrdnerl
Rainbow trout (try),
Sal«o
Duration
Effect
Retult
jug/I) Reference
Rainbow trout (fry).
Rainbow trout (fry),
Salijp qalrdnerl
Rainbow trout (fry),
Salao Qalrdnerl
Rainbow trout (fry),
Salao galrdnerl
Rainbow trout (fry),
Salno flalrdner1
Rainbow trout (fry),
Salxa oatrdnerl
Rainbow trout (fry),
Sal«o
200 hrs
200 hrs
200 hrs
200 hrs
>10 days
14 days
1 hr
24 hrs
24 hrs
24 hrs
96 hrs
96 hrs
48 hrs
96 hrs
LC50
LCIO
LC50
LCIO
Threshold LC50
LC50
Avoidance behavior
LC50
LC50
LC50
LC50 (field)
LC50
LC50 (field)
LC50
— Ai«^BHB«~b-
15
8
21
7
94
B70
0.1
950
450
150
251
250-680
70
250
Chopaan, In pr&si
Ctt^pMdn, In press
Chapaan, In press
Chapaan, In press
Fogels & Spraguo,
Calanarl & Harchettl ,
1973
FolMr, 1976
Cairns, et al. 1978
Cairns, et al. 1973
Cairns, et al. 1978
Hale, 1977
Lett, et al. 1976
Colaiurl &Marchattl,
1975
Goettl, et al. 1972
3-57
-------
Table 6. (Continued)
R«*ult
trout (try).
alrdnerl
Rainbow trout (try),
Salic palrdnerl
Rainbow trout (try),
Salao galrdnerl
Rainbow trout,
Salao galrdoerl
Rainbow trout,
Salao
Rainbow trout,
Sajaio galrdnerj
Rainbow trout,
Sal»o galrdnerj
Rainbow trout,
Sal«o galrdnerl
Rainbow trout,
Sal«
Rainbow trout,
Sal«
Rainbow trout,
Sal»o galrdfter I
Rainbow trout,
Sal»o flalrdnerl
Rainbow trout,
Sal«o galrdnarl
Rainbow trout.
Sjlmu gdlrdntir I
Pur at Ion
24 hrs
24 hr«
72 hrs
>15 days
>I5 days
>I5 days
>I5 days
>15 days
>I5 days
48 hrs
48 hrs
48 hrs
72 hrs
48 hrs
Elt*ct
UC50
LC50
Threshold LC50
Threshold LC50
Threshold LC50
Threshold l£50
Threshold LC50
Threshold UC50
LC50
LC50
LC50
UC50
LC50
(f p/l ) Refer*
140 Shaw i
130 Shaw I
MO Brown,
19 Miller
54 Miller
48 Ml 1 ler
78 Miller
18 Miller
96 Miller
500 Brown.
750 Brown
150 Cope,
t,\00 Lloyd,
nc*
Brown, 1974
Brown. 1974
et al. 1974
A McKay, 1980
& McKay, 1980
A McKay. I960
1 McKay. 1980
& McKay, 1900
& McKay. 1980
I960
i Dal ton, 1970
1966
l%!
270 Hurbert & VdixJyku,
1964
B-58
-------
Table 6. (Continued)
Specie*
Atlantic sal«on.
Sal no salar
Atlantic sal»on,
Salao calar
S^ •
Atlantic MIMA.
Sal«o Mlar
Atlantic salnofl,
Salao salar
Brown trout.
Sal NO trutta
Brook trout,
Salve) Inus fontlnalls
Crook trout,
Salvellnus fontlnalls
Brook trout ,
Salvellnus fontlnalls
S toner ol ler,
Caapostonla anonealun
Goldfish,
Carasslus auratus
Goldfish,
Carasslus auratu&
Goldfish,
Carasslus auratus
Golden shlnsr,
Notealgonlus cry&olaucas
Golden shlnar,
Nota«lgonlus crysolaucai
Golden shiner.
Notealgonlus crysolaucas
Duration
7 days
7 days
21 days
27-38 hrs
21 days
24 hrs
21 days
337 days
96 hrs
24 hrs
24 hrs
24 hrs
24 hrs
24 hrs
24 hrs
Effect
• i i in •
Incipient lethal
level
Incipient lethal
level
Median period of
survival
Median period of
survival
Median period of
surv 1 va 1
Significant change
In cough rate
Significant changes
In blood Chun Is try
Significant changes
In blood chuMistry
LC50
LC50
LC30
LC50
LC50
LC50
LCt>0
Result
1.510
330
230
270
Reference
Sprague, 1964
Sprague & Kdasay,
1965
Grande. 1966
Zltko A Carson, 19 Ib
Grande, 1966
Oruoniiond. et al. 1973
McKJ«, et al. 1970
McKI«. et al. 1970
Geek ler, of al. 1976
Cairns, at al. 1978
Cairns, ut al. 1978
Cairns, et al. 1978
Cairns, et al. 1978
Cairns. «t al. 1978
Cairns, et al. 1978
B-59
-------
Table 6. (Continual)
Species
Striped shiner.
NotropU chrysocepha I es
'^^T*W*^*^'
Striped thlner.
Motroplt cnrysocephales
Striped shiner,
Notropls cnrysocephales
Strlp«d shiner,
Notropls chrytocephales
Striped shiner,
Notropls chry&ocephales
Striped shiner,
Not/ up Is chrysocepholus
Bluntnose
Pl»ephdles notatus
bluntnose •Innov,
Pl«aphala!» notatus
•Innow,
Plaaphalus groaalas
Fathead "Innon,
Plaephalet propel as
Fathead Minnow,
Plaepttalet pjoaelas
Fathaad
Pluephalas prooelns
Fathead rntnne*.
Plt»phales prpaelas
Duration
hrs
96 hrs
* hrs
hrs
hrs
9b hrs
46 hrs
96 hrs
96 hrs
Effect
LC50
LC50
LC&O
UC!X)
LCM)
Decrt»
-------
Table 6. (Continued)
Result
Specie*
Fathead Minnow,
PlMephales proMelas
Fathead Minnow,
PlMMf*ales proMelas
'••mYiPHi .i,
FaftlM < plnnow,
PlMOfcales proMelas
Fathead Minnow,
PlMephales proMelas
Fathead Minnow,
PlMephales proMelas
Fathead Minnow,
PtMephales proMelat
Fathead Minnow,
PlMephales proMelas
Creek chub,
Seaotllus atrotaculatus
Creek chub,
SoMotllus atroMaculatus
Brown bullhead,
Ictalurus nebulosus
Channel catfish,
Ictalurus punctatus
Channel ca tils'),
Ictalurus punctatus
Channel catfish,
Ictalurus punctatus
Channel catfish.
Ictalurus punctatus
Duration
96 hrs
96 hrs
96 hrs
96 hrs
96 hrs
96 hrs
Lite cycle
96 hrs
96 hrs
96 hrs
94 hrs
24 hrs
24 hrs
24 hrs
Effect
UC50 (TOC - 36
LC50 (TOC - 28
•9/1)
LC50 (TOC - 15
LC50 (TOC - 34
M9/I)
LC50 (TOC - 30
•9/1)
LC50 (TOC • 30
•9/1)
Chronic Halts
LC50
LC50
LC50
Decreased blood
osMolarlty
LC50
LC50
LC50
1,129
1.001
2,050
2,336
66-120
11,500
1,100
11,000
2,500
1.730
2,600
3,100
Reference
Llnd, et ol.
Manuscript
Llnd, et al.
Manuscript
Llnd, *t 4l.
Manuscript
Llnd, «t dl.
Manuscr 1 pr
Llnd, et al.
Manuscript
Llnd, et al.
Manuscript
Brungs, et al.
Geckler, et al.
Geckler, et al.
Geckler, et al.
Lewis & Lewis,
Cairns, et al.
Cairns, et al.
Cairns, et al.
1976
1976
1976
1976
1971
1978
1978
1978
B-61
-------
Table 6. (Continued)
Result
Duration
Effect
Reference
~T i ' i
F leftist.
Jor4w»lU f lor 1 doe
Ho*4)ultofUh,
GaaUiila attlnls
Guppy,
Poecllla retlculata
Rainbow darter,
Etheostana caeruleu*
Rainbow darter,
Etheosteaa caeruleum
Rainbow dai tor,
ttheosltMa caeruleu*
Johnny darter,
Ethoosteaa nlgrunl
Orangethroat darter,
Etneostoma spectabHe
Orangethrodt darter,
E theostoM spectabl le
Orangethroat darter,
Etheostoaa spectabl le
Orangethroat darter,
Etheostoaa spectabl le
Rock bass,
Aobloplites relpest/ Is
Bluegll 1.
LepOMiU macrochlrus
blueglll.
Lepomls nacrochlrus
10 days
96 hrs
24 hrs
96 hrs
96 hrs
96 hrs
96 hrs
96 hrs
96 hrs
96 hrs
96 hrs
96 hrs
24-36 hrs
40 his
LC50
LC50 (750 *g/l
turbidity)
LC50
LC50
LC50
LC50
LC50
LC50
LC50
LC50
LC50
Altered oxygen
consuMpt Ion rates
LC50
600
75,000
1,250
4,300
5,900
2,800
6,800
9,800
7,900
5,400
5,000
1,432
300
2,000
(•oqels & Spraguu,
1977
Nal len, et dl. 1957
Hlnlcuccl, 19/1
Geckler, et dl. 1976
Geckler. ft dl. 1976
Geckler. ot dl. 1976
Ceckler, et dl. I9761
Geckler, et dl. I97b
Geckler, et dl. 1976
Geckler, et dl. 1976
Geckler, et dl. 1976
Lfnd, et dl.
Manuscript
O'Hara, 1971
Cope, 1966
3-62
-------
Table 6. (CofltlnuwJ)
Blueglll,
Laosls macrochlrus
Blu*fllM,
Macrochlru*
Blueglll,
macrocMrus
Colonial hydrold,
Caapaoularla flaxuosa
Colonial hydrold,
CaMpanularla flaxuosa
Colonial hydrold,
EIrene vlrldula
PolychaeTa worm,
Clrrlfprala splrabractia
Polychaate worn,
Phyllodoce oaculata
Polycha«t« DOT*,
Keanthes araoacaodanfata
Poly cheat* HOT*.
Neanthas aranacaodantaTa
Bay seal lop,
Argopacteo trradians
Bay seal lop,
Argopecteo trradlans
Aaerlcan oyster (larva),
Crassostrea vlrgtnica
Duration
96 hrs
% hrs
96 hrs
96 hrs
Ettect
LC50
LC50
LC50
LC50
SALTWATER SPECIES
II days Growth rata
Inhibition
Eniyae Inhibition
14-21 days Gronth rate
Inhibition
26 days 50J Mortality
9 days 50$ Mortality
28 days 50* Mortality
28 days 50< Mortality
42 days EC50, growth
119 days IOOJ Mortality
12 days 501 Mortality
(Mfl/l) Rafarenca
16,000 GacKter, at at. 1976
17.000 Cockier, et at. 1976
740 Trama, 1956
1,800 Turnout I, *>1 al. 1954
10-13 Stabbing, 1976
1.43 Hoor« A Stabbing.
1976
30-60 Karbe. 1972
40 Mllanovlch, -it al.
1976
80 Mclusfcy 4 Phillips,
1975
44 P«sch & Morgan, 1978
100 P«sch & Morgan, 1978
5.8 U.S. EPA, J980
5 U.S. EPA, 1980
46 Calabraso, at al.
1977
B-63
-------
6. (CCMtlMMd)
Black **• Ion*.
HvllotU crach«rodll
ft* (felon*,
HajlotU ruf ascans
Northar* ouahaug (larva)
Harcaoarla M*rf*narla
Northern quaoaug,
Harcanarla M»rc*narla
Soft shallad C|M.
Hya aranarla
Hussal,
Hytl lus «du| Is
Channeled whelk.
Busycon cana 1 1 cu 1 atu«
Hud snail,
Nassarlus obsoletus
Calanold copepod,
Acartla clausl
Calanold copepod,
Acartla tonsa
Co pa pod,
Hetrldla paclflca
Co pa pod.
Phial Idaiui sp.
Calanold copepod,
Acartla tonsa
Copepod,
fuchaeta •arina
Duration
4 days
4 days
8-10 days
77 days
7 days
1 days
77 days
3 days
2 days
6 days
24 hrs
24 hrs
24 hrs
24 hrs
Eflact
Hlstopathologlcal
gill atnoTMalltlas
Hlstopathologlcal
gill atnorMlltlae
50| •ortallty
531 Mortality
50| Mortality
50| Mortality
501 Mortality
Decrease In ocygen
con SIMP t ion
501 Mortality
501 Mortality
LC50
LC50
LC50
LC50
>32
>32
30
25
35
200
470
100
34-82
9-73
176
36
104-31 1
188
Rafaranca
Hart In. at al. 1977
Hart In, at al. 1977
Calabrase, at al.
1977
Shustw A Prlngl*,
1968
Elslar. )977
Scott & Major, 1972
Botzar i Yevlch, 1975
Haclnnes 1 Thurberg,
1973
Horaltou-
Apostolopoulou, 1978
SosnowsHI, at al.
1979
Roav«, at al. 1976
Reeve, et al. 1976
Reeve, et al. 1976
Reave, et al. 1976
B-64
-------
TabU 6. (Continued)
Spaclat
Copepod,
Undlnula vulgar 1 5
(nauplll),
Rotlfar.
Brachlonus pllcatUls
Ctenophora,
Mnaalopsls •ccrodyl
Ct«oophor«,
Plaurobrachla pilaus
Larval annallds,
Mlxad spaclas
ChaeTognalh,
Sayltta hlsplda
Shrimp,
Euphausia pacltlca
Duration
24 hrs
24 hrs
24 hrs
24 hrs
24 hrs
24 hrs
24 hrs
EMact
LC50
LC50
LC50
LC50
1X50
LC50
LC50
Copepod.
Labldocera scottl
A*erlcan lobstar.
Hoaarus a>«rlcMiMS
Coral-ra«f «chlnold,
Cchlocwtatra Mthaal
Saa urchin,
Arbacla punctulata
Sea urchin,
Paracontrotus llvldus
HuMMlchog,
24 hrs
13 days
4 days
4 days
21 days
UC50
90| Mortality
Supprasslon of
larval skeletal
dav«lop«ent
56| dacraasa In
Spar* wot) 1 Ity
Retardation ot
growth of plutaal
larvaa
Hlstopathologlcal
Fundulus hetaroclltus
Ias tons
Rasult
(ug/ll Rafaranca
192 Roeve. at ol. 1976
90 Raava. at al. l'>76
100 Haava. at al. 1976
17-29 Reave, et ol. 1976
33 Raava, et al. 1976
69 Raave. at ot. 1976
43-460 Rdeve, at al. 1976
14-30 Reeve, et
-------
Table 6.
MuMlcnog.
FuAdulus heteroclltus
Atlantic silvers! d«,
HMtldla Men Id la
Pacific herring (eMbryo),
Clupea harengut pallntl
Pacific harrlng (larva).
Clupea harengui pal las!
Atlantic Menhaden,
Brevoortla tyrannus
Spot,
lelobtomus xonHiuiub
Atlantic crodker,
Mlcropagun undulatus
Plnllsh,
layodon rhoaboldes
Plaice,
Pleuronectes platessa
Winter flounder,
Pseudopleuronectes
nMTrrlrnnit"
Alga,
Laminar la hyporborla
Duration
4 days
6 days
2 days
14 days
14 ddys
14 days
14 days
4 days
14 days
28 days
UUct
Enzyae Inhibition
Hlstopatho loylcal
lesions
Incipient LC50
Incipient LC50
50J Mortality
50) Mortality
50| Mortality
50} Mortality
Hlstopathologlcal
lesions
Growth decrease
Result
(H9/I) N*f*r«fi
ice
600 Joe Ma, 19/3
<500 Gardner & LaRochu,
1973
33 Rice &
900 Rice i
610 tngel.
160 En9el.
210 Engel,
150 Engol,
750 Saward,
180 Baker,
50 Hopk 1 ns
rtirrlson, 19/b
hbrrlboii, 19/8
et al. 1976
et al. 19/6
et al. 19/6
et al. 1976
et al. 1975
196?
& Koln, 1971
* Dissolved copper; no other Measurement reported
3-66
-------
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B-70
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B-75
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-------
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B-79
-------
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B-SO
-------
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-------
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3^34
-------
Mammalian Toxicology and Human Health Effects
INTRODUCTION
Copper is widespread in the earth's crust, and the extensive
use of copper and its compounds by man since prehistoric times has
added copper to the environment and the ecosystem in highly vari-
able concentrations.
From 1955 to 1958 the annual United States production of re-
coverable copper was about 900,000 metric tons. By 1975, the pro-
duction had risen to 1,260,000 metric tons (D'Amico, 1959; U.S.
Bur. Mines, 1976) . The world trade in refined copper amounted to
2,271,150 metric tons in 1973 (World Metal Statistics, 1974).
Hunan exposure to copper can occur from water, food, and air,
and through direct contact of tissues with items that contain cop-
per. Copper is essential to animal life; consequently, abnormal
levels of copper intake can range from levels so low as to induce a
nutritional deficiency to levels so high as to be acutely toxic.
EXPOSURE
Ingestion from Water
Water can be a significant source of copper intake depending
upon geographical location, the character of the water (i.e.,
whether it is soft or hard), the temperature of the water, and the
degree of exposure to copper-containing conduits.
Schro«der, et al. (1966) place considerable emphasis on drink-
ing water as a source of copper. They reported that the mean values
of copper in human livers (56 cases) from Dallas, Denver, and Chi-
cago varied from 410 to 456 ug/g of ash, and that, the mean value
C-l
-------
from Miami was 578 ug/g of ash . The municipal water supplies of
these cities each provided relatively hard potable waters with mea-
sured hardness ranging from 75 to 125 mg/1. On the other hand, 143
human livers from seven cities with relatively soft waters ranging
from 10 to 60 mg/1 had mean levels of copper varying from 665 to 816
ug/g of ash. Of the cases from soft water areas, 37.1 percent had
hepatic copper of 700 or more ug/g of ash. compared with only 14.3
percent of the samples from the hard water cities. Of the 56 indi-
viduals from three cities with the hardest water, only two showed
such high values. Unfortunately no studies were made of cities
with very hard water.
Schroeder, et al. (1966) suggested that the higher copper
levels in residents of cities with soft water might be due to the
ability of soft water to corrode copper pipes and fittings, thereby
increasing the intake of soluble copper. Another explanation may
lie in the ability of calcium or magnesium ions in hard water to
suppress the intestinal absorption of copper.
Schroeder, et al. (1966) reported on the progressive increase
of copper in water from brook to reservoir to hospital tap, and the
considerable copper increment in soft water, compared with hard
water, from private homes (Table 1). The authors found that
the daily increment of copper ingested from soft water may amount
to 10 to 20 percent of dietary intake.
The values cannot readily be converted to total copper content
present in liver on a wet weight basis since they were secured at
autopsy. Information regarding the individuals from which samples
came was minimal.
C-2
-------
TABLE 1
Copper in water Plowing through Copper Pipes3'
Item ug/1
Spring water, Brattleboro, Vermont, mountain 1.2C
Municipal water, soft, Brattleboro
Brook, inlet to reservoir 16
Reservoir, lake 55
Water, main end 150
Hospital, at tap
cold, running 30 rain 170
hot, running 30 min 440
cold, standing 12 hr 550
cold, standing 24 hr 730
Spring water, soft, private houses, Brattleboro,
Vermont, at tap
No. 1 from spring, unpiped 2.8
running 30 min 190
cold, standing 24 hr 1,400
hot, standing 24 hr 1,460°
No. 2 1,240
No. 3 75
Well water, private houses, Windham County, at tap
No. 4, hard 36
No. 5, hard 4.4C
No.
No.
NO.
6,
7,
8,
hard
hard,
soft
at
at
well
tap
40
4
36
278
c
c
aSource: Schroeder, et al. 1966.
bWater from the main was taken after it had passed through the
treatment plant at the entrance to hospital supply system,
from whence it ran through copper pipes. This water was
chlorinated. Spring and well waters were untreated.
°By chemical, method using diethyldithiocarbamate after
evaporatingr 1 liter water.
C-3
-------
Hadjimarkos (1967), on the contrary, suggested that drinking
water may be only a minor source of copper. He reported that the
mean drinking water concentration of copper is 0.029 mg/1, which
could mean a daily intake of 58 ug of copper in water, or 1 to 8
percent of total daily intake if food intake is 3,200 ug of copper
per day.
It is probable that the difference in intakes estimated by
Schroeder, et al. (1966) and Hadjimarkos (1967) is due to a differ-
ence in location. However, it is difficult to pinpoint local cop-
per concentrations in drinking water sources, since the only readi-
ly available information on concentrations of copper in stream
water is from areas of 10,000 square miles or greater (Kopp and
Kroner, 1968; Thornton, et al. 1966).
Robinson, et al. (1973) in New Zealand have suggested that
soft water used exclusively from the coldwater tap to make up daily
beverages may add as much as 0.4 mg of copper per day per indivi-
dual, but that if hot water from the same source is used for the
same purposes, it would add at least 0.8 mg of copper per day to an
individual's intake.
The average concentration of copper in the United States water
systems is approximately 134 ug/1 [U.S. Department of Health, Edu-
cation and Welfare (U.S. HEW), 1970]. The highest concentration
reported was 8,350 ug/1? a little over 1 percent of the samples ex-
ceeded the drinking water standard of 1 mg/1.
The 1 mg/1 copper standard was established not because of tox-
icosis but because of the taste which develops with higher levels
of copper in the water (U.S. HEW, 1970). It is most commonly ex-
C-4
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ceeded in soft water that is acidic in nature; however, it is race
that the concentration of copper in drinking water is high enough
to affect its taste or to produce toxicosis (McCabe, et al. 1970;
Fed. Water Quality Adro., 1968). For this reason, regulatory agen-
cies have not treated copper in public water supplies as a signifi-
cant problem. In New York City, copper is intentionally added to
the water supply to maintain a concentration of 0.059 mg/1 in order
to control algal growth (Klein, et al. 1974).
Prolonged contact of acidic beverages with copper conduits,
such as occurred in earlier models of drink dispensing machines,
may produce sufficient copper concentration to cause acute copper
toxicosis (see Acute, Subacute, and Chronic Toxicity section); how-
ever, because of taste problems, modern equipment does not contain
copper conduits.
The national impact of a water-borne contribution of copper is
difficult to detect, predict, or evaluate because information is
either absent or irretrievable. The current trend for recycling
waste (animal wastes, sewage solids and liquids, channel dredging,
and Industrial waste) to the land offers very real possibilities
that imbalance* in organisms may unwittingly be created, because
•uch wastes are commonly high in trace element concentration.
These trace elements may directly alter crop production and indi-
rectly affe«t the consumer (Patterson, 1971).
Anothet source of copper in water is the use of copper sulfate
to control «Lq«e. Some idea of the distribution of copper sulfate
-Y be g«ined fro. the work of Button, et al. (1977), who applied
9t.nul« coppr .ulfat. to the surface of Hoover Reservoir, Frank-
C-5
-------
lin County, Ohio. Soluble and particulate cupric copper concentra-
tions at several depths were measured by atomic absorption spectro-
photometry for four days after application. The soluble cupric
copper concentration decreased to near baseline values in 2 to 6
hours when 0.2 or 0.4 gms of copper sulfate per square meter were
added to the surface. Most of the copper sulfate was dissolved in
the first 1.75 meters of water column, and only 2 percent of the
total copper sulfate reached the depth of approximately 4.5 meters.
A concentration of 0.4 gms of copper per square meter controlled a
diatom bloom.
Ingestion from Food
Levels of copper in various foods are given in Table 2. Some
foods, such as crustaceans and shellfish (especially oysters),
organ meats (especially lamb or beef liver), nuts, dried legumes,
dried vine and stone fruits, and cocoa, are particularly rich in
copper. The copper content of these items can range from 20 ug/g to
as high as 400 ug/g (McCance and widdowson, 1947; Schroeder, et al.
1966). On an "as-cooked and as-served" basis, calves' liver, oys-
ters, and many species of fish and green vegetables have- recently
been classed as unusually good sources of copper (more than 100 ug
copper/100 kcal).
High levels of copper may also be found in swine because of
the practice, common in the United Kingdom and elsewhere, of feed-
ing to swine diets that are high (up to 250 ug/g) in copper in order
to increase daily weight gain. Levels of copper in swine liver
vary greatly depending on the copper content of the feed. A high
copper diet fed continuously until slaughter may produce levels of
C-6
-------
TABLE 2
Copper in Foods (Wet Weight)
Item
Sea food
Clams, raw
Clams, fresh frozen
Oysters
Sardines, canned Portugese
Kipper snacks, Norway, canned
Anchovies, canned Portugese
Pan fish, dried, V.I.
Lobster, frozen
Shrimp, frozen
Mean, excluding oysters
Meat
Beef liver
Beef kidney
Beef fat
Pork kidney
Pork loin
Pork liver
Lamb kidney
Lamb chops
Chicken leg and wing
Mean
Dairy products
Egg yolk
Egg white
Dried skimmed milk
Whole milk, dairy 1
Whole milk, dairy 2
Butter, salted
Mean
ug/g
3.33
0.48
137.05
1.12
1.70
0.81
0.58
0.51
3.40
1.49
11.00
0.42
0.83
5.30
3.90
3.72
0.95
7.13
1.99
3.92
2.44
1.70
2.09
0.26
0.12
3.92
1.76
ug/ioo
calories
694
100
27,410
38
85
27
49
42
297
167
769
34
21
441
130
260
96
381
99
249
70
460
63
40
18
49
117
^Source: Schroeder, et al. 1966
^* /""*•. 1 J*. ~^ 2 *mm ••A'1..*._.^ .K £ f .A. .A. J ^ A u .AM*. ^ A \t.^^^ d. ^ .^ ^ «h ^ ^3 'O \A Tj9 J jj J«^*.»^* ^%M
1947
V.I. - indicates that the sample came from St. Thomas, virgin
Islands.
C-7
-------
TABLE 2 (cont.)
Copper in Fooda
Item
Vegetables
Peas, green
Peas, split, green dry
Peas, green, V.I.
Peas, split, green, V.I.
Lentils
Yam, white, V.I.
Yam, yellow, V.I.
Turnip, white
Turnip greens
Beets
Carrots
Tomato, V.I.
Pepper, green, No. 1
Pepper, green, No. 2
Pepper, green, V.I.
Pepper, hot, red, V.I.
Cucumber, No. 1
Cucumber, No. 2
Christofine, V.I.
Egg plant, V.I.
Asparagus
Celery
Cabbage
Parsley
Rhubarb
Mushrooms
Mean
Fruits
Banana, V.I.
Papaya, V.I.
Coconut, V.I.
Coconut seed, V.I.
Apple, Macintosh
Mean, excluding coconut seed
ug/g
0.45
12.30
1.14
2.25
1.41
0.32
0.41
1.84
0.73
0.15
3.42
0.34
0.68
0.28
0.90
0.56
0.07
0.47
0.18
0.06
0.37
0.31
0.70
0.20
0.34
0.65
1.17
0.66
1.06
0.19
3.31
1.39
0.82
ug/100 .
calories
70
410
181
75
47
37
47
1,022
663
32
1,487
143
453
187
600
-
70
470
257
40
205
344
350
-
567
929
362
86
265
100
-
278
182
C-8
-------
TABLE 2 (cont.)
Copper in Foods
»-
Grains and cereals
Wheat seed 1.09 33
Wheat, whole 2.48 75
Wheat germ 0.15
Wheat head, chaff and stalk 0.14
Bread, white 0.19 8
Bread, whole wheat 0.63 25
Oats, whole 0.40 10
Corn, No. 1 0.46 13
Corn, No. 2 0.65 19
Rye, No. 1 0.92 27
Rye, No. 2 4.12 123
Rye, dry, flour 4.20 124
Benzene extract 10.82
Residue 1.87
Barley 3.83 106
Buckwheat 8.21 227
Rice, brown, U.S. 0.47 13
Rice, Japanese, polished 3.04 84
Bengal gram, India, 1 4.23 120
Bengal gram, India, 2 0.56 16
Grapenuts 14.95 415
Millet 2.34 67
Doughnut, cream filled 2.32 66
Mean, excluding grapenuts and extracts 2.02 58
C-9
-------
TABLE 2 (cor.t.
Copper in Foods
Item
Oils and fats
Lard, canned, 1
Lard, canned, 2
Lard, canned, 3
Lecithin, animal
Lecithin, egg
Cod liver oil, Norway
Castor oil, refined
Corn oil
Corn oil margarine
Cottonseed oil
Olive oil
Sunflower oil
Linseed oil, pressed
Peanut oil, pressed
Lecithin, vegetable, pure
Lecithin, soy, 90 percent pure
Lecithin, soy, refined
Mean, excluding lecithins
Nuts
Hazelnuts
Peanuts
Walnuts
Brazil nut
Pecans
Almonds
Mean
Condiments, spices, etc.
Garlic, fresh
Garlic powder
Mustard, dry
Pepper, black
Paprika
Chill powder
Thyme, ground
Bay leaves (laurel)
Cloves, whole
Ginger, ground
Ginger, root, V.I.
Caraway seeds
Vinegar, cider
Yeast, dry, active
Molasses
Sugar, refined
Mean
ug/g
3.06
2.50
2.13
26.38
10.52
6.80
1.70
2.21
24.70
1.26
3.20
5.44
1.75
0.83
5.31
4.37
20.95
4.63
12.80
7.83
12.70
23.82
12.64
14.11
14.82
3.15
0.75
3.04
20.73
8.47
5.98
23.58
3.68
8.67
2.63
1.87
4.31
0.76
17.79
2.21
0.57
6.76
ug/ioo
calories
34
28
24
—
-
-
-
25
274
14
36
60
19
9
-
-
-
58
233
131
231
370
211
234
235
—
-
—
—
—
—
—
—
—
—
—
—
—
—
85
14
-
C-10
-------
TABLE 2 (cont.)
Copper in Foods
Beverages
Gin, domestic 0.03 1
Vermouth, French 0.88 102
Vermouth, Italian 0.38 44
Whiskey, Scotch 0.35 14
Whiskey, Bourbon 0.18 7
Brandy, California 0.45 18
Bitters, Angostura 0.75
Wine, domestic, red 0.28 33
Beer, canned 0.38 76
Cola 0.38 100
Grape juice 0.90 136
Orange drink, carbonated 0.20 43
Orange juice, packaged 0.89 234
Coffee, dry, ground 2.35
Coffee, infusion 0.22
Tea, infusion 0.31 -
Mean, excluding dry coffee 0.44 20
Miscellaneous
Chocolate bar, Hershey 0.70 18
Ice cream, vanilla 0.29 15
Gelatin, Knox 3.87 148
Purina laboratory chow 15.61
Aspirin, Squibb 3.12
Saccharin 5.43
C-ll
-------
up to 400 to 600 ug/g in the liver. However, swine will rapidly
eliminate copper once it is removed from the diet. Sheep also ac-
cumulate copper in direct proportion to the level of copper in the
diet, but they eliminate excess copper very poorly [NRC-42, 1974;
National Academy of Science (NAS), 1977; Barber, et al. 1978],
Animal and industrial wastes (including sewage solids) common-
ly yield high concentrations of copper and other trace elements.
The current emphasis on recycling these wastes may unintentionally
supply excessive amounts of copper and these other elements to the
soil. Such recycling could indirectly affect consumers if the
yield of crops were reduced or if copper were increased in feed
products (NAS, 1977).
The National Academy of Science (1977) noted that the consump-
tion of sheep or swine livers that are high in copper could result
in excessive levels of copper, especially in baby foods where the
actual amount of copper might exceed the copper requirements of
very young children.
Dairy products, white sugar, and honey rarely contain more
than 0.5 ug copper/g. The nonleafy vegetables and most fresh
fruits and refined cereals generally contain up to 2 ug/g. Cheese
(except Eramental), milk, beef, mutton, white and brown bread, and
many breakfast cereals (unless they are fortified) are relatively
poor sources of copper, i.e., they have less than 50 ug copper/100
kcal [World Health Organization (WHO), 1973].
The refining of cereals for human consumption results in sig-
nificant losses of copper, although this loss is not so severe as
it is for iron, manganese, and zinc. Levels of copper in wheat and
wheat products are given in Tables 3 and 4.
012
-------
TABLE 3
Mineral Content of Known Wheats, the Flours Milled from them
and the Products Prepared from the Floursa'
«
Wheat, common hard
Flour, Baker1 s patent
Bread, sponge-dough
Bread, continuous-mix
Wheat, common soft
Flour, soft patent (cake)
Cake
Flour, straight-grade
Cracker
Flour, cut-off (cracker)
Cracker
Wheat, Durum
Semolina
Marcaroni
Humber
of
Samples
5
5
5
5
4
6
6
5
5
2
2
2
2
2
Moisture
11.0
13.9
36.3
35.3
10.6
11.9
22.8
11.4
4.9
12.6
4.5
10.7
14.7
9.6
Ash
1.87 + 0.10
0.49 + 0.03
3.39 + 0.19
3.42 T 0.30
1.73 + 0.17
0.42 + 0.03
2.71 + 0.11
0.50 + 0.05
3.42 ? 0.50
0.71 + 0.04
3.09 + 0.34
2.03 + 0.01
0.83 + 0.01
0.82 T 0.01
Copper
M9/g
5.1 + 0.5
1.9 + 0.2
2.3 ? 0.3
2.0 + 0.2
4.5 + 0.5
1.6 + 0.3
0.8 + 0.1
1.6 * 0.2
1.6 T 0.1
2.6 + 0.1
2.4 + 0.1
4.8 + 0.1
2.2 + 0.1
2.5 + 0.1
^Source: ZooK, et al, 1970
DMean and standard deviation, dry weight basis.
'Includes two flours prepared by air classification.
C-13
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TABLE 4
Mineral Content of Consumer Products Purchased in Ten Cities
a,b
Product
Cereal- to-be-cooked
Shredded wheat
Wheat flakes
Bread, whole wheat
Bread, white
Conventional dough
Continuous-mix
Rolls/ hamburger
Doughnuts, cake
Biscuit mix
Flour, all-purpose
Total
Samples
Collected
No.
24
47
28
38
52
29
52
28
23
31
Producers Sampled
Total
No.
7
6
3
26
37
17
34
20
8
19
Per
City
Range
1-3
4-6
2-3
2-8
3-9
1-4
4-9
1-5
1-4
3-4
Model
City
No.
3
4
3
2
4
2
4
3
2
3
Moisture
t
9.5
8.0
4.8
37.8
35.8
36.7
33.6
21.9
9.8
12.9
Ash
%
1.85 + 0.07
1.87 + 0.12
3.78 + 0.17
3.87 ± 0.12
3.23 + 0.12
3.10 + 0.13
2.85 + 0.08
2.61 + 0.20
4.28 + 0.26
0.56 + 0.03
Coppe r
wg/g
5.3 + 0.2
6.1 + 0.4
4.7 + 0.3
5.1 + 0.5
2.1 + 0.2
2.3 + 0.3
2.5 + 0.2
1.7 + 0.2
1.6 + 0.2
1.8 + 0.2
^Source: Zook, et al. 1970
and standard deviation, dry weight basis.
C-14
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Schroeder, et al. (1966) have suggested that since copper oc-
curs widely in human foods, it is difficult to prepare a diet of
natural foods that provides a daily copper intake of less than 2
mg, the level that is considered to be adequate for normal copper
metabolism (Adelstein, et al. 1956).
Tompsett (1934) reported that the normal daily intake of cop-
per from food appeared to be 2 to 2.5 mg per day for human subjects.
Daniels and Wright (1934) reported an average intake of 1.48 mg
copper per day in young children, with a requirement of not less
than 0.10 ug/kg of body weight per day.
Most American and western European diets supply adults with 2
to 4 mg of copper per day. This is evident from studies in England,
New Zealand, and the United States.. Lower estimates have been made
for certain Dutch and poorer Scottish diets, while Indian adults
consuming rice and wheat diets have been shown to ingest from 4.5
to 5.8 mg of copper per day (Schroeder, et al. 1966).
Scheinberg (1961) has contended that most adult diets supply a
substantial excess of copper. Klevay, on the other hand, has sug-
gested on the basis of recent food analyses that the copper content
may be less than earlier analyses indicated and has cautioned that
United States diets may not be adequate to provide 2 mg of copper
per day (Klevay, 1977; Klevay, et al. 1977).
Dr. Walter Mertz in a personal communication reported that in
1978 the analysis of diets of more than 20 individuals employed at
the Institute of Nutrition of the U.S. Department of Agriculture,
Beltsville, Md., showed that only two approached an intake of 2 mg
of copper per day. The diets of these individuals included soft
C-15
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drinks, water, and snacks, suggesting that food subjected to modern
processing and preparation methods may be much lower in copper than
was supposed based on earlier analyses, and that many individuals
eating these foods may be receiving considerably less than the 2 mg
of copper per day.
Engel, et al. (1967) conducted studies on young girls which
indicated that 2 u5 coppsr/g cf diet was adequate for good nutri-
tion. Petering, et al. (1571) mention that the copper content of
hair appears to be related to the age of the individual and suggest
that the need foe copper may differ between the sexes.
Because of the essentiality of copper, the copper balance in
newborn infants has been examined (Cavell and Widdowson, 1964). It
was noted that breast milk ranged from 0.051 to 0.077 rag/100 ml and
that total copper intakes of the babies ranged from 0.065 to 0.1
mg/kg/day. In the first week of life, some infanta excreted more
copper than was contained in the milk that they consumed. Of 16
babies, 14 were in negative balance.
As a general statement it would appear that, at least in the
United States, there is a greater risk of inadequate copper intake
than of an excess above requirements.
A bioconcentration^factor (BCP) relates the concentration of a
chemical in aquatic animals to the concentration in the water in
which they live. An appropriate BCF can be used with data concern-
ing food intake to calculate the amount of copper which might be
ingested from the consumption of fish and shellfish. Residue data
for a variety of inorganic compounds indicate that bioconcentration
factors for the edible portion of most aquatic animals is similar,
C-16
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except that for some compounds, bivalve molluscs (clams, oysters,
scallops, and mussels) should be considered a separate group. An
analysis (U.S. EPA, 1980) of data from a food survey was used to
estimate that the per capita consumption of freshwater and estua-
rine fish and shellfish is 6.5 g/day (Stephan, 1980). The per cap-
ita consumption of bivalve molluscs is 0.3 g/day and that of all
other freshwater and estuarine fish and shellfish is 5.7 g/day.
A bioconcentration factor of zero was reported for copper in
the muscle of bluegill sunfish (Benoit, 1975). Data are available
for several species of saltwater molluscs:
Species
BCP
Reference
Bay scallop, 3,310
Argopecten irradians
Bay scallop 4,160
Argopecten irradiana
American oyster, 28,200
Crasaostrea virginica
American oyster, 20,700
Crasaostrea virginica
Northern quahaug, 88
Mercenaria mercenaria
Soft shelled clam, 3,300
Mya arenaria
Mussel,. 208
Mytilua. edulis
Mussel,. 108
Mytilua edulis
Mussel, 90
Mytilus edulis
Mussel, 800
Mytilus galloprovincialis
Zaroogian, 1978
Zaroogian, 1978
Shuster and
Pringle, 1969
Shuster and
Pringle, 1969
Shuster and
Pringle, 1968
Shuster and
Pringle, 1968
Zaroogian, 1978
Zaroogian, 1978
Phillips, 1976
Major! and
Petronio, 1973
C-17
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If the values of zero and 290 are used with the consumption
data, the weighted average bioconcentration factor for copper and
the edible portion of all freshwater and estuarine aquatic orga-
nisms consumed by Americans is calculated to be 36. The geometric
means for scallops, oysters, clams, and mussels are 3,708, 24,157,
539, and 200, respectively, and the overall mean is 290.
Inhalation
The principal sourca of elevated copper levels in air is cop-
per dust generated by copper-processing operations. However, since
the economic value of copper encourages its capture from industrial
processes, extraneous emissions are reduced. Other possible
sources of copper in air may be tobacco smoke and stack emissions
of coal-burning power plants.
Copper has not been considered a particularly hazardous indus-
trial substance because the conditions that would produce excessive
concentrations of copper dust or mist in a particle size that could
be absorbed and generate toxic effects are apparently quite rare.
Investigations of Chilean copper miners have shown that liver and
serum concentrations of copper are normal, despite years of expo-
sure to copper sulfide and copper oxide dust, both of which are in-
soluble {Scheinberg and Sternlieb, 1969). However, workers can be
exposed to excess concentrations of copper in any of its forms, and
when this occurs, undesirable health effects can result. A 24- to
28-hour illness characterized by chills, fever, aching muscles,
dryness in the mouth and throat, and headache, has been noted where
workers are exposed to metal fumes within closed areas as a result
of the welding of copper structures (McCord, 1960).
C-18
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The U.S. Occupational Safety and Health Administration (OSHA)
has adopted standards of exposure to airborne copper at work. The
time-weighted average for 8-hour daily exposure to copper dust is
limited to 1 rag/m of air. The standard for copper fume was changed
in 1975 to 0.2 mg/m3 (Gleason, 1968; NAS, 1977).
In 1966, a National Air Sampling Network survey showed that
the airborne copper concentrations were 0.01 and 0.257 ug/m in
rural and urban communities, respectively (Natl. Air Pollut. Con-
trol Admin., 1968). Even near copper smelters, where high levels
(1 to 2 yg/m ) are reached, the dose of metal that would be acquired
through inhalation of ambient air would comprise only about 1 per-
cent of the total normal daily intake (Schroeder, 1970).
Generally speaking, inhalation of copper or copper compounds
is of minor significance compared to other sources, e.g., copper in
foods, drinking water, and other fluids, and use of copper for med-
ical purposes.
Dermal
Copper toxicity has resulted from the application of copper
salts to large areas of burned skin or from introduction of copper
into the circulation during hemodialysis. The source of the copper
in hemodialysia may b« the membranes fabricated with copper, the
copper tubing* or the heating coils of the equipment. Copper stop-
cocks in circuits can also cause potentially hazardous infusions of
copper (Holtzman, et al. 1966; Lyle, et al. 1976).
Studies with monkeys indicated that copper used as dental
fillings and placed in cavities in the deciduous teeth of the mon-
key caused more severe pulp damage than any of the other materials
C-19
-------
studied. This is additional evidence that tissues exposed directly
to copper or copper salts will suffer adverse effects due to the
direct absorption of the copper by the tissues (Mjor, et al. 1977).
Recent papers from Australia (Walker, 1977? Walker, et al.
1977) suggest the possibility of copper absorption through the skin
as a result of perspiration action on the copper bracelet, some-
times worn as treatment for arthritis, although the therapeutic
value of this has little support.
Concern has been directed toward the absorption of copper as a
result of the use of the intrauterine device (IUD) as a contracep-
tive measure (NAS, 1977). Analysis of lUDs that have been _in utero
for months to years shows that about 25 to 30 mg of copper are lost
each year. Some of the metal is excreted with endometrial secre-
tions. Experimental evidence to date does not indicate that use of
an IUD results in harmful accumulations of copper (see Absorption
section for additional information).
PHARMACOKINETICS2
Absorption
Tracer studies provide the basis for the conclusions that most
absorption in man takes place in the stomach and the duodenum.
Copper absorption appears to be regulated by the intestinal mucosa,
and maximum copper levels occur in the blood serum within one to
three hours after oral intake.
Acknowledgement is made of the courtesy of the late Dr. Karl E.
Mason and Dr. Walter Mertz who allowed the author to read their
manuscript, Conspectus on Copper, to be published in the Journal of
Nutrition.
C-20
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Much of the information on copper absorption in humans has
come from studies of patients with Wilson's disease. Studies con-
ducted with these patients using radioactive copper indicate that
about one-half of the copper in the diet is not absorbed but is ex-
creted directly into the feces. The average absorption in these
individuals has been reported to be approximately 40 percent
(Sternlieb, 1967; Strickland, et al. 1972a). Investigations by
Cartwright and Wintrobe (1964a) indicated that the daily intake of
copper in Wilson's disease patients was 2 to 5 mg, of which 0.6 to
1.6 mg were absorbed, 0.5 to 1.2 mg were excreted in the bile, 0.1
to 0.3 mg passed directly into the bowel, and 0.01 to 0.06 mg ap-
peared in the urine.
Information from these studies indicates that absorbed copper
is rapidly transported to blood serum and taken up by the liver,
from which it is released and incorporated into ceruloplasmin. Any
copper remaining in the serum is attached to albumin or amino acids
or is used to maintain erythrocyte copper levels (Weber, et al.
1969; Beam and Runkel, 1954, 1955; Beckner, et al. 1969? Bush, et
al. 1955; Jensen and Kamin, 1957).
Estimates of the amount of the copper that is actually ab-
sorbed by normal individuals vary considerably and must be consid-
ered inconclusive. The values obtained have ranged from as low as
15 percent tff as high as 97 percent (Weber, et al. 1969), although
it seems probable that subjects having these extreme values were
not in a steady state. The uncertainty of these values is con-
founded by the lack of accurate information regarding the excretion
of copper in its various forms by way of the biliary system. Even
C-21
-------
Less information is available regarding the reabsorption of copper
or copper compounds from the intestine after they have been excret-
ed in the bile. Most of the values that have been obtained with
normal subjects suggest that 40 to 60 percent of the dietary copper
is absorbed (Van Ravensteyn, 1944; Cartwright and wintrobe, 1964a;
Bush, et al. 1955; Matthews, 1954; Weber, et al. 1969; Strickland,
et al. 1972a,b; Sternliebf 1967)>
Animal studies have shown that copper is absorbed by at least
two mechanisms, an energy-dependent mechanism and an enzymatic
mechanism (Crampton, et al. 1965) , and that many factors may inter-
fere with copper absorption, including competition for binding
sites as with zinc, interactions with molybdenum and with sulph-
ates, chelation with phytates, and the influence of ascorbic acid.
Ascorbic acid will aggravate copper deficiency by decreasing copper
absorption. In cases of excess copper intake, ascorbic acid can
reduce the toxic effects (Gipp, et al. 1974; Hunt, et al. 1970;
Voelker and Carlton, 1969).
Studies with laboratory animals have shown that once copper
enters the epithelial cells, it is taken up by a cellular protein
similar to liver metallothionein (Evans, et al. 1973; Evans, 1973;
Starcher, 1969). Absorbed copper is bound to albumin and trans-
ported in the plasma. Approximately 80 percent of the absorbed
copper is bound in the livec to metallothionein. The remaining
copper is incorporated into compounds such as cytochrome-c-oxidase
or is sequestered by lysosomes (Beam and Kunkel, 1954, 1955).
Little information is available concerning absorption of copper
into the lymphatics, although in pathological conditions this may
be significant (Trip, et al. 1969).
C-22
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Several studies have been conducted on humans and laboratory
animals concerning absorption of copper as a result of the use of
copper XUDs. Studies with the IUD in rats have suggested that as
much as 10 to 20 mg of copper may be absorbed (Oreke, et al. 1972).
This amount/ which is small compared to the dietary copper usually
ingested, may or may not be metabolized and excreted by the same
homeostatic mechanisms that operate with ingested copper. If an
IUD were used for many decades and the absorbed copper were re-
tained, it would result in amounts of copper similar to those re-
tained from dietary copper by patients with Wilson's disease. Such
levels could result in chronic toxicosis.
Japanese investigators (Okuyama, et al. 1977} have compared
effects of using the IUD with copper and the IUD without copper in
two groups of women/ using a third group as controls. Pregnant
women with an IUD in place were also examined. No significant dif*
ference was found in the endometrial copper levels in the three
groups. There was a tendency toward an increase above controls in
the endometrial level of copper during the secretory phase in those
women using the IUD with or without copper. No significant differ-
ence was found between women who had used an IUD more than 13 months
and those who had used it less than 13 months. The copper content
of the chorion and the decidua of the pregnant women with lUDs in
place did not-differ from the levels noted in pregnant women with-
out lUDs. Apparently, the long-term use of copper-containing lUDs
did not lead to an accumulation of copper in the uterus.
Tamaya, et al. (1978) have studied the effect of the copper
IUD on the histology of the endometrium in the proliferative and
C-23
-------
the secretory phases of women. Their result
*ftdtca$)d
copper IDD affected the secretory endoraetriu* h««.
"• °at not t!* proliut
ative endometr iuni, "
In another study, Israeli women with the Lat
contains both copp*r and zinc, showed Increased
— -*•"»• w^»
ala if they had had low serum levels of cooper tnd ^^
section. However, their copper and tine levels did
upper limits of normal values. No significant statistic*!
ence was found between the serum levels of coppet
insertion of the ItTD.
It has been suggested that diabetic WOWH
ently feoai normal healthy wowen to the UM of a
diabetics, the presence of a copper IUO did not
lytic activity in th« endo**triu», although svcft a* effwt «•»«•*>
served in nondiabetlcs. Slnc« there is evidene* tfttt «^S**SM^
of the endo**trial fibrolytic activity pr*v««t* a*M*l4» •* M»
plantation of ovs, th* results ««y etplaia tB* rvport *f UMB «**!*
»bie contraceptive effect of the nn> In diadetttf <*•»• fUftMfe «t
•I. if77).
A matter of studies of th« effect of «PP*€ ^» fwtlUff
tit «« «- lfTflt
of «U
IUO« la rats have ail «<**•««•<
treeti howler
-------
Distribution
The amount and distribution of copper in body tissues varies
with sex, age, and the amount of copper in the diet. Copper content
of fat-fre« tissues of most animals ranges upward from about 2
ug/g. The highest concentrations of copper in both animal and
human tissues are found in the liver and the brain, with lesser
amounts in the heart/ the spleen, the kidneys, and blood (Cart-
wright and Wintrobe, 1964a,b; Smith, 1967; Schroeder, et al. 1966).
Some tissues are very high in copper, e.g., the iris and the cho-
roid of the eye, which may contain as much as 100 vg/gra (Bowness and
Morton, 1952; Bowness, et al. 1952).
Estimates of the total amount of copper in a 70 kg man have
ranged from 70 to 120 mg. Approximately one-third of body copper
is found in the liver and the brain, one-third is found in the mus-
culature, and the remaining one-third is dispersed in other tis-
sues. It has been estimated that, on the average, about 15 percent
of the total body copper is contained in the liver (Tipton and
Cook, 1963; Surainor et al. 1975; Sass-Rortsak and Beam, 1978).
The relatively high percentage of liver copper is related to the
liver's function as a storage organ for cooper and as the only site
for the synthesis and release of ceruloplasrain, the most abundant
copper proteinr in the blood.
In th» brain, the striaturn and both components of the cortex
(gray matter) have the highest copper content, with the cerebellum
(white matter) being the lowest (Hui, et al. 1977; Cumings, 1948;
Earl, 1961). The brain appears to be the only tissue in which there
is a consistent increase in copper content with age. Other tissues
appear to be under a homeostatic control.
C-25
-------
Copper levels in hair vary widely with respect to age, sex,
and other factors, and therefore have little meaningfulness in
evaluating copper levels in man (Underwood, 1977). However, Jacob,
et al. (1978) have suggested that the copper in hair may be useful
in evaluating the total liver content of copper. Engel, et al.
(1967) surveyed over 180 adolescent girls in the 6th to 8th grades
for dietary intake and nutritional status. They found that the
mean concentration of copper in hair samples was 31 + 23 ug/g. No
significant difference was found between girls who had experienced
menarche and those who had not.
Levels of copper in the blood of normal adults average 103
ug/100 ml of blood. The amount of copper in blood serum can range
widely from 5 ug/100 ml to 130 yg/100 ml. In practically all spe-
cies, copper deficiency is first manifested by a slow depletion of
body copper stores, including the blood plasma, eventually result-
ing in a severe anemia identical to that caused by iron deficiency
{Cartwright, et al. 1956).
Both the plasma and the erythrocytes have two pools of copper,
a labile pool and a stable pool, which contain approximately 40 and
60 percent respectively, of the copper in the blood (Bush, et al.
1955). Ceruloplasrain represents the predominant portion of cooper
in the serum pool. There appears to be little or no interchange
between ceruloplasnin copper and other forms of copper in the blood
stream (Sternlieb, et al. 1961). Mondorf, et al. (1971) indicate
that the blood contains an average of 30 ug of ceruloplasmin/100 ml
of blood. This is in reasonable accord with accepted levels of
copper in the blood of normal adults (approximately 103 ug total
C-26
-------
copper/100 ml of blood). white blood cells contain a small amount
of copper, about one-fourth the concentration in erythrocytes
(Cartwright, 1950) .
The distribution of copper in the fetus and in infants is
quite different from that in the adult. The percentage of copper
in the body increases progressively during fetal life (Shaw, 1973).
Chez, et al. (1978) found that concentrations of copper in amniotic
fluid increased between the 26th and 33rd weeks of pregnancy, but
that there did not appear to be a correlation between maternal and
fetal copper concentrations.
At birth, the liver and spleen contain about one-half the cop-
per of the whole body (Widdowson and Spray, 1951). A newborn in-
fant contains about 4 mg/kg as compared to approximately 1.4 mg/kg
in the 70 kg man (Widdowson and Dickerson, 1964). The liver of the
newborn has approximately 6 to 10 times the amount of copper in the
liver of an adult man on a per gram basis (Bruckmann and 2ondek,
1939; Nusbaum and Zettner, 1973; Widdowson, et al. 1951).
The concentration of copper in the serum of newborn infants is
significantly lower than in 6- to 12-year-old healthy children, but
by five months of age the serum concentration of copper is approxi-
mately the same as in older children. There is no difference be-
tween copper levels in male and female infants, although breast-fed
infants see* to have somewhat higher copper levels by one month
than bottle-fed infants (Ohtake, 1977). The liver copper content
of the fetus is several times higher than maternal liver copper
(Seeling, et al. 1977).
C-27
-------
Metabolism
The copper content of red blood cells remains remarkedly con-
stant, but the plasma copper is subject to striking changes asso-
ciated with the synthesis and release of ceruloplasmin, which is
the most abundant copper protein that responds to deficiencies or
excesses (Gubler, et al. 1953; Lahey, et al. 1953).
Some 20 mammalian copper proteins have been isolated, but at
least three are identical and others have more than one name. Most
of this information has come from animal studies, and its applica-
bility to humans is uncertain. Evans (1973) and others have re-
viewed this subject (Mann and Keilin, 1938; Osborn, et al. 1963;
Morell, et al. 1961; Sternlieb, et al. 1962).
Copper plasma levels during pregnancy may be two to three
times the normal nonpregnant level. This is almost entirely due to
the increased synthesis of ceruloplasmin (Henkin, et al. 1971;
Markowitz, et al. 1953; Scheinberg, et al. 1954). The source of
this copper appears to be the maternal liver. The increase in
maternal plasma copper levels appears to be associated with estro-
gen, since either sex receiving estrogen shows an increase in cop-
per level of the plasma (Eisner and Hornykiewicz, 1954; Gault, et
al. 1966; Humoller, et al. 1960; Russ and Baymunt, 1956).
The use of oral contraceptives causes a marked increase in
serum copper levels that may be greater than those observed during
pregnancy (Oster and Salgo, 1977; Smith and Brown, 1976; Tatum,
1974) .
Infant levels of serum copper are low at birth but promptly
increase due to the synthesis of ceruloplasmin by the infant's
liver (Henkin, et al. 1973; Schorr, et al. 1958).
C-28
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There are two inherited diseases that represent abnormal cop-
per metabolism, Menkes' disease and Wilson's disease. Menkes' dis-
ease is a progressive brain disease caused by an inherited sex-
linked recessive trait. It is often referred to as the "kinky
hair" disease ot "steely hair" disease (Danks, et al. 1972). The
primary characteristic of Menkes1 disease appears to be a dimin-
ished ability to transfer copper across the absorptive cells of the
intestinal mucosa (Danks, et al. 1972, 1973). The general symptoms
of the disease are similar to those observed in animals suffering
from coppec deficiency (Oakes, et al. 1976). The prospects for
more effective therapeutic measures as a result of early diagnosis
appear to be limited.
Wilson's disease, which has also been designated "hepatolen-
ticular degeneration," is caused by an autosomal recessive trait
(Beam, 1953) . The disease is actually a copper toxicosis with
abnormally high levels of copper in the liver and brain (Cumings,
1948). Symptoms include increased urinary excretion of copper
(Spillane, et al. 1952? Porter, 1951), low serum copper levels due
to low ceruloplasmin (Scheinberg and Gitlin, 1952), decreased in-
testinal excretion of copper, and occurrence of Kayser-Pleischer
rings due to excessive accumulation of copper around the cornea.
If therapy with d-penicillamine is instituted during the early
phases of Wilson's disease, it can assure a normal life expectancy,
especially when accompanied by a low-copper diet (Deiss, et al.
1971; Sternlieb and Scheinberg, 1964, 1968; Walshe, 1956).
Other abnormalities of copper metabolism are primarily associ-
ated with low levels of copper. Hyoocupremia, which is defined as
C-29
-------
80 ug or less of copper/100 ml (Cartwright and Wintrobe, L964a),
usually refers to a low ceruloplasmin level. In most cases it is
probably due to a dietary deficiency of copper or to a failure to
synthesize the apoenzyme of ceruloplasmin (Kleinbaum, 1963). Hypo-
cupremia can also result from malabsorption that occurs during a
small bowel disease (Sternlieb and Janowitz, 1964).
Hypercupremia, abnormally high levels of copper, occurs with a
number of neoplasms (Delves, et al. 1973; Herring, et al. I960;
Goodman, et al. 1967; Janes, et al. 1972). Elevated serum copper
levels occur in psoriasis (Kekki, et al. 1966; Molokhia and Port-
noy, 1970) .
It is well recognized that copper is necessary for the utili-
zation of iron. Much of this work has been done in animals, and the
subject is well covered by Underwood (1977). It appears that ceru-
loplasmin is essential for the movement of iron from cells to plas-
ma (Osaki, et al. 1966). Reticulocytes from copper-deficient ani-
mals can neither pick up iron from transferrin normally nor synthe-
size heme from ferric iron and protoporphyrin at the normal rate
(Williams, et al. 1973).
The ratio of copper to other dietary components, e.g., zinc,
iron, sulfate, and molybdenum, may be almost as important as the
actual level of copper in the diet in influencing the metabolic
response of mammalian species (Smith and Larson, 1946). The car-
diovascular disorder "falling disease", reported by Bennetts, et
al. (1942), is associated with a copper deficiency in cattle. Sim-
ilar conditions have been observed in pigs and chickens (O'Dell, et
al. 1961; Shields, et al. 1961). In this disorder the elastic tis-
C-30
-------
sue of major blood vessels is deranged, markedly reducing the ten-
sile strength of the aorta. This appears to be associated with a
biochemical lesion, the reduced activity of lysyl oxidase, a cop-
per-requiring enzyme necessary for elastic tissue formation and
maintenance (Hill, et al. 1967) .
Evans has discussed the metabolic disorders of copper metabo-
lism including nutritional disorders, inborn order errors of proper
homeostasiSr and disorders due to the lack of copper-requiring en-
zymes (Evans, 1977).
Particular attention has been given to the role of copper as
associated with cardiovascular diseases (Vallee, 1952; Adelstein,
et al. 1956). More recently there has been considerable interest
in the role of copper and its ratio to zinc as a factor in the level
of cholesterol and cholesterol metabolism as it may relate to is-
chemic heart disease (Klevay, 1977) . It has been suggested that a
low copper-high zinc ratio may result in an increased level of
cholesterol, particularly that part of the blood cholesterol in the
serum low density lipoprotein which has been associated with in-
creased susceptibility to ischemic heart disease (Allen and Klevay,
1978a,b; Petering, 1974; Lei, 1978; Klevay, et al. 1977). In a
different context, Harman (1970) has suggested that copper in the
diet in excess of needs may result in free radicals that cause ad-
verse effects in the cardiovascular system.
Excretion
It has been noted that perhaps 40 percent of dietary copper is
actually absorbed (Cartwright and Wintrobe, 1964a). These esti-
mates are largely based on the difference between oral intake and
C-31
-------
fecal excretion. Urinary excretion of copper plays a very minor
role. The fecal excretion represents unabsorbed dietary copper and
the copper that is excreted by the biliary tract, the salivary
glands, and the gastric and intestinal mucosae (Gollan and Deller,
1973). It should be noted that some of the excreted copper is re-
absorbed in the course of its movement down the intestinal tract.
Some loss of copper may occur by way of sweat and in the female
menses.
One of the principal routes of excretion is by way of the
bile; however/ because of the difficulty in studying biliary excre-
tion in normal subjects, the evidence for quantitative values of
copper excretion by this route is fragmentary. Cartwright and Win-
trobe (1964a) suggest that 0.5 to 1.2 mg per day is excreted in the
bile. This is in reasonable accord with the report (Frommer, 1974)
that excretion was approximately 1.2 mg/day in ten control sub-
jects. It is possible that very little of the copper excreted in
the bile is reabsorbed (Lewis, 1973).
Some copper (approximately 0.38 to 0.47 mg/day) is excreted in
the saliva, but there is little evidence as to whether this copper
is or is not absorbed in the intestine (DeJorge, et al. 1964).
It is possible that the gastric secretion of copper approxi-
mates 1 mg of copper per day, but there is very little published
information on this subject (Gollan, 1975).
The amount of copper excreted in the urine is small. Esti-
mates range from 10 to 60 ug/day and average 18 ug/o*ay (Cartwright
and Wintrobe, 1964a; Zak, 1958). It is possible, of course, that
copper may be reabsorbed from the kidney tubules (Davidson, et al.
1974) .
C-32
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Studies in New Zealand conducted on young women with a copper
intake of 1.8 to 2.09 mg/day showed an excretion in the feces of
between 65 and 94 percent of the intake. The urinary excretion
amounted to 1.7 to 2.2 percent of the intake (Robinson, et al.
1973) .
Under some conditions a considerable amount of copper may be
lost through sweat, perhaps as much as 1.6 mg of copper per day or
about 45 percent of the total dietary intake (Consolazio, et al.
1964).
There is very little information on the loss of copper by way
of the menstrual flowr but an average value of 0.11 £ 0.07 mg per
period seems reasonable (Ohlson and Daunt, 1935? Leverton and Sink-
ley, 1944) .
Sternlieb, et al. (1973) note that 0.5 to 1.0 mg of copper is
catabolized daily by the adult liver, and about 30 mg of cerulo-
plasmin, which contains 0.3 percent copper, is excreted into the
intestine (Waldmann, et al. 1967). The copper excreted into the
intestine in the bile may not be readily available for reabsorption
because it is bound to protein; the copper found in the feces seems
to come from various secretions, as well as the copper that is not
absorbed from food (Gollan and Deller, 1973).
In summary it may be said that most copper is excreted by way
of the biliary system with additional amounts in sweat, urine,
saliva, gastric and intestinal mucosae, and menstrual discharge.
Examination of the pharmokinetic data points up the fact that
the biological half-life of copper is very short. This provides
significant protection against accumulations of copper even with
intakes considerably above levels considered adequate.
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EFFECTS
Acute, Subacute, and Chronic Toxicity
Copper toxicity produces a metallic taste in the mouth, nau-
sea, vomiting, epigastric pain, diarrhea, and depending on the
severity, jaundice, hemolysis, hemoglobinuria, hematuria, and oli-
guria. The stool and saliva may appear green or blue. In severe
cases anuria, hypotension, and coma can occur.
Toxic levels of copper ingested are promptly absorbed from the
upper gut, and the copper level in the blood is rapidly increased,
primarily because of its accumulation in the blood cells. Hemoly-
sis occurs at high copper levels. A high level in the blood can
also result from absorption through the denuded skin, as when ap-
plied to burns, because of dialysis procedures, or because of ex-
change transfusions. The hemolysis is due to the sudden release of
copper into the blood stream from the liver that has been damaged
by an increasing load of copper and is unable to utilize the copper
in the synthesis of ceruloplasmin, which in turn can be excreted by
way of the biliary system (Chuttani, et al. 1965; Bremner, 1974;
Cohen, 1974; Deiss, et al. 1970; Roberts, 1956; Bloomfield, et al.
1971; Ivanovich, et. al. 1969; Bloomfield, 1969).
Chatterji and Ganguly (1950) describe a nonfatal type of cop-
per poisoning in which the symptoms are laryngitis, bronchitis,
intestinal colic with catarrh, diarrhea, general emaciation, and
anemia.
Burch, et al. (1975) have estimated that the toxic intake
level of inorganic copper for an adult man is greater than 15 mg per
dose. The vomiting and diarrhea induced by ingesting small quanti-
C-34
-------
ties of ionic copper generally protect the patient from the serious
systemic toxic effects which include hemolysis, hepatic necrosis,
gastrointestinal bleeding, oliguria/ azotemia, hemoglobinuria,
hematuria, proteinuria, hypotension, tachycardia, convulsions, or
death (Chuttani, et al. 1965; Davenport, 1953).
Because most of the information about acute copper toxicity in
humans has come frora attempts at suicide or from the accidental
intake of large quantities of copper salts, the information about
the changes occurring with acute toxicity are meager.
Acute copper poisoning does occur in man when several grams of
copper sulfate are eaten with acidic food or beverages such as vin-
egar, carbonated beverages, or citrus juices (Walsh, et al. 1977).
Some cases of acute poisoning have occurred when tablets containing
copper sulfate were given to children (Forbes, 1947).
When carbonated water remains in copper check valves or drink-
dispensing machines overnight, the copper content of the first
drink of the day may be increased enough to cause a metallic taste,
nausea, vomiting, epigastric burning, and diarrhea (Hooper and
Adams, 1958). Drinks that are stored in copper-lined cocktail
shakers or vessels can have the same effect (Pennsylvania Morbidity
and Mortality Weekly Reports, 1975; McMullen, 1971).
Salmon and Wright (1971) have reported the possibility of
chronic copp«r poisoning as a result of water moving through copper
pipes. They document a case in which a family moved into a house in
North London with a hot water system entirely composed of copper.
The water was stored in a 40-gallon copper tank which reached a
temperature of 93°C at night. The family used hot water for all
C-35
-------
cooking and beverages. After two months, the electric kettle was
coated inside with a thick green film of the copper complex. The
child in the family was admitted to the hospital after five weeks
of behavior change, diarrhea, and progressive marasmus. When it
was first seen, the clinical picture was that of "pink" disease
with prostration, misery, red extremities, hypotonia, photophobia,
and peripheral edema. The liver was palpable 2 cm below the costal
margin. The serum copper level was 286 ug/100 ml, compared to a
normal range of 164 + 70 ug/100 ml. Analysis of water in the home
found 350 yg/1 of copper in the cold water and 790 ug/1 of copper in
the hot water. Cold and hot water levels in the hospital were 40
and 300 ug/1, respectively, and in North London the values were 80
and 160 ug/1.
Walker-Smith and Blomfield (1973) treated the male infant de-
scribed in the preceeding paragraph, who had received high levels
of copper front contaminated water over a period of three months,
with d-penicillamine and prednisolone. The infant made a slow re-
covery. The method of Eden and Green (1940) was used to determine
copper levels. It is possible that the infant was exhibiting Wil-
son's disease and responded to the appropriate treatment.
Eden and Green (1940) reported on a male infant who received
high levels of copper from contaminated water ingested over a peri-
od of thre« months. The result was chronic copper poisoning.
Treated with d-penicilliamine and prednisolone, the infant made a
slow recovery.
In general, however, the problems associated with high levels
of copper in drinking water are more or less controlled because of
C-36
-------
(1) taste (since high levels of copper in water produce a metallic
taste), and (2) cosmetic considerations (since water with high cop-
per content develops a surface scum due to the formation of insolu-
ble copper compounds).
Chronic toxicity has been studied in animals, and there ap-
pears to be a wide variation in the tolerance of different species
for high levels of copper in the diet. Sheep are very susceptible
to high copper intakes, whereas rats have been shown to be very
resistant to the development of copper toxicity.
Swine will develop copper poisoning at levels of 250 ug of
copper/g of diet unless zinc and iron levels are increased. Suttle
and Mills (1966) have studied dietary copper levels ranging up to
750 ug/g in the diet of swine. Toxicosis does develop with hypo-
chromic microcytic anemia, jaundice, and marked increases in the
liver and serum copper levels as well as serum aspartate ami no
transferase. These signs of copper toxicosis in swine can be elim-
inated by including an additional 150 ug of zinc and iron/g in
diets containing up to 450 ug of copper/g; the addition of even
more zinc and iron, 500 to 750 ug/g, will overcome the effects of
750 ug of copper/g of diet.
Chronic oral intake of copper acetate in swine and rats can
produce a condition comparable to hepatic hemosiderosis in man
(Mallory andt Parker, 1931). Some question exists as to whether
hemosiderosis in man is a result of copper toxicity, because people
consuming comparatively high levels of copper do not develop this
condition regularly.
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Sheep are quite susceptible to high Levels of copper in the
diet. Copper levels of 35 ug/g of feed have resulted in toxicity
when fed over a period of nine months to one year (Fontenot, et al.
1972) . Cattle are much more resistant to copper in the diet; 2 g of
copper sulfate given daily did not produce toxic reactions (Cun-
ningham, 1931) .
It is well known that with ruminant animals, molybdenum and
sulfate interact with the copper. Copper toxicity is counteracted
by inclusion of molybdenum and sulfate in the diet of ruminants
(Dick, 1953; Kline, et al. 1971; Wahal, et al. 1965).
Synergism and Antagonism
There is some evidence that copper may increase the mutagenic
activity of other compounds. Using strain TA100 of Salmonella
typhimurium, Omura, et al. (1978) studied the mutagenic actions of
triose reductone and ascorbic acid. They found that the addition
of the copper to triose reductone at a ratio of 1:1,000 lowered the
most active concentration of the triose reductone to 1 mM from 2.5
to 5 mM.
Another enediol reductone, asborbic acid, had no detectable
mutagenic action by itself, but a freshly mixed solution of 5 mM of
ascorbic acid and 1 or 5 uM of cupric copper had an effective muta-
genic action. Ascorbyl-3-phosphate had no mutagenic function even
in the presence of cupric copper. The investigators suggested that
it was the enediol structure in the reductones that was the essen-
tial for mutagenicity.
In the Acute, Subacute, and Chronic Toxicity section, it was
pointed out that the dietary levels of zinc and iron are as impor-
C-38
-------
tant as the level of copper in determining the toxic level of
copper.
Teratogenicity
There is very little evidence in the literature to suggest
that copper has a teratogenic effect in either animals or humans,
Mutagenicity
No data were found to suggest that copper itself has a muta-
genic effect in either animals or humans; however/ one report
exists suggesting that copper may increase the mutagenic activity
of other compounds {see Synergism and Antagonism section).
Carcinogen id ty
There is very little evidence in the literature to suggest
that copper has a carcinogenic effect in either animals or humans.
Pimental and Marques (1969) noted that vineyard workers in France,
Portugal, and southern Italy, exposed to copper sulfate sprays
mixed with lime to control mildew, developed granulomas in the
liver and malignant tumors in the lung (Pimental and Menezes, 1975;
Villar, 1974). Because of the route of exposure, quantitative
estimates are, at best, speculative.
It has been noted earlier that the conditions in industry that
would produce- excessive concentrations of copper as a dust or a
mist with particle sizes that would result in toxic effects if the
copper were absorbed, are apparently quite rare. Some investiga-
tors have suggested that lung cancer, which is prevalent in copper
smelter workers, is actually due to the arsenic trioxide in the
dust and that the copper itself did not play any etiologic role in
the development of the cancer (Kuratsune, et al. 1974; Lee and
:-39
-------
Fraumeni, L969; Milham and Strong, 1974; Tokudome and Kuratsune,
1976) .
Some studies have reported that, with the development of vari-
ous tumors, the copper content in both blood and the tumor tissue
is likely to increase, although this is not always the case (Ped-
rero and Kozelka, 1951; Dick, 1953; Kline, et al. 1971; Wahal, et
al. 1965). However, when an increase occurs, it appears to be a
result of an inflammatory response or stress rather than any direct
causative relationship.
Polish workers (Legutko, 1977) have suggested that the copper
level of the serum is a particularly sensitive indicator of the
clinical condition and effectiveness of treatment of lymphoblastic
leukemia in children, but again no particular relationship to the
development of the leukemia is indicated.
Russian scientists (Bezruchko, 1976} have also studied the
copper and ceruloplasmin in patients with cancer and noted that the
levels of both ceruloplasmin and copper were increased in metastat-
ic cancer of the mammary gland, in skin melanoma, and in ovarian
cancer. The serum levels of ceruloplasmin increased 27, 20, and 44
percent, respectively, for those tumors, and the copper increased
by 41, 35, and 51 percent, respectively, for those same tumors as
compared with normal tissue. Again, no correlation was found be-
tween the tumor and copper as a causative agent.
Workers in Hong Kong (Fong, et al. 1977) have been investigat-
ing copper concentrations in cases of esophageal cancer in both
humans and animals. They report that serum copper is increased
slightly and that this is paralleled by a decrease in zinc content.
C-40
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In summary, it must be stated that evidence for the oncologi-
cal effects of copper, even at high concentrations, is essentially
nonexistent. With the exception of the references cited, there
appear to b« no definitive reports of copper as a causative agent
in the development of cancer. There is much more evidence that a
deficiency of copper will have adverse effects both in animals and
in humans due to its essential role in the functioning of many en-
zyme systems.
C-41
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CRITERION FORMULATION
Existing Guidelines and Standards
Par more attention has been given to the problems of copper
deficiency than to the problems of excess copper in the environ-
ment. The 1 mg/1 standard that has been established for copper
levels in water for human consumption has been adopted more for
organoleptic reasons rather than because of any evidence of toxic
levels (Fed. Water Quality Admin., 1968).
Cohen, et al. (1960) noted that various investigators have
reported adverse taste of water containing 3 to 5 mg/1, 2 mg/1 and
1.5 mg/1 of copper. The choice of 1 ppm as a level that was organo-
leptically satisfactory and below any values of health concern for
humans was therefore considered reasonable. This study was used as
a basis for the current drinking water standard.
The U.S. Occupational Safety and Health Administration has
adopted standards for exposure to airborne copoer at work. The
time-weighted average for 8-hour daily exposure to copper dust is
limited to 1 mg/ra of air. The standard for copper fume was changed
in 1975 to 0.2 rag/m3 (Gleason, 1968; Cohen, 1974).
As indicated below, the Food and Nutrition Board of the Na-
tional Academy of Sciences (1980) recommends a daily allowance of
0.5 to 1.0 mg/day for infants, 1.0 to 2.0 mg/day for pre-schoolers,
2.0 to 2.5 mg/day for older children, and 2.0 to 3.0 mg/day for
teenagers and adults.
Age (yrs) RDA (mq/day) Age (yrs) RDA (mq/day)
0.0-0.5
0.5-1.0
1-3
0.5-0.7
0.7-1.0
1.0-1.5
4- 6
7-10
11-Adult
1.5-2.0
2.0-2.5
2.0-3.0
C-42
-------
There are no standards for copper in medical practice such as
the treatment of burns or dialysis or for parenteral feeding.
Current Levels of Exposure
As has been mentioned earlier/ principal concern has been for
conditions of copper deficiency rather than copper toxicity. It
has been suggested earlier that copper intakes in food and water
may range from 6 to 8 mq per day, and that the percentage absorbed
varies with the nutritional status. On the other hand, because of
changes in food processing and, perhaps, because of better methods
of analysis, copper intakes may not reach the 2 mg per day consid-
ered an adequate nutritional intake (Klevay, et al. 1977; Diem and
Lentner, 1970; Robinson, et al. 1973; Schroeder, et al. 1966? WHO,
1973; Cartwright and wintrobe, 1964a).
The average concentration of copper in United States water
systems is approximately 134 ug/1 with a little over 1 percent of
the samples taken exceeding the drinking water standard of 1 mg/1
(McCabe, et al. 1970). When the U.S. Public Health Service studied
urban water supply systems, they found that only 11 of 969 systems
had copper concentrations greater than 1 mg/1 (U.S. HEW, 1970}.
In 1966, the National Air Sampling Network found airborne cop-
per concentrations ranging from 0.01 to 0.257 ng/m in rural and in
urban communities, respectively. Levels of copper as high as 1 to
2 yg/m were* found near copper smelters, but this was not consid-
ered hazardous (Natl. Air Pollut. Control Admin., 1968? Schroeder,
1970) .
C-43
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Special Groups at Risk
Increased copper exposure, with associated health effects, has
occasionally occurred in young children subjected to unusually high
concentrations of copper in soft or treated water that has been
held in copper pipes or stored in copper vessels. Discarding the
first water coming from the tap can reduce this hazard. Similar
problems have developed in vending machines with copper-containing
conduits where acid materials in contact with the copper for per-
iods of time have dissolved copper into the vended liquids.
Other groups that may be at risk are medical patients suffer-
ing from Wilson's disease and those patients who are being treated
with copper-contaminated fluids in dialysis or by means of paren-
teral alimentation. These are medical instances in which the cop-
per content of the materials used should be carefully controlled.
There is also a reasonable likelihood that exposure to ele-
vated levels of copper (ca. 1.0 ppm) from community drinking water
may be a contributory factor in the precipitation of acute hemoly-
sis in individuals with a glucose-6-phosphate dehydrogenase
(G-6-PD) deficiency. Approximately 13 percent of the American
black male population has a G-6-PD deficiency (Beutler, 1972).
G-6-PD deficient humans were found to be markedly more sensitive to
several indicators of oxidant stress as measured by increases in
raethemoglobin levels and decreases in the activity of red cell
acetylcholinesterase indicating that susceptibility to copper-
induced oxidative stress is associated with the presence of low red
cell G-6-PD activity {Calabrese and Moore, 1979; Calabrese, et al.
1980).
C-44
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A final group that may be subject to risk of copper toxicity
consists of those people occupationally exposed to copper, e.g.,
industrial or farm workers.
In reviewing the medical and biologic effects of environmental
pollutants, the National Academy of Science (1977) pointed out that
use of livers from animals fed high levels of copper in the diet
could produce a baby feed product that was excessively high in cop-
per. The Committee also raised the question of exposure to copper
from intrauterine contraceptive devices (lUDs), but subsequent re-
ports have failed to demonstrate any abnormal accumulation of cop-
per because of the use of these devices.
Basis and Derivation of Criterion
Copper is an essential dietary element for humans and animals.
A level of 2 mg per day will maintain adults in balance (Adelstein,
et al. 1956) and has been considered adequate, although because of
interactions with other dietary constituents that limit absorption
and utilization, a requirement level must be considered in conjunc-
tion with such constituents as zinc, iron, and ascorbic acid. The
minimum level meeting requirements for copper intake in intravenous
feeding is 22 ug copper/kg body weight (Vilter, et al. 1974).
The short biological half-life of copper and the homeostasis
that exists in humans prevents copper from accumulating, even with
dietary intakes considerably in excess of 2 mg per day. In the
opinion of many investigators, there is much more likelihood of a
copper deficiency occurring than of a toxicity developing with cur-
rent dietary and environmental situations.
C-45
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Although acute and chronic levels of intake may occur, there
are no data that adequately define these levels. It has been sug-
gested that intakes above 15 mg of copper per day may produce ob-
servable effects, but if zinc and iron intakes are also increased,
much higher levels may be consumed without adverse reactions. The
data for acute toxicity are even more uncertain, since practically
all human information stems from cases of attempted suicide.
The available literature leads to the conclusion that copper
does not produce teratogenic, mutagenic, or carcinogenic effects.
The limited information available indicates that where such action
has occurred, e.g., with mixtures of copper sulfate and lime, arse-
nic, or enediols, the copper should be considered as interacting
with the other materials and not as the active material.
The current drinking water standard of 1 mg/1 is considered to
be below any minimum hazard level, even for special groups at risk
such as very young children, and therefore it is reasonable that
this level be maintained as a water quality criterion.
Since the current standard and hence the water quality crite-
rion of 1.0 mg/1 are based on organoleptic effects (U.S. HEW, 1970)
and are not toxicological assessments, the consumption of fish and
shellfish is not considered as a route of exposure.
C-46
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