Click here for

DISCLAIMER

Document starts on next page
EPA 

United States EPA 440/5-80-036 

Environmental Protection October 1980 

Agency 

Office of Water 

Regulations and Standards 

Criteria and Standards Division 

Washington DC 20460 

Ambient 

Water Quality 

Criteria for 

Copper 
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 

i 
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. 

ii 
FOREWORD 

Section 304 (a)(1) 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)(1) 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 satisfaction of paragraph 11 of the Settlement Agreement 

in Natural Resources Defense Council, et. al. vs. Train, 8 ERC 2120 

(D.D.C. 1976), 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)(1) 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 effects. 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. 

Guide lines 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 

iii 
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 

Technical Support Services Staff: D.J. 

William B. 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 D. Lutkenhoff, 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 

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. 

Clerical Staff: C.A. Haynes, S.J. Faehr, L.A. Wade, D. Jones, B.J. Bordicks, 

B.J. Quesnell, C. Russom, B. Gardiner. 

iv 
TABLE OF CONTENTS 

Page 

Criteria Summary 

Introduction A-l 

Aquatic Life Toxicology 

Introduction 

Effects 

Acute Toxicity 

Chronic Toxicity 

Plant Effects 

Residues 

Miscellaneous 

Summary 

Criteria 

References 

Mammalian Toxicology and Human Health Effects 

Introduct ion 

Exposure 

Ingestion from Water 

Ingestion from Foods 

Inhalation 

Dermal 

Pharmacokinetics 

Absorption 

Distribution 

Metabolism 

Excretion 

Effects 

Acute, Subacute and Chronic Toxicity 

Synergism and Antagonism 

Teratogenicity 

Mutagenicity 

Carcinogenicity 

Criteria Formulation 

Existing Guidelines and Standards 

Current levels of Exposure 

Special Groups at Risk 

Basis and Derivation of Criterion 

References 

B-1 

B-1 

B-4 

B-4 

B-8 

B-11 

B-11 

B-12 

B-13 

B-15 

B-67 

C-1 

C-1 

C-1 

C-1 

C-6 

C-18 

C-19 

C-20 

C-20 

C-25 

C-28 

C-31 

C-34 

C-34 

C-38 

C-39 

C-39 

C-39 

C-42 

C-42 

C-43 

C-44 

C-45 

C-47 

v 
CRITERIA DOCUMENT 

COPPER 

CRITERIA 

Aquatic Life 

For total recoverable cooper the criterion to protect freshwater aquatic 

life as derived using the Guidelines is 5.4 μg/l as a 24-hour average and 

the concentration (in μg/l) 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/l as CaCO3 the concentration of total recoverable copper 

should not exceed 12, 22, and 43 μg/l at any time. 

For total recoverable copper the criterion to protect saltwater aquatic 

life as derived using the Guidelines is 4.0 μg/l as a 24-hour average and 

the concentration should not exceed 23 μg/l at any time. 

Human Health 

Sufficient data are not available for copper 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 is 1 mg/l. It should be 

recognized that organoleptic data as a basis for establishing a water quality criteria have limitations and have no demonstrated relationship to potential adverse human health effects. 

vi 
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 (Stecher, 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: Cu I (cuprous) and Cu II (cupric). Cuprous 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 presence of excess cupric ion. Cupric ions are also adsorbed by clays, sediments, and organic particulates and form complexes with several inorganic 

and organic compounds (Riemer and Toth, 1969; Stiff, 1971). Due to the complex 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, temperature, alkalinity, and the concentrations of bicarbonate, sulfide, and organic ligands. Based on equilibrium constants, Stumm and Morgan (1970) calculated copper solubility in a carbonate-bearing water. They found that cupric ion (Cu2+) would be the dominant copper species up to pH 6, and from 

pH 6 to 9.3 the aqueous copper carbonate complex (CuCO3 aq) would dominate. 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-1 
Zirino and Yamamoto (1972) developed a model to predict the distribution 

of copper species in seawater. Mixed ligand complexes and organic chelates 

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)2, CuCO3, and Cu2+ 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. CuC03 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 sediments and particulates in freshwater may be released as soluble copper when 

it comes in contact with seawater in estuarine environments. 

Copper is ubiquitous in the rocks and minerals of the earth's crust. In 

nature, copper occurs usually as sulfides and oxides and occasionally as metallic copper. Weathering and solution of these natural copper minerals results in background levels of copper in natural surface waters at concentrations generally well below 20 μg/l. Higher concentrations of copper are usually from anthropogenic sources. These sources include corrosion of brass 

and copper pipe by acidic waters, industrial effluents and fallout, sewage 

treatment plant effluents, and the use of copper compounds as aquatic algicides. Potential industrial copper pollution sources number in the tens of 

thousands in the United States. However, the major industrial sources include the smelting and refining industries, copper wire mills, coal burning 

industries, and iron and steel producing industries. Copper may enter natural waters 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 
The levels of copper able to remain in solution are airectly depenaent 

on water chemistry. Generally, ionic copper is more soluble in low pH, 

acidfc wdters and less soluble in high pH, alkaline raters. 

A-3 
RE FERENCES 

Carrels, R.M. and C.L. Christ. 1965. Solutions, Minerals and Equilibria. 

Har?er and Row, Yew York. 

Riemer, O.N. 3r.d 5.:. Tzth. 1363. A2sstp:ion of copper by clay minerals, 

humic dci d, and bottom vwcis. iuur. Am. kiter Works Assoc. 62: 195. 

Stecher, P.G. (ed.) 1968. The Merck Index. Merck and Co., Inc., Rahway, 

New Jersey, 

Stiff, M.J. 1971. The chemical states of copper In polluted fresh water 

and a scheme of analysis of differentiating them. Water Res. 5: 585. 

Stumn, W. and J.J. Morgan. 1970. Aquatic Chemistry - An Introduction Emphasizing Chemical Equilibria in Natural Waters. John Wiley and Sons, Inc., 

New York. 

Thomas, O.J. and E.V. Grill. 1977. The effect of exchange reactions between Fraser River sediment and seawater on dissolved Cu and Zn concentrations in the Strait of Georgia. Estuarine Coastal Mar. Sci. 5: 421. 

Zirino, A,. and 5. Yamamoto. :9?2. A PH dependent model for the chemical 

speciation of copper, zinc, cadmium, and lead in seawater. Limno. Oceanogr . 17: 661. 

A-4 
Aquatic Life Toxicology* 

INTRODUCTION 

concentrations of copper. Chronic data are available for only one species, 

Acute toxicity tests on cooper have been conducted with 45 freshwater 

species 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 sensitivities from 28 μg/l for the summer flounder to 600 μg/l 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 

but bioconcentration tests have been conducted with a wide variety of 

species. 

ion in free and complex forms, is a minor nutrient for both plants and aniCopper, which occurs in natural waters primarily as the divalent cupric 

mals at low concentrations but is toxic to aquatic life at concentrations 

not too much higher. Concentrations of 1 to 10 μg/l are usually reported 

for unpolluted surface waters in the United States, but concentrations in 

the vicinity of municipal and industrial outfalls, particularly from smelting, refining, or metal plating industries, may be much higher. 

*The reader is referred to the Guidelines for Deriving Water Quality Criteria for the Protection of Aquatic Life and Its Uses in order to better understand 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 toxicity as described in the Guidelines. 

B-1 
The cupric ion 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 complicates the interpretation and application of available toxicity data, because 

the proportion of free cupric ion present is highly variable and is difficult 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 criterion 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 commonly occurring forms not measured by the total recoverable procedure, e.g., 

copper occluded in suspended mineral particulates, are farms 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 total recoverable copper, however, does measure those forms directly toxic to 

aquatic life, e.g., the free ion, and those labile forms (hydroxide, carbonate, and some phosphate precipitates) readily converted to more toxic forms 

under various natural conditions. Since the criteria are derived on the 

B-2 
3asis 3L tests conducted lising solubye inorganic c3Doer ja:tS, tots; Jo,: 

total recoverable cooper concentrations in the tests should be nearly equivalent, and the results are used interchangeably. 

Because a majority of the reported test results (Tables 1 and 2j nave 

been conducted with oligotrophic raters 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 conditions, 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 relationship of toxicfty to other factors, i.e., temperature, alkalinity, size 

of organism, and total organic carbon, are available for a limited number of 

soecies and wfll be dfscussed later. 

The follouing data on the effects of copper on aquatic biota (Tables I 

through 6) have been summarized front the literature from 1950 to 1980. Effqrts to.obtain residue data, or effects data on algae and other plants, 

were not exhaustive, since previous reviews have indicated. that these 

S-3 
effects are of nrinor impot:ance relative to toxicity of copper to fish and 

jnvertebrate species. 

11: concentrations are reoorted as cooper, not as the compound. 

EFFECTS 

&cute Toxicity 

Acute toxicity tests with czpper have been conducted on 18 invertebrate 

and 27 fish species (Table l), 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/l for Oaphnia pulicaria in soft water to 10,200 

;rg/l for bluegills tested in hard water. The majority of tests conducted 

since about 1970 have been flow-through tests with measurements of both 

total and dissolved copper. For comparative purposes, only values expected 

to be equivalent to total recoverable copper were included in the tables. 

?esults of Cairns, et al. (1978) (Table 6) indicate that daphnids are 

more resistant to copper at low temperatures in acute tests. Since such 

data were not available for other species or for longer tests, no generalizations could be made.fot criteria derivation, Chakoumakos, et al. (1979) 

and Howarth and Sprague (1978) (Tables 1 and 6) have reported that larger 

(10 to 30 g) rainbow trout are approximately 2.5 to 3.0 times more resistant 

to copper than juveniles. This factor is obviously a source of variation in 

Table 1. However, insufffcient data are available for other species to 

allow adjustment of *test results or on which to base criteria recomendations. An additional complicating factor is the general lack of knowledge 

of the range of sensitivity of various life stages of most invertebrate species, or the effects on susceptibility, of starvation and other stress factors under natural conditions. 
Lind, et al. (Yanuscrigt) (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 relationships have been demonstrated for only a few species (Daphnia magna, fathead 

minnow, and rainbow trout), the effects shown should be generalizable 

through chemicai effects on cupric ion activity and bioavailability. Lind 

et al. (Yanuscript) 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 

approximate1.y 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/l usually found fn the waters used for toxicity tests. 

An exponential equatfon 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 hardness. Sufficient data were available for Daphnia maqna, 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 regression equations ranged from 0.67 for chinook salmon to 1.34 for Daphnia 

magna with an arlthrnetlc mean of 0.94. The close agreement of the slopes 

and the hig)rly sfgnlffcant (p = 0.01) regressions In each case reflect the 

quality of tht toxicological data available and confirm the premise that the 

effect of hardness on the acute toxicity of copper is simflar for various 

aquatic animals. 

In the absence of the contradictory data, it is assumed that the hardness relationship holds for the acute toxicity of copper t0 all freshwater 

B-5 
aquatic animals. The mean slope (0.94) was fitted throl;gh the geomevic 

rrean toxicity value and hardness for each species to obtain a lcgarithmic 

intercept for each soecies. The species mean intercept, calculated as tne 

exponential of the logarithmic intercept, was used as a measure of rel'ative 

soecies sensitivlty to copper (Table 3). 

Daphnia pulicaria was found to be the most sensitive species. Two other 

daphnid soecies 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 approximately 3 to 11 times more resistant. Bluegi 11s and other centrarchids are 

approximately 10 to 100 times more resistant than salmonids. 

A freshwater Final Acute Intercept of 0.29 ug/l was obtained for copper 

using the species mean acute intercepts listed in Table 3 and the calculation procedures described in the Guidelines. Thus the Final Acute Equation 

is ,(0.94[ln(hardness)]-1.23). 

The saltwater invertebrate data (Table 1) include investigations on 

three phyla: annelids, molluscs, and arthropods (crustaceans). The acute 

sensitivities of crustaceans ranged from 31 pg/l for Acartia tonsa (Sosnowski and Gentile, 1978) to 600 ug/l for shore crab, Carcinus maenus (Connors, 

1972). Adult polychaete worm +cute values ranged from 77 ug/l (Pesch and 

Morgan, 1978) to 480 *g/l (Jones, et al. 1976). Pesch and Morgan (1978) determined that the 96-hour KS0 for Yeanthes arenaceodentata increased from 

77 Ug/l in a flowing water system to 200 Ug/l in the presence of a sandy 

sediment. Jones, et al. (1976) irdicated that Nereis diversicolor exhibited 

a variable response to salinity ever a range of 5 to 34 g/kg with the 

greatest toxicity occurring at 5 gikg. The lowest reported acute value fcr 

the bivalve molluscs was 39 gg/l fzr the soft-shelled clam, +& arenaria 

3-6 
'Eisier, !977), ard the highest was 560 ug/l for the adult ?acific oyster, 

Grassostrea gigas (Okazaki, 1976). Eisler (1977) indicated that the sensitivity of Mya arenaria to coouer varied according to the seasonal tempera- 

'tJ?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 species tested, with an acute value of 31 Ug,'\ for Acartia tonsa (Sosnowski and 

Gentile, 1978), and the least sensitive of ali animals tested, with an acute 

value of 600 ug/l for larvae of the shore crab, Carcinus maenus (Connor, 

1972). Sosnowski, et al. (1979) showed that the sensitivity of field populations of Acartia tonsa to copper was strongly correlated with population 

density and food ration (Table 6), whereas cultured A. tonsa manifested a 

-- 

reproducible toxicalogical response to copper (Table 1) through six generations (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 hfstory stages (Table 1). Acute toxicity ranged from 28 

,,g/l for summer flounder embryos, Paralichthys dentatus (U.S. EPA, 1980) to 

510 Dg/l for the Florida pompano, Trachinotus carol inus (Birdsong and Avavit, 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 apparently are not resistant to copper and because other acute values are not 

available for these specfes. 

Studies err- the effect of salinity on the toxicity of copper indicate 

that it is more toxic to adult pomoano at 10 g/kg than at 30 g/kg (Birdsong 

aod Avavit 1971). Other species of saltwater fish were tested for sensitivity to copper, but the experimental conditions were not suitable for inclu8-7 
sion in either the acute or chronic tables; consequently, these data ;Irere 

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/l was obtained for copper using 

the species mean acute values in Table 3 and the calculation procedures 

described in the Guidelines. 

Chronfc Toxicity 

The data base for chronic toxic'ty of copper to freshwater aquatic animals (Table 2) includes chronic values for four invertebrate and eleven fish 

specfes. Life cycle test results are available for two snails, Daphnia magna 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 catffsh at two hardnesses. The chronic values range from a low of 3.9 ug/l for 

early lffe stage tests wfth 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/l. A series of tests 

wfth Oaphnfa magna in a hard pond water (Table 6) wfth unmeasured copper 

concentrations resulted in chronic values of about 49 ug/l. 

The data available concerning the effect of hardness on the chronic toxicfty of COQQW is somewhat nebulous. The total range of chronic values is 

3.9 to 60.4 ug/l (Table 2). which is much less than the range of 0.23 to 260 

*g/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 

kfnds of tests, but it may also indicate that hardness affects chronic tox8-8 
iCity crf copper differently t?an it affects acute tOXic'ty. Indeed, ii 

chronic tests with Daphnia magna, 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 factors were not expected to ;aqait 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 effect of hardness on chronic toxicity. The slope of 0.26 is not statistically 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 (8rungs, 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 Sam- 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 sens!tive species have ratios above 4. 

Also, the ratio seems to increase with hardness. 

B-9 
The 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 quite a variety of aquatic animals and Dresent a 

good indication of the range of chronic sensitivity to copper. The 

Freshwater final Chronic Value for copper, derived from the species mean 

chronic values llsted in Table 2 using the calculatjon procedures described 

in the Guidelines, is 5.6 ug/l. 

The only chronic value reported (Table 2) for a saltwater species was 

that for the mysid shrimp, Mysidoosis bahia (U.S. EPA, 1980). The chronic 

toxicity of copper to this saltwater invertebrate was determined in a flowthrough life cycle exposure in which the concentrations of copper were 

measured by atomic absorption spectroscopy. Groups of 20 individuals were 

reared in each of ffve copper concentrations (control - 2.9 f 0.5 ug/l, 24.2 

2 7.0 ug/l, 38.5 2 6.3 ug/l, 77.4 f, 7.4 ugll, 140.2 2 11.8 ugll) for 46 days 

at 20'C and 30 g/kg salinjty. The biological responses examined included 

time of appearance of first brood, the number of spawns, mean brood size, 

and growth. The appearance of embryos in the brood sac was delayed for 6 

and 8 days at 77 ug/l and 140 ugil, respectively. The number of spawns recorded at 77 ~g/l was significantly (p < 0.05) fewer than at 38.5 ug/l. The 

number of spawns at 24 and 38 ug/l was not signiffcantly different from the 

control. Brood size was sfgnificantly (p < 0.05) reduced at 77 ugll but not 

at lower=concentratlons, and no effects on growth were detected at any of 

the coopw concentrations. Based upon reproductive data, adverse effects 

were observed at 38 ugll, but not at 77 ug/l, resulting in a chronic value 

of 54. ug/l. Using the acute value of 181 ugll, the acute-chronic ratio for 

this species is 3.4. 

The species mean acute-chronic ratios of 38 and 156 appear to be high 

(Table 3), but the other seven are al! ,dithin a factor af 10. The geometric 

3-10 
mean of :.+ese seven is 5.73. 1' the Saltwater Final acute Val3e 3; 22.3 

ug/7 is divided by the acute-chronic ratio of 5.78, a Saltwater Final 

Chronic 'Value of 4.0 ug/l is obtained, 

Dlant Effects 

Copper has been widely used as an algicide and herbicide for nuisance 

aquatic olants. Although it is known as an inhibitor of photosynthesis and 

plant growth, toxicity data on individual species (Table 4) are not numerous. The relationship of toxicity to water chemistry and the importance of 

the culttire medium on toxicity has only recently been recognized (Gachter, 

et al. 1973). 

Copper concentrations from 1 to 8,000 ug/l 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 values were based on measured concentrations. 

For saltwater algae the concentrations 

cent reduction in photosynthesis or growth 

species of macro-algae and eight species of 

of copper which cause a 50 perare tabulated in Table 4 for one 

micro-algae. The most sensitive 

species were Thalassiosira pseudonana and Scrippsiella faeroense which were 

inhibited by 5 ug/l. 

Residues 

Bioconcentration factors 

2,000 for the alga Chlorella 

(Table 5) ranged from zero for the bluegill to 

regularis. Because copper is a required element for animal nutrition, the significance of copper residues has never 

been established, and few tests have been run for the purpose of determining 

bioconceotration factors. 

3-11 
Cspoer is 3~ essential eiefrent in the respiratory pi;merlts 2i sxe sa::- 

water invertebrates, especially Crustaceans, and plants have enzymes which 

csntain copper and are recessary for ohotosynthesis. However, copper is 

also Sioconcentrated in excess of any known needs by several saltwater soecjes (Table 5). The polychaete worm, Neanthes arenaceodentata, bioconcentrated copper 2,550 times (Pesch and Morgan, 1978), whereas in a series of 

measurements witn algae by Riley and Roth (1571) the highest reported concentration factor was 617 for Heterunastix Longifillis. 

The highest bioconcentration factors for copper are those for the bivalve molluscs. Shuster and Pringle (1969) found that the American oyster 

could concentrate copper 28,200 times after a 140day continuous exposure to 

50 ug/l. 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 instances recorded that oysters have been unmarketable because of their green 

appearance due 

Because no 

freshwater nor 

to high copper content. 

maximum permissible tissue concentration exists, neither a 

a saltwater Final Residue Value can be calculated. 

Miscellaneous 

The results of many additional tests of the effects of copper on freshwater aquatic 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-in Table 6 were conducted in dilution waters which were known to 

contain matvials which would significantly reduce the toxicity of copper. 

These reductfons 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 Pulicar3-12 
ia and fathead minnow in waters with concentrations of T.O.C. ranging up to 

34 mgll. Similarly, Geckler, et al. (1976) and Brungs, et al. (1976) conducted tests with many species in stream water which contained a iarge 

amount of effluent from a sewage treatment plant. Also, Wallen, et al. 

(1957) tested mosquitofish in a turbid pond water. Until chemical measurements which correlate well vrith the toxfcity 0.f 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 &- 

Jopecten irradfens (U.S. EPA, 1980). which suffered mortality and reduced 

growth at concentrations of S and 5.8 ug/l, respectively. Even though 

several studies have been reported on the sublethal effects on survival, 

growth, and reproductfon, 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. 

Sumnary 

Acute toxicity data are available for 45 species of freshwater animals. 

The approximatqly 175 acute values range from 7.2 ug/l for Daphnia pulicaria 

in soft water to 10,200 vg/l for the bluegill in hard water. Statistically 

significant regressions of acute toxicity on water hardness are available 

for seven spccIcs, with toxicity decreasing as hardness increases. Additfonal 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 species could survive in copper concentrations over 100 times that which would 

8-13 
be readily lethal to the more sensitive species. Among the more sensitive 

species are daphnids, scuds, midges, and snails which form the major focdwebs for both narm- 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 fnvertebrate species. 

Chronic values are available for I5 freshwater species, ranging from a 

low of 3.9 ug/l for brook trout to 60.4 ug/l for northern pike. Hardness 

does not appear to affect the chronic toxicity of copper. Fish and invertebrate species seem to be about eoually sensitfve to the chronic toxicity of 

copper. The two most sensitive species, bluntnose minnow and 5. pseudolimnea, are both important food organisms. 

Copper toxicity has been tested on a wide range of plant species, with 

results aoproximatfng those for animals. Complexing effects of the test 

media and a lack of good analytical data make interpretation and aoplication 

of these results dlfffcult. Protection of animal species, hawever, appears 

to offer adequate protection of plants as well, Coooer does not appear to 

bioconcentrate very much in the edible portion of freshwater aouatic soecies. 

The acute toxicity of copper to saltwater animals ranges from 17 ug/l 

for a calonoid cupepod to 600 ugll for the shore crab. A chronic lifecycle 

test has beer? conducted with the mysid' shrimp, and adverse effects were 

observed at 77 ug/1 but not at 38 ~g/l which resulted in an acute-chronic 

ratjo of 3.4. Several saltwater algal species have been tested, and effects 

were obsewcd between 5 and 100 ug/l. Oysters can bioaccumulate copper UP 

to 28,200 times, and become blu'sh-green, apparently without significant 

mortdlity. In long-term exposures, the bay scallop was kflled at 5 ug/?. 

CY?!WIA 

For total recoverable copper the criterion to protect freshwater aauatic 

life as derived using the Guidelines is 5.6 ugll as a 24-hour average, and 

3-14 
the concentration (in Vgll) should not exceed the numerical value given ?y 

e~0~g4~'n~hardness~~~1.23~ at any time. For example, at hardnesses of 50, 

100, and 200 mg/l as CaC03 the concentration of total recoverable copper 

should not exceed 12, 22, and 43 ugll at any time. 

For total recoverable cooper the criterion to protect saltwater aauatic 

life as derived using the Guidelines is 4.0 ug/l as a 24-hour average, and 

the concentration should not exceed 23 pg/l at any time. 

B-15 
Spmcios Method. 

worm, 

Limodriiur hoft~irtwi 

s, u 

Snai i Iadult), 

Amicoia rp. 

s, hi 

Snai I, 

Csrpoim deciur 

Slldli, 

Gyraulus clrcurstrlatus 

s, u 

3n.311, 

Physd lnteyra 

c I adocer an, 

Daphla s 

C IiWtOCW~n, 

Oaphn la maqna 

C iadoceran, 

Daphnla magna 

C Iadocaran, 

Oaphn is magna 

Cladoceran, 

qnphnis magna 

Ciadoceran, 

Daphnla maqna 

FT, M 

s, IJ 

R* u 

s, u 

s, u 

s, tJ 

s, u 

C I atieran, 

Ddphn I a rayna 

s, M 

rabio 1. Acute vaius la- coppu 

tiUclrWS 

bg/l u Lc50~50 

ChriUi C&O,) tJIQ/i 1.8 

FREWATER SPECIES 

Copper 

WI tat4 

Copper 

sul tate 

Wwr 

w I fate 

Copper 

WI tat8 

CopPer 

su I fate 

G=vPchloride 

Copper 

ch iorida 

c0Pl-r 

ch ioride 

Copper 

su I tate 

Wvr 

sui tate 

Qvper 

chloride 

tipper 

y1 i tato 

loo 

54) 

50 

35-55 

100 

100 

35-55 

226 

45.3 

99 

99 

la0 

52 

102 

PO 

900 

1,700 

IO8 

69 

39 

200 

9.8 

65 

30 

12.7 

100 

26 

Nurtr 6 Llridges, 1961 

f-&h*oldt, et al. 19711 

Fbhroldt, et al. 1973 

kthur 1. Leonsd, 1970 

Wurtz 4 Bridges, I961 

wurtr a tifidy3,s, I%61 

CabeJsrek & stosiolt, 

1960 

Ulesingef 6 

Christensen, 1972 

Mema I LLeyoot-Van 

ZIJI, I972 

Adean L byoot-Van 

ZIJI, 1972 

Anderson, I946 

kb-ingaann A Kuhn, 1959 

chapcan, at al. 

Hanuscr I pt 
Tabi. 1. iccet lauui) 

Specla Mean 

i.CW/ECM Acut Value 

(i&J/i I*’ (w/l 1’. 

30 

MetiKlli~ 

s, J4 

s. Jd 

s, M 

R, M 

ChviCal 

Wwr 

chloride 

Species 

C iadocei~n, 

Daphnia magna 

Ciadoceran, 

Daphnia maqno 

Ciadoceran, 

Daphnia w3gna 

C iadocoran, 

Daphnio lrsgna 

Cidocwm, 

Dapbnia puiox 

CiSdDCUSn, 

Dephnla pullcarla 

C I adocuan, 

Daphnia puilcaria 

Cidoceran, 

Daphnis pullcarla 

Ciadoceran, 

Daphnia pullcario 

C iadoceran, 

Daphnia pi icaria 

C iadoceran, 

Daphnia pui lcaria 

C iadocefan, 

Daphnla puilcaria 

Cladocaran, 

Oaphnla pul Icarla 

Scud, 

Carrarus pseudollmaeulr 

Reterence 

Chapmm, et al. 

lbnuscr Ipt 

Chawan, et al. 

kuruscr lpi 

Chapman, et al. 

WMuscript 

Calms, et al. 1978 

hPPN 

ctriorlbe 

I06 

207 69 

cAiorlde 

co9w 

sui fate 

tipper 

uI I fat0 

45 IO 

45 IO alms, et al. 1978 

48 il.4 Llnd, et al. 

Mmuscr ipt 

Lind, et 41. 

Manuscript 

L:nd, et al. 

Honuscr I pt 

Lind. et al. 

kmuscr lp? 

llnd, et al. 

Uanuscr I pt 

Llrld, et a\. 

kmuscr Ipt 

Llnd, et al. 

Wanuscr I pt 

I IlId, ot aI. 

Wanuscr I pt 

9.06 

R, M 

R, M 

R, M 

R, M 

R, M 

R,.M 

18 7.24 

44 IO.8 

45 9.3 

95 17.8 - 

I45 23.7 

245 27.3 

f-r, n @rwr 

sul fate 

35-55 20 

B-L? 
Tsblo 1. uhntIau84) 

specIss 

SCUd, 

Gamerus sp. 

Crayflsh, 

Orconectes rustlcur 

SiOflef If, 

Acrctneurls Iycwlss 

Oi¶Wt3lfly, 

lJnldantlfled 

Caddlsf ly, 

Unldentltled 

HotIter, 

Phi lodlna acut lcornls 

RotIt=, 

Phl lodlna acutlcornls 

AmerlCM eel, 

Angullla rostrata 

American eel, 

Angul I la rostrats 

Cub salr*n (adult), 

Oncmhynchus k I sutch 

c&o salron lycwllng), 

Oncorhynchus hlrutch 

coho 56lmcm (ywrllngl, 

Oncorhynchus klsutch 

Method’ 

s, M 

s, M 

S, M 

R, U 

R, U 

S, M 

FT, M 

5. n 

s. M 

Cherlcal 

CoPPer 

su I fate 

Ww 

su I fate 

f%vr 

sul tate 

wwr 

chloride 

CoPPer 

ch lor I de 

Copper 

Ch lorIde 

loo- I25 

40 

50 

50 

SO 

40 

25 

81 

53 

55 

xl 

89-99 

89-99 

3,ooo 

0,31yJ 

4,600 

30 

6,200 

I60 

700 

I, loo 

6,400 

6,‘300 

46 

74 

70 

tlubsctlludn, I967 

Wlrnlck 4 Bel I, I969 

Huhuoldt, et al. I973 

Retrroldt, et al. 1973 

Elulkemd, or al. I977 

tlutkena, et al. 1974 

tluIkemd, et at. I974 

Rehrol(jt, tit dl. I971 

Rehroldt, tit al. 1972 

Chdpman 4 Steven5, 

I978 

Lorz 4 WcPhersoc1, I976 

Lor z a W&hwson, 1976 
Table I. (comtlwadl 

tbr&as 

tdlu 

spoclmsmeam 

u34vEc50 hart* Value 

hu/l)‘~ 

60 

zi 

19 

38 

IO 

22 

85 

IXI 

x7 

Spwlos C&X) 

89-99 

Rotumcs 

Coho saimon (seolt), Laz 4 McPherson, 1976 

Oncorhynchus klsutch 

Chlnook SUI~XI (elovln), 

Oncorhynchus tshmViscM 

Chlnoak salmon (swlrrup), 

Oncorhynchus tshmytscho 

ChInook salon (parr), 

Oncarhnychus tshwytscha 

Chlnook salmm (smelt), 

Oncorhynchus tshwytscha 

Chlnook salmm, 

Oncorhynchus tshauytscha 

Chlnook sa bon, 

Oncorhynchus tshawytscha 

Chlnook zdlmon, 

Oncorhynchus tshawytscha 

Chlnook salmon, 

ticarhynchus tsharytscha 

Cutthroat trout, 

Salao clarkl 

-- 

Cutthroat trout, 

Salao clarkl 

-- 

Cut throat trout, 

Salno clarkl 

-- 

Cut thraat trout, 

Sala clarkl 

-- 

Cutthroat trout, 

Salvo clarkl 

-- 

25 Chap-, 1978 

25 Chapran, 1978 

25 xhdpman, 1978 

25 abapman, 1978 

I3 Chapman 4 MaCrady, 

i977 

Chapman h Wrcldy, 

i977 

Chapman A tirady, 

i977 

46 

I82 

Chapran 6 Wrady, 

1977 

chdkouMk6s, tit al. 

1979 

Chakouraakos. et al. 

1979 

.ZL 

Wper 

chloride 

CQpper 

chlorlda 

Ww 

chloride 

FI, M 186 

I8 xi.8 ChakcMlmdkc6, et el. 

1979 

ChakourdtG5. et di. 

1979 

204 232 

83 162 Cbkourdws, et dl. 

1979 

B-19 
lablm I. Kclntlaued) 

Hsrdnur 

hlglr u 

Cdx,) 

31 

SPecler Dl+a 

LC50m Acut0 Valu 

(Pa/l )‘a fPg/l)‘~ 

73.6 

Mathod* 

FT, M 

Cherlcal Re f wence 

Ct~kouwkos, et al. 

IYIY 

C.lokouwkos, ot dl . 

1379 

Chakowdko5, et al. 

I’)79 

SPecIes 

Cutthroat trout, 

Salvo clarkl 

-- 

Cutthrmt trout, 

Salmo clerk1 

-- 

Cutthroat trout, 

Sala clsrkl 

-- 

Cutthroat trout, 

Sala clarkl 

.-- 

Ra I ntau trout. 

Salu, galrdnerl 

Ha I nba* trout, 

Salmo galrdnerl 

Hdtnti trout, 

Sslmo qdtrdncrrt 

Rd I nbo* trout, 

SdlW CJdIrdnw 1 

Rdlnbow trout, 

Salmo gslrdnerl 

Ha I nbou trout, 

Salw gulrdnerl 

Ra I nban trout, 

Salmo galrdnerl 

Ra I nbam trout, 

Salmo gelrdnerl 

Ralnbou trout, 

Salmo galrdner I 

Ralnba trout, 

Salmo galrdnerl 

Wwer 

chloride 

Copw 

ChlOrlde 

CQPPer 

drlorlde 

Wwr 

dblorlde 

FT, M I60 

74 

91 

FT, M 44.4 

FT, M 

FT. M 

FT, M 

FT, W 

13.7 Cnakourakm, et dt. 

IV19 

CopPer 

su I fate 

30 19.9 

22.4 

tiwar-th b Sprague, 

1378 

Wv*r 

5u I fat8 

32 bdrth 4 Sprague, 

I’)ltl 

%wr 

bul fate 

Capper 

su I fate 

31 28.9 tkwdri h 6 Sprague, 

I978 

FT, M 31 ttrarth A Sprague, 

1978 

Copper 

su I fdte 

30 Wwarth h Sprague, 

197&i 

tT, M hPP8f 176 

su I fate 

Wwr 

sultate 

Wwr 

sulfate 

IO1 tioudrih & Sprayue, 

1978 

il, n 40 tiuwdr.th A Sprdgu8, 

1918 

FT, M 99 33.1 tkmarlh 6 Sprdyw, 

I978 

tl, M 30.1 

t-T, W 

Copper 

sulfate 

Qwper 

sulfate 

102 

IO1 

tkwdrth A Sprdguo, 

1970 

46.3 tkudr-th 6 Sprdgue, 

l97tJ 

9-20 
Table I, EantIwoll) 

Specl~s 

Ralnbmf trout, 

Salao galrdnerl 

Ra I nbom trout, 

Sa Im 9alrQnwl 

Ra I nbar trout, 

Salm galrdnul 

Rnlnb0m trout, 

Salm galrdnsrl 

Ralnbcu trout, 

Salm galrdnul 

Ralnbw trout, 

Salm gslrdnerl 

Ralnbw trout, 

Sd lm gd 1 r doer I 

Halntu trout, 

Salu qalrdn8rl 

Ra 1 nbu trout, 

Lalm galrdnerl 

RaInbow trout, 

Salm qalrdnerl 

Ralnbcu trout, 

Salm galrdnerl 

Ralnbcu trout, 

Salm galrdnerl 

Ralnba trout, 

Salm galrdnerl 

Ra I nbar trout, 

Salm galrdnerl 

Chadcal 

Wper 

Y I fate 

CoPper 

w I fate 

CopPer 

su I fate 

QPPW 

sulfate 

Copw544 Ifate 

Copper 

sulfate 

bPP@r 

SUItat 

Copper 

chloride 

Copper 

&llorldI3 

Copper 

chloride 

CoPPer 

CiIlorlde 

Hardfmsr 

@l/l as 

C8&) 

99 

loo 

loo 

90 

370 

3.6 

371 

3661 298 

194 169 

194 85.3 

I94 83.3 

I94 

194 274 

194 

48.1 

tit.1 

85.9 

232 

70 

82.2 

103 

I28 

Spocla Weon 

Acat* Valu 

ROf YWI 

Houarth 4 Sprague, 

1978 

bdfth i Sprague, 

I970 

tiwarth A Sprague, 

197l3 

IClwarth & Sprague, 

1978 

Harorth 4. Sprague, 

1978 

kmarth A Sprague, 

I978 

tkmarth 6 Sprague, 

1970 

tkwarth 6 Sprague, 

1978 

Chakowkos, et al. 

1979 

ChakOllMkos, et al. 

1979 

Chakooaakcs, et dt . 

1979 

Chakaurakos, at al. 

1979 

CbkOumkOS, Lit dt . 

1979 

Chakouankos, et al. 

1979 

B-Zi 
Table I. UhdlWOd) 

Sp0CI.S 

Ralntlal trout, 

salm galrdnul 

Ralnbcu trout, 

Salm Qalrdnorl 

Ra I nbau trout, 

Salm galrdnerl 

Ralnbo* traut, 

Selm galrdnwl 

Ralnbcv trout, 

Sslm galrdntwl 

Ralnhn trout (alevln)~, 

Salmo galrdnerl 

Ralnbou trout (sulrup), 

Salro galrdnerl 

RaInbow trout (parr), 

Sola galrdnorl 

Halnbon trout (molt), 

Solr, galrdnerl 

RaInbow lruut (adult), 

Sala galrdnerl 

Ralnboa trout, 

Salm galrdneri 

Aalnbou trout, 

Sale galrdnerl 

Ralnbcw trout, 

Salma galrdnerl 

Ralnbw trout, 

Salm gdlrdnerl 

MethlxP 

FT. W 

FT, n 

FT, n 

FT, II 

f-f, M 

tl, M 

t4udnoss 

a!$- 

194 221 

I94 165 

194 197 

194 514 

194 243 

25 

25 

25 

25 

42 

350 

I25 

125 

I25 

28 

17 

18 

29 

57 

I02 

200 

IW 

210 

R.1 Y@#BcI 

Chak~kos, st al. 

1979 

Ch&omakas, et al. 

1979 

Chakowlakos, et al. 

1979 

~hakoumekos, et al. 

1979 

Chdtoumakos, et al. 

1979 

Chspan, 1970 

Chapman, 1978 

chapran, 1978 

Chapman, 1978 

Chapman I Stuvons, 

1978 

Fogels a Spr.+yue, 1911 

spear, 1971 

Sped, 1977 

Spew, 1977 

9-22 
Table 1. Koatlnud) 

SpOClOS 

Ralntxm irout, 

Sala galrdnerl 

At lant Ic sa Illon, 

Salao salar 

-- 

At lant Ic we lm, 

Salm salar 

-- 

Atfantlc Sal-, 

Sala salsr 

-- 

Brook trout, 

SalvelInus fontlnafls 

Stoner01 ler, 

Caqnntora an- lur 

Goldflsh, 

Carasslus suratus 

Goldflsh, 

Carasslus auratus 

Carp. 

Cyprlnus carplo 

Carp. 

Cyprlnus carplo 

LongfIn &ce, 

AQOS la chry sogast-r 

Strlped shiner. 

Notrapls chrysocephalus 

Strlped shInor, 

Notrdpls drry+ocephalus 

bluntnose rlnnou, 

Plwphafes notatus 

%wsulfate 

Copper 

sulfate 

COPPer 

sul fate 

CoPper 

a.11 fate 

QVPnl trata 

Wvr 

su 1 tate 

Ww 

w I tat0 

Copper 

su I fate 

tkudness 

(&I as 

!z?!aL 

290 

20 

e-10 

I4 

200 290 Gwkler, et al. 197b 

20 

52 

53 

55 

LC5O/ECSJ 

bls/l)~~ 

890 

48 

125 

32 

100 

36 

300 

810 

000 

fJ60 

7po 

Speck Mean 

Aalto volw 

(m/l I- R0fWUM.X 

Calwiarl 6 Marchettl, 

1973 

Sprague, I W4 

Yllson. 1972 

Sprague 6 Ramsey, I%3 

McKlr I fienolt, I971 

Plcheflng & HBndersw, 

I%6 

Tsal 6 McKee, 1980 

Rehwoldt, et al. 1971 

Rchroldt, et al. 1972 

Leuls, 1978 

Geckler, et al. 1976 

Geckler, et al. 1976 

Geckler, et al. 1976 

B-23 
Tabfo 1. Kant Iwed) 

Species 

bluntnose mlnncu, 

P lmepha les notatur 

Bluntnose minnow, 

Plmephales notatus 

Bluntnose mlnnau, 

Plmephales notatus 

fl I untnose m Innou, 

Plaephales notatus 

Bluntnose l lnnou, 

Plmnphafes notatus 

Uluntnose mlnnou, 

Plmaphales notatus 

b I untnosu l lnncu, 

Plwphales notstus 

f afhadd alnnou, 

Plmephales promelas 

Fathead l lnnou, 

Plmephales prcnelas 

Fathead olnnow. 

PImphalos prwelas 

Fathead mlnaou. 

Plmephales prmlas 

Fathead l lnnou, 

Plmephales prowl45 

Fathead l lnnou, 

Ploephales prmelas 

Fathead l lnna, 

Plmephales promnlas 

ChOdclrl 

Wvr 

sulfate 

Wper 

suf fate 

Copper 

su I fate 

Copper 

su I fate 

Copper 

su I fate 

Copper 

Su I fate 

Cwpefsu I fate 

54 iate 

copper 

su I fate 

Wwr 

5u I fate 

CoPper 

sul fate 

f%per 

su I fate 

HUdmS 

k!!&- 

200 

200 

a00 

200 

194 

194 

194 

202 

M2 

200 

45 

X0 

20 

200 

260 Geckler. ut al. 1976 

200 Heckler. et al. 1974 

340 

210 

220 

270 

460 

490 

790 

200 

1,450 (2)“. 

23 f4).*’ 

430 

- 

Retuonce 

Gecklor, et al. 1976 

Gecklur, et dl. I976 

ttornlng d Nelhn 

1979 

Isel, 

llornlng 6 Nelhn llbrtl, 

1979 

Hurnlng & t&lhelsel, 

1979 

Plckerlng, et al. 1917 

Plckerlng, et al. 1977 

Andrew, 1976 

Andre*, I976 

Plckerlng A Mndorson, 

1966 

Plckerlng 4 Rendarson, 

I%6 

b&Int, 1966 

B-24 
Tobla I. KwtImu4d) 

SpeclOS 

fatha+d rlnncn, 

PImeph8les prcmelas 

F atheaa ~lnnoa, 

Plmeplmles pr”l+s 

fathead l lnncu, 

PImphalos prcnelar 

Fathead l fnncq 

Plmeph4les promelas 

Fathead l lnna, 

Plaephales pr-las 

fathead l lnaow, 

Plmephales promalas 

Fathead rlnnow, 

Plm@4les prowalas 

fathead minnow, 

Pleeph4les prorelas 

Blacknose date. 

Rhlnlchthya atratuluS 

Creek chub, 

Seaotllus 4trcwaculatus 

Brown hrl Ihesd, 

lctalurus nobulosus 

Bran bul Ihrad, 

lctalurus nebulosus 

Banded kllllflsh, 

fundulus dlaphsnus 

banded k I I I If Ish, 

Fundulus dlaphanus 

ctmm1cu1 

CaQwr 

sulfate 

Copper 

sulfate 

Wper 

su I tote 

CoPper 

su I fate 

c0pP.r 

sulfate 

UUCIWSS 

( IU 

c%, ) 

200 

31 

31 

200 

200 

40 

45 

46 

Copper 

su I fate 

CQPper 

sulfate 

Copper 

sulfate 

CoPPer 

su I fate 

Copper 

nl trate 

200 

202 

200 

53 

55 

ZsO 

470 

Ii4 

75 

440 

490 

I 14 

121 

08.5 

320 

310 

spoclu MEan 

Acut Valw 

I80 (2)*‘* 

540 

860 

wit 

Refernce 

Mount 6 Stephan, I%9 

Mount b stsphan, I%9 

Mount & Stephan, I%9 

Geckler, et al. 1976 

Geckler. et al. I916 

llnd, et al. 

Manuscr I pi 

Llnd, et al. 

Manuscr I pt 

Llnd, et al. 

Manuscr I pt 

Geckler, et al. I976 

Geckler, at al. 1976 

Brungs, et al. 1975 

Geckler, at al. 1976 

Rehwoldt. et al. 1971 

Rehwoldt, et al. IYR 

B-25 
labI* 1. mantIrwl) 

spec1rs 

f lagflsh, 

.lofdaneI la f Icvldae 

W=PY, 

Pueclll4 retlculata 

GUPPY, 

r0diia retlculata 

GUPPY, 

Poocllla rotlculata 

Yhlto perch, 

Morone amrlcanus 

Yh I te parch, 

MU onrc OIldc lcanus 

-- 

511 lyad tuss, 

k4ono saxatllls 

Strlped bass, 

-one saxatllls 

Sfrlped fass, 

Worow saxat I I Is 

Strlped bass flsrva), 

Morone ssxst 1 I Is 

Strlped bass f larva), 

Mwcme saxat I Is 

Strlped bass fflngerllng), 

)(aonla saxat Ifs 

Ralnbcu darter, 

Etheostm caeruleum 

Ordngethroat darter, 

ftheostm spectsblle 

s. M 

S, JJ 

s. u 

s, u 

s. u 

s, u 

cbomlcal 

coppsul fata 

Qwper 

nl trste 

Copper 

nl trste 

Copper 

su I fate 

Wwer 

su I fate 

Copper 

su I fate 

llU&US 

(q/las 

se%L 

350-375 

20 

87.5 

67.2 

53 

55 

53 

55 

35 

68.4 

68.4 

68.4 

SpeclwnMn 

Aane V@hm 

h/l)- Rd Y0aco 

FogsIs A Sprague. 1977 

36 PIckwIng 1 thnderson, 

I%6 

112 Chynoueth, et al. 1976 

138 Chynoueth, et al. 1976 

6,200 Rehroldt, ot 41. 1911 

6,400 

4,3@ 

4.000 

620 Yol Iham. I%9 

50 Hugl~s, 1973 

100 lkIghes. 1971 

150 liughes, 1971 

3m Heckler, et al. l97b 

850 Gackler, ot al. 19/b 

Rehwoldt, et al. 1972 

Rehroldt, et 41. 1971 

fkhroldt, et al. l9?2 

3-26 
Tsbia 1. mmt iawd) 

LCMIECSO 

l&I 1.’ 

2,400 

2,700 

1,240 

I,= 

Sp8ci.s 

PUrpkin~ed, 

L+omi s g I bbsus 

Pwpk inseed, 

le@mis gibtxms 

Plqk inseed, 

i.oixmis gibiWur 

Puqkinswd, 

L-is gibbosus 

Puqkinsesd, 

Lapais gibhosus 

Purpk I nreod, 

Lefmais gibbosus 

PurQk inseed, 

Lepomis gibtMAsus 

Puapk inseed, 

Lepmis gibbosus 

Pumpk inseed. 

lepamis 9ibhosus 

Blwgiii, 

Cepomi s mcrochirus 

EiiU~iii, 

Lspomis macrochirus 

Biwgiii, 

le~omis aacmchirus 

BlUegill, 

Lepais wcrochirus 

fiiwgii I, 

~epoais macrochirus 

ChricSi 

CoPPer 

nitrate 

Henwoidt, et ai. 1972 

Wpsr 

&I I fate 

CQPper 

su I tate 

bpprr 

su I fate 

Wvr 

su I fate 

Cw-- 

su I fate 

Wvr 

sul fate 

WPW 

8411 fate 

Copw 

su I fate 

125 Spear, 1971 

I25 spear. 1977 

125 1,670 Spear, 1977 

125 I.940 

125 1,240 

125 

I25 

45 

1.w 

1,740 

1,100 

a.- 

10,900 

spear, 1977 

spear, 1977 

5pear, 1977 

3pear, 1977 

Benoit, 1915 

CoPper 

su I fete 

Wper 

chloride 

copper 

su I fate 

Geckier, et al. 1976 

Geckier, st al. 1976 

1,250 

660 

Patrick, et al. 1968 

20 Pickering I tkmderson, 

I%6 

B-27 
labi. 1. ckmtIwui) 

Biwgi I I, 

Lepomir wcrochirus 

Biwgii I, 

leponis acrochirur 

Largmnouth tars, 

Microptams salmolder 

Poi ychaete uorm, 

Neanthes srenaceodentata 

Polychaete worm, 

Neanthes aronaceodentats 

Pol ychaete worm, 

Nereis diversicolor 

Pol ychaete wora, 

Nereis diversicoior 

Poiycheeto voca, 

He-is divarsicoior 

Poi ychaete mm, 

kareis dlverrlcoior 

Pol ychaets wa, 

Phyi la&co macuiata 

Pacific oyster, 

Crassoslrea gigas 

Awri can oyster, 

Crassostrea virginica 

black &lone, 

tbllotls cracharodll 

Mmaod’ 

s, u 

FT, W 

FT, M 

fl, M 

5, u 

s, u 

5. u 

s* u 

s. u 

5, ” 

s, u 

Copper 

ni trots 

copper 

ni trato 

coppw 

at I fate 

Copper 

SuItsto 

CoPper 

rullate 

Ww 

su I fate 

Copper 

w I fate 

tipper 

chloride 

~iwr 

su I fate 

HuheM spoclrb8m 

( IW 

c%. J g$F 23” ( R*tuwca 

360 10,200 Pickering I tbnQrsoe, 

1966 

35 2,400 O’htra, 1971 

IO0 6,9’Eo Bir’ge 1 Black, 1919 

SALTWATER SPECIES 

77 

200 

200 

445 

480 

410 

120 

560 

I28 

30 

63 

I24 

364 

I20 

560 

I28 

50 

Pesch A Cbrgan, 1978 

Pesth & Wocgan, 1978 

Jonti, et si. 1976 

Jones, et al. 1916 

Jones, et al. 1976 

Jwgi, et al. 1916 

KLusky & Phliilps, 

1975 

(Irazaki, 1976 

Calabrese, et al. 1913 

Martin, et al. 1971 

HartIn, et dl. IYll 

B-28 
Tablr 1. 1Gmt Inuedd) 

ifWdWSS 

bg/lu Li3fvEc50 

Caco~l (us/l 1” 

I I4 

Species Wean 

krta Valw 

(~Q,/i~” 

86 

Mdhod~ 

s, u 

5, u 

5, u 

s, u 

% u 

s, u 

s, u 

species 

Red abalone (IarvaJ, 

Hallotis rulescens 

Soft shelled cl-, 

& areaaria 

Calanoid copepod, 

Acwtia ciausi 

-- 

Calanoid copepod, 

Acartia tonsa 

-- 

Caian0ld copepod. 

Acart la tonsa 

-- 

CalMbold copepod, 

Acartia tonaa 

-- 

Cwmod, 

Luryttmora dffinis 

COpeP~, 

Psovdodlaptcws corooatus 

Copepod l 

Tlyriopus Japonicus 

Mysid shriq~, 

Wysidopsis bahia 

Mysid shrimp, 

Hysidopsls bigelwi 

American lobster f iafva), 

Homarus aaer icanus 

fmericau lobster (adult), 

Humiwus americanus 

Urorn sbrtrl, (larva), 

Crangon crsngorr 

ChwiCai Ret wence 

CoPper Martin, et al. 1977 

su I fate 

Cwper 

chloride 

hwr 

chloride 

59 

52 

I7 

55 

31 

526 

I58 

39 Cisler, 1971 

52 U.S. EPA, 19&l 

Copper 

ch lor I de 

%-wr 

ch lorlde 

Scsnowskl 4 Gentlla, 

i9!8 

So:,nouski 6 Cent I la, 

l9?8 

51 So2nousk I 6 (;ent L Iu, 

19tt.J 

Wwr 526 u. -A. EPA, 19LUI 

chloride 

s, u 

s. u 

t1, M 

.tT, f4 

s, u 

s, u 

s, u 

Cwper 

Chioricb 

@pm 

chloride 

Copper 

nitrate 

Qvw-r 

ni irate 

Ww 

nitrate 

%wr 

su I fate 

tipper 

w I fate 

I38 U.j. EPA, l9w1 

481 487 U.S. CPA, 1960 

I81 181 U.S. Lt’A, TYtKI 

I41 141 U.S. WA, 1980 

48 Johnson d CentlIe, 

1979 

100 

330 

69 NcLetr5tl, I914 

350 Connor, I912 

B-29 
T4bio I. lcodi~~ 

speciw 

Shore crab I larva), 

Carcinus menus 

fiorida pqm.no, 

Trachinotus caroiiaus 

Fiwida -0, 

lrachieotus caroiinus 

Florida -no, 

Trachinotus caroiinus 

Atiant ic si ivwsida 

1 larva), 

Menidia wnidia 

-- 

Surer t lounder ferbcyo), 

Para I l chthys dent&us 

Ylnter llounder (odryo). 

P’srudop ieuronectes 

aver icanus 

Mmthod. cbamicai 

s, u 

3z* 

s, u WIsui fat. 

s. u COPPWI fate 

copper 

su I fate 

%-v-r 

nitrate 

Copper 

chloride 

Copper 

ni trato 

IfUdRWS 

(m&urn 

fXXJ,J lbg/iJe’ 

600 600 

360 

380 

510 412 

I36 17Jkfi’ I36 

28 131*** 28 

129 f9J*** 129 

Aafwwa 

connor, 19n 

Ulrdsong s, Avavit, 

I971 

8irdsaq I Avsvlt, 

1971 

Ulrdsong I Avavlt, 

I971 

U.S. EPA, l9Mt 

U.S. WA, 1980 

U.S. tPA, l9MU 

” s= static, R = t la-through, R - reneuai, U = unneasured, M - lleasured 

.* Results LUO expressed as copper, not as tha co+xmd. 

“akArith4tic w of (NJ rosuits. 

Frashrater; 

kute toxicity vb. hardness 

Ciadoceran, Daphnia mqna: slope = 1.34, intercept = -2.64, r - 0.80, p = 0.01, N = IO 

Ciadoceran, Uaphnia put Icarla: slope - 0.70, intercept - 4.40, r = 0.94, p = 0.01, N = 8 

Chinook salmon, Uncwhynchus tsharytscha: slop a 0.67, intercept = 0.93, r - 0.93, p = 0.01, N = 8 

Cutthrmt trout, Salao clarkl: -_I_ slope = 0.88, Intercept = 0.79, r = 0.78, p = C.01. N a 9 

B-20 
RaInbat trou$, tilr, galrdnerli shpe - 0.87, Intercept - 0.33, r = 0.78, p - 0.01, N - 39 

fath3ad l lnlyI*, Plmphales prmolas: sbpe * 1.12. lntercapt - O.)e, r = O.%, p = 0.01, N = 15 

Filuegl Il. LefK.dr rscrochIl-us: slope = 1.00, Intercept - 3.40, r = 0.95, p - 0.01, N - 7 

AfltImotlc Dem sutm slop. * 0.94 

B-31 
5pUI.S 

Snal I, 

c8apf3lour declslm 

Snal I, 

Physa lntegra 

C I a-an, 

Daphnla magna 

Cladoceran, 

Odphnla raqna 

Cl4&K4rdn, 

Daphn la mqnrl 

Scud, 

Gdlmdr-us pQwdol lrnaeus -- 

Halnbw trout, 

5s Imo qa lrdner I 

l3roun h-out, 

Sdlmo trutta 

-- 

Isrook trout, 

Salvellnus tontlnalls 

crook trout, 

Salve1 lnus fontlnal Is 

Brook trout, 

SalvelInus fontlnalls 

Urcwk trout, 

SalvelInus tontlnalls 

Lake trout, 

S~~lval lnus ntiycush 

T-t’ 

LC 

Lc 

Lc 

LC 

LC 

LC 

ELS 

ELS 

LC 

ELS 

tLS 

LLS 

CLS 

Chadcal 

CopQer 

w I fate 

&PW 

ch IwIde 

hw-- 

chloride 

Wwer 

chloride 

CoPper 

5u I fate 

Wper 

5ul tat4 

Cwper 

SkII tste 

CoPper 

w I tate 

Copper 

5u I fait4 

Qvper 

514 Ifate 

copper 

w I fate 

FIUWATLH SPECItS 

45 

45 

51 

I04 

211 

45 

45.4 

45.4 

45 

45.4 

37.5 

187 

45.4 

8-14.8 10.9 

8-14.8 IO-9 

11.4-16.3 13.6 

20-43 29.0 

7.2-12.6 9.5 

4.6-8 6. I 

11.4-31.7 I9 

Arthur h Leonard, 

I970 

Arthur h Leonard, 

1970 

ctmpran, et al. 

Mmuscr Ipt 

chapmm, et 01. 

Hanuscr I yt 

Chapran, et al. 

Mdnuscr Ipt 

Arthur 4 Leoncud, 

IY70 

McKlm, et al. 1976 

22.0-43.2 xl.0 McKlm, et al. 1978 

9.5-17.4 12.9 WcKlr & Uenolt, 1971 

22.3-43.5 31. I McKlm, et al. IYM 

3-5 3.9 Sauter, et al. 1YIb 

5-8 6.3 Saute, et dl. 1916 

22.0-42.3 30.5 MLKlm, et al. 1978 

Chrmlc V.lw 

Cm/l 14. ftofwanco 

9-32 
Iable 2. 4coatIumd~ 

Species 

Rorthern pike, 

Esox luclus 

-- 

B luntnose l lnncu, 

PImphales notatus 

Fathead mlnnom, 

Plaeplmlu promlu 

Fathead l lnncm, 

~hOQtUbh6 WOrtAO 

Fathead l lnnou, 

PInphale5 prcnelas 

Fathead rlnncu, 

Plaephaies promlas 

Yhlle suchef, 

Catostaus C’Suel 

Channel catf Ish, 

lctalwus puactatus 

Chanhel atf Ish, 

IctalWbls punctatus 

BluegIll, 

Lefmmls macrochlrur 

Hal leye, 

Stlzostedlon vltreua 

TasP 

ELS 

Lc 

u 

Lc 

lc 

ElS 

ELS 

ELS 

ELS 

LC 

ElS 

Chemlcsl 

copw 

sulfate 

CoPper 

ullfate 

copprr 

WI tat4 

COPF 

5u I fat0 

c0pp.c 

sul fat. 

Copper 

su I fate 

coQp-- 

sul tat0 

CePpv 

5ul fate 

nBr&mss 

(m&l m 

CdBq) 

45.4 

I91 

I98 

30 

200 

45 

45.4 

36 

I86 

45 

35 

SALTWATER SPECIES 

Mysld shriw, 

Mysldi~psls lmhla 

LC Copw 

nl trate 

54 

LIDIts 

(Irg/l* 

34.9- 104.4 

clwoalc V~luo 

(QQjl)- 

60.4 

4.3-M 8.8 

14.5-33 21.9 

IO.6 18.4 14.0 

24-32 27.1 

13. t-26.2 

12.9-33.8 

12-M 

u-19 

2140 

13-21 

38-J7 

18.5 

20.9 

II. 1 Sauter, et al. 1976 

15.7 Sauter, et al. 1916 

29.0 

16.5 Sauter. et al. 1976 

54 

Reterence 

McKin~, et al. 1978 

Horning I Nelheisei, 

1979 

Mount, 1960 

Mount 4 Stephbn, 1909 

f’lckerlng, et al. 

1977 

Lind, et al. 

M4muscr Ipt 

FkKlr, et al. 1978 

BermIt. 1975 

U.S. EPA, 1980 

l LC = tlfe cycle or partial llte cycle; ELS - early life stage 

l Hesui ts we expressed a5 copper, not 05 the oolpcund. 

B-33 
Tablo 2. GMtInuul) 

w 

Snal I, 

~lcmo declsw 

Small, 

PhVu Intwa 

cladocuan, 

Oaphnla rgM 

Cledocoran, 

Oaphnle mgna 

C I sdocrran, 

Daphnla magna 

Scud, 

Gaw8ru5 pseudol Inaous 

Brook trout, 

SalvelInus focrtlnalls 

8 I untnoso l lnna, 

Plmphalos fbotatus 

Fathead rlnacw, 

PlmQha1.S prarrlas 

Fatlmad rlnnor, 

elnphalos promoIas 

Fathead olnnou, 

PIurhales pcalas 

fdlmad mlnmou, 

PlPphnI.8 pramlss 

t3lu+Jlll, 

Lepomls mcrochlrus 

Wysld shrlq, 

f4Vsldopsis bahla 

AcuteChronIc Rat lo6 

iiardnoas 

(q/i - kutr Value 

Cd;ol) QbQ/I) 

45 I,Mo 

45 39 

57 ifI 

I04 34 

211 69 

45 20 

45 100 

I94 233 

I98 430 

30 75 

200 415 

45 lo6 

45 1,100 

I61 

Chrallc Value 

fpQ/l) 

10.9 

Rat lo 

156 

IO. 9 3.6 

13.6 I.9 

29.0 1.2 

9.5 I.3 

&I 3.3 

12.9 1.0 

8.8 26 

21.9 

14.0 

21.1 

18.5 

29.0 

54 

20 

5.4 

I7 

5.8 

36 

3.4 

--- - 

B-34 
labI* 2. &ontlamd) 

Rmk* 

I5 

I4 

13 

12 

II 

IO 

9 

8 

7 

6 

5 

4 

3 

Freshwater Species Mean Chronic Valuqs 

SQOCll3S 

W-them pl ko, 

Esox luclus 

-- 

Speck WBsn 

Chonlc Valus 

(w/l, 

60.4 

tkwn trout, 

klmo trutta 

-- 

Lske trout 

klvellnus naaaycush 

30.8 

30.5 

Blurglll, 

Lappals mcrochlrus 

Whl to sucker, 

Catostaws C’SM I 

29.0 

20.9 

Fathead alnncw, 

Plrepbles proretas 

19.9 

Fblnbom trout, 

Salvo galrdnerl 

19.0 

Yal Iaye, 

Stlzostedlm vltreu 

16.5 

clsdocwan, 

Oaphnla magna 

15.5 

Channel catt I ah, 

Ictalurus punctatus 

15.2 

ball, 

Physa lntegra 

Snail, 

Carpelm declsur 

10.9 

IO.9 

k3ok trout, 

Saiveilnus fmtlnal Is 

10.0 

9-35 
Tablo 2. mlatIund) 

R&l&. SpbCl9S 

2 Bluntnose l lnnou. 

Plmophaler not&r 

Speclas Mean 

ChroaIIc Value 

Crs/l) 

8.8 

l Ranked frcr load sansltlvo to wart sewltlw hosed an spocles mean cRonlc vslw. 

FreshwOw Flnal Chronic Value - 5.56 &I 

8-36 
Table 3. CamtIau4) 

Rank’ 

31 

30 

29 

28 

27 

26 

25 

24 

23 

22 

21 

20 

I9 

I8 

SPuler 

Hot lfer, 

Phi lodlne mxtlcornls 

StrIped tass, 

l&n-on. saxstl I Is 

Strlpcd shiner, 

Motropls chrysocephalus 

orangethrvmt darter, 

Etheostora spectabl le 

Laogf In date, 

Agosls chryscgaster 

flagtlsh, 

Jordanel la f lw Ida4 

Atlantic salmon, 

Salvo salar 

-- 

GOldtlSh, 

carssslu5 aufstus 

Fathead rlnnor, 

Pimphales pramlas 

Brook trout, 

Salvellnus fontlnalls 

Yom, 

Nals sp. 

Ralnbor darter, 

Etheostm cawuleum 

Blacknose Qce, 

Hhlnlchthys atratulus 

tifan bul Ihecld, 

Ici.3lurus nobuIcEiu5 

Sprlw mean speclos llwn 

Acute lntr4mpt kutdhfOrlC 

(Vg/l) Ratlo 

14.4 

IO. I 

a.41 

5.61 

5.37 

5.00 

4.fJ5 

3.91 

3.29 

2.80 

2.28 

2.20 

2.20 

2. I3 

IO. I 

7.8 

3-38 
Tablm 3. Spades mom acute Intercepts 8nd values wt4f auto-clwonlc ratios fw COQPW 

45 

44 

43 

42 

41 

40 

39 

38 

37 

34 

35 

34 

33 

32 

Sprclw Mean Spmcla ban 

kut* I aterapt Acuta-Chalc 

spacl# lr!dl) a&lo 

fRESHWATEl? SPECIES 

stonet I y, 

Acrabeurla lycwlas 

260 

Caddlrf ly, 

Unldentifled 

I50 

White porch, 

fkuae amurlcmus 

I48 

Amulcan eel, 

A0qul I la rostrata 

ckmxlfly, 

Unldmtlfled 

145 

II7 

Largemouth bass, 

Wlcropterus salaldes 

91.8 

BluegIll, 

&xmls mcrochlrus 

hat I, 

caqnblaml docI5ur 

lhyt Ish, 

Orconectes rustlcus 

35.2 

Scud, 

Garsrus sp. 

23. I 

soal I, 

lrrnlcols sp. 

22.9 

Purpk I nseed, 

Laporls glbbosus 

Banded kll Ilflsh, 

fundulus dlaphanus 

21.8 

20.1 

carp, 18.9 

Cypr lnus carplo 

a-37 
18bh3 3. (Cod Inuedk 

Rimk~ 

17 

14 

15 

14 

13 

I2 

II 

IO 

9 

8 

7 

6 

Speclor 

Crrtek chub. 

SemtIlus atromculatus 

WJPY # 

Pcecl f la retlculata 

Stoner01 ler, 

Campostcem anamafua 

Bluntnose IpJnnou, 

Plmaphales notatus 

Cutthroat trout, 

Salm clarkl 

-- 

Snail. 

Gyraulus clrcumstrl~tus 

Worm, 

Clnmdrl Ius hoffmlsterl 

Coho salmon, 

Oncorhynchus kfsutch 

Snal I, 

Physa Inteqro 

Halnbau trout, 

Salm qalrdnerl 

ChInook SalDon, 

Oncorhynchus t-shswytscha 

Snail, 

Physa heterostropha 

Wldge, 

Unldent I fled 

scud, 

Gamarus pstludollamaeus 

Species Mean specl.5 tin 

Acute Intercept ACUiO-CkrOllIC 

cps/r, Rat lo 

2.13 

2.12 

1.99 

I.83 

1.68 

26 

I.42 

I.34 

I.23 

I.01 3.6 

1.02 

0.91 

Cl.91 

CL 76 

0.55 3.3 

B-39 
Rank’ Smcla 

3 Clsdocoran, 

oaphrls ragns 

2 Clatiran, 

Oaphnls pulex 

I Cladoceran, 

Oaphnla JBJII lcarla 

22 

21 

20 

I9 

18 

I7 

I6 

15 

I4 

spalr NnM spulr wwr 

Aato Irhrapt &UtcckOrlC 

(I&I J adlo 

0.43 2.6 

0.28 

0.23 

Spelw hea Spula m 

Acute Value Acvh-CLrorlc 

SJUIM (p&l) R8t10 

SALTWATER SPECIES 

Shore carb, 

Carolnus hiwmus 

600 

Pacl f Ic. oyster, 

Crsssostraa glws 

N-pod, 

Eurytemra aff lnlo 

560 

526 

~pep~, 407 

1lQrlopus Japu4Ilcus 

Florlda pcqmno, 

Trschlnotus carol lnus 

412 

Pol ychaeto ucwm, 

Merols dlverslcolor 

344 

Bran shlq, 

Cranqon crangon 

330 

Mysld shrlq, 

Mysldop sls balIIs 

Mysld shrlrp, 

~ysldopsls blqelarl 

I81 

I4 I 

B-GO 
Tablo 3. 

Rbrlkfi 

I3 

I2 

II 

IO 

9 

8 

7 

6 

IContInued) 

Species 

CopePod, 

Pseudodlaptwius cwonatus 

At lant Ic sl lversl df3, 

wklaia lenldla 

-- 

Winter flounder, 

Pseudoplwrww3ctes 

tWWICi3nUS 

Am8rlcan oyster, 

Crassostrea vlrglnlca 

Pol ychaete uorm, 

Neanthes arenaceoduntat~ 

Pol ychaete worm, 

Phy I lodoce mcu latd 

Red abalone, 

fiallotls rutescens 

Amer lcsn lobster, 

fkmarus amirlcanus 

Calanold aopepod, 

Acartla clausl 

-- 

Black &~lone, 

Hsllotls cracherodll 

Soft shelled clam, 

w artbnar la 

Calmold copepod, 

Acsrt la toasa -I_ 

Summer f lounder, 

Paral lchthys dcrntatus 

Speclms Mean Speclar MOM 

Acute Valtbe AcMm-chronlc 

(p&l/l 1 Ratio 

- 

138 

I36 

IB 

I28 

I24 

I20 

86 

69 

52 

50 

39 

31 

28 

B-41 
Tablo 1, (Cont1nu.d) 

l Ranked trcm least sensltlve to mxt senrltlve based on species mean 

acuto value or Intercept. 

Freshrater 

Flnal Acute lntercspt = 0.29 rg/l 

ktural logarithm of 0.29 a -1.23 

Acute slope - 0.94 (see Table I) 

FI,-,~, Acute Equation I e(0.9411n(hardness) I-I.231 

Sal Water 

Flnal Acute Value = 22.9 us/l 

Acute-mrfmlc Rot lo - 5.7% 

Flnal Chronic Value - (22.9 ug/ 

(see hurt) 

1)/5.78 - 4.0 rg/l 

B-42 
Table 4. Plant vdur tar cqlpu 

Speclu 

Alga, 

Aaabnona f la-aqua 

Alga, 

Anabaena varlabl I Is 

Ahw, 

Aaacystls nldulsns 

Alga, 

Chlemydomnas sp. 

Alga. 

Chlorel la pyrenoldosa 

Alga, 

Chloreffa pyrenoldosa 

Alga, 

Chlorel la reqularls 

Ww. 

Chlorel la sp. 

Ah% 

Cfilorel la vulgar Is 

Alga. 

Chlorof la vulqarls 

Alga. 

Chiofella vufgurls 

Alga, 

Cyclotef la mmeghlnlsna 

Alga, 

Eudorlna callfornlca 

Alga, 

Scenedesmus acwlnatus 

RmUIt 

Etfut hi/l 1 

WfkSffUATER SPtCIES 

751 growth 

InhIbItIon 

Growth 

lnhlblt Ion 

Grouth 

InhIbIton 

Growth 

recluct Ion 

Lag In gath 

Grouth 

InhIbItIon 

Lag In south 

Photosynthesis 

InhIbIted 

Growth 

lnhlblt Ion 

EC50 wowth, 

33 days 

%$ growth 

reduct Ion 

Growth 

reduct lw 

Grouth 

lnhlblt Ion 

40s grouth 

reduct luff 

zoo 

100 

100 

8,0@ 

I 

100 

20 

6.3 

200 

WI 

100-200 

&oofJ 

5,0(10 

300 

R*tYe#blX 

Young 4 Llsk, 1972 

Young i Llsfc, I972 

Young I Llsk, 1972 

Calms, et al. 1978 

Steeran+ el sen 6 

Hlum-Andersen, 1970 

Steemawf4Irlsell 4 

Kaq-NI el sun, I970 

Sakaguchl, et al. 

1977 

Gachter, et al. 

1973 

Young & Llsk, 1972 

Rosko A Rachlln, 

1977 

Stokes a 

HutchInson, I916 

blrns, et al. 1978 

Young 6 LIti, 1972 

Stokes d 

HutchInson, 1976 

B-43 
Table 4. Icoetlnuoa) 

“pecles 

Alga, 

Sceeedesaus quadr t cauda 

Ihreshoid 

torIcIty 

Alga, Growth 

Scanedesus quadr lcauda reduct Ion 

Algae, 

Mlxed culture 

Blue green algae, 

Wlxed culture 

Dlatom, 

Nltzschfa llnaarls 

Dlatwn, 

NJ tzschla palea 

OUCkuWd, 

Lemna minor 

-- 

Wirrophyte, 

E lodea canadensls 

Eurasian uattumllfoll, 

Myrlophyl I- splcatua 

Green alga, 

Selenastrum capr lcornutun 

Alga, glant kelp, 

Macrocyst Is pyr I tera 

Alga, 

jhalassloslra psoudon~n~ 

Effect 

Slgnlf lcant 

reductlar, In 

photosynt hes I s 

50s reduct Ion In 

photosynthesls 

I20 lK Hi50 

Coclplrte growth 

lnhlbltlon 

EC50, 7 day 

50# reduction In 

photosynthetlc 02 

product Ion 

509 root relght 

reduct Ion 

Grouth 

reduct Ion 

Result 

(WI 1 

150 

8.ooO 

5 

25 

7958 I5 

5 

II9 

I50 

250 

50 

SALlWAlER SPECIES 

96 fu EC50 

photosynthrrsls 

lnact I vat Ion 

loo 

I2 hr EC50 

yrouth rate 

5 

Referewe 

Brlnwan & Kuhn, 

1959 

Calms, et al. 1978 

Elder A fkrne, I978 

Strwoti-Nlel sen A 

Bruun-Laursen, IS76 

Patrlck, et df. 

1968 

Steeran-Ml el stw b 

Wlum-Anderson, 1970 

Yal bridge, 1977 

Brown 6 Ratt Igdn, 

1979 

Stanley, 1974 

Bartlett, et al. 

1974 

Clendennlng & 

Mar-th , I959 

trlckson, 1972 

B-44 
Table 4. Kaatlnued) 

Spacler 

Alga, 

hphldlnlur, carter1 

Al a, 

01 7 sthodlscus luleus 

Alaa, 

Skeletonem costatum 

Alga, 

ytschla closterlua 

Alga. 

Scrlppslells feeroense 

Akm 

Proiocentrur deans 

Alga, 

Gymodlnlu splendons 

tttut 

I4 day EC50 

grcmth rote 

I4 day EC50 

grath rate 

I4 day EC50 

gradh rate 

%hrECw 

growth rate 

5 day EC50 

gr”rth rate 

5 day EC50 

grath rate 

5 day EC50 

grcuth rate 

Result 

tJlg/l, 

C50 

33 

5 

IO 

20 

Reference 

trIckson, et al. 

;970 

trlckson, et al. 

1910 

trIckSon, et al. 

1970 

Rosko & Ruchlln, 

1975 

Salful lah, 1978 

Salfullah, 1978 

Selfullah, 1978 

a-15 
Sped= 

A km 

Chlorella rwulerlr 

Sionof ly, 

Pteronarcys callfornlca 

fatbed rlnnou (larva) , 

Plnphales praaelas 

BluegIll, 

Lepods mcrochlrus 

Polychcmta YOTII, 

Clrr ItorrId splrabracha 

Polychaete worm, 

Neanthes arenacfmcbntata 

Polychaete worm, 

Nerels dlverslcolor 

Pol ychaete worm, 

Phyllcdoce raculata 

Bay scallop, 

Argapecten lrradlans 

Bay scallop, 

Argopacten lrradlans 

Aatvlcm oyster, 

Crassostrtm vlrglnlca 

American oyster, 

Crassostrsa vlrqlnlca 

Northern quahaug, 

wtw cwmr la ow-cenar la 

Tablo 5. fhsldum tar aqlpu 

Bl-lrmtla huat loa 

TIS*w fbdor (days) Hofwma 

fRESHHATER !iPECIES 

2,~ 20 hrs Sskeguchl , et al. 

1977 

203 I4 Nehr Ing. 1976 

msc le 

290 

0 

30 Llnd, et al. 

ebnuscr lpi 

660 Benol t, 1975 

SALTWATER SPECIES 

250. 24 

2,550. 

203. 

1,750* 

3,310 

4, I60 

28,200 

20,100 

88 

26 

24 

21 

I I2 

I I2 

140 

140 

70 

Mllanavlch, et al. 

1976 

Pesch & kwgm, 1978 

Jones, et al. 1976 

ClcLusky A Phi I I Ips, 

1975 

ikrooglan, 1918 

Zwocglan, 1978 

Shuster 6 Prlngle, 

I%9 

Shuster- 6 PI Inyle, 

I%9 

Shuster & Pr Inyle, 

I%8 

3-46 
Table 5. uhnt bwu) 

6l-tratl0- 

factor 

3, JO0 

Ourat loa 

(ueya) 

35 

SPOCI*S 

Sott shelled cla=, 

w aremarLa 

Wurs.1, 

mm 

ti*lrul, 

WI lus euu!ls 

MUSSII, 

Byl luc edul Is 

wUSS61, 

Wvtl lus ~lcwx3vlnclol Is 

Alga, 

Dunsllella prlolects 

A ha, 

Dunallella tectlolecta 

Alw, 

Ch I amydomonss spc 

Alw. 

Chlorella ssllns 

Alga. 

Stlchococcus baclllarls 

Rduence 

Shuster I Prlngle, 

I%8 

2(r, 1 I2 lJ,s, fPb, 19fMJ 

we 112 U.S. EPA, l9aD 

90 I4 Phllllps, l97f 

800 25 WaJoorl & ?etrmlo. 

1973 

153* 25 Riley S filth, 1971 

IMP 25 Hliey & kth, 1971 

135* 25 Riley a Roth, I971 

74* 25 

25 

Riley 6 Kuth, f9?1 

Riley & Roth, 1971 

Alga. 273’ 25 Riley a Roth, 1971 

tiemlselmls vlrescens 

Alga. 

Hemlselmls brunescens 

Alga, 

0llsthodlscus luteus 

Alga. 

Aster lone1 la Jqmnlca 

Akm. 

Phaeodactylw t! lcwnutum 

553= 25 Hlley a Roth, 1971 

25 Riley & Roth, 1971 

309’ 25 RI ley I Hoth, 1971 

323’ 25 Hlley & bth, I971 

5-47 
Table 5. uhnt1lw.d) 

Spules 

Al!% 

Akvr 

Pseudopedlnella pyrlforals 

A kw, 

Hetoromastlx longltlllls 

T I ssuo 

Bl-centrotlan Ourat Ion 

factor hAays) 

IXIB’ 25 

B5’ 25 

617” 25 

Reference 

Riley A Roth, I971 

Hlley b Roth, 1971 

Hlley b Roth, 1971 

Alga. 

MI cronnms rquawta 

Alga, 

Totraselrls tetrathele 

279’ 25 Hlley 6 fblh, 1971 

265a 25 RI ley A lath, 1971 

l lJry relght to wet uelght converslon 

3-18 
SpUlOS 

Aacul Id ua-a, 

kolo+ay hmdlwl 

Amal Id warm, 

Aaotoscma hmadleyl 

Amnalld rora, 

Amol- tmadloyl 

AnnalId worm, 

Amolosors hmadloyl 

Annel Id YWD, 

Aooloscra hrsdleyl 

Snal I (erbryo), 

Avrlcol* rp. 

Snal I, 

GonIobnsls llvescens 

Snsl I, 

Lyme8 emarqlnata 

Smll, 

Nltrocrlr sp. 

Snsl I, 

Wltrocrlo rp. 

Snsl I, 

Wltrocrls sp. 

Snal I, 

Nltrocrls sp. 

Snsll, 

Nltrocr Is sp. 

Claboceran, 

Daphnla amblgua 

l&bl* 6. Mhu dmta for alppar 

Result 

Dwatloa Ettut wa/l) 

40 lws 

ul IUYE 

a h-s 

4a hrs 

4B lwr 

96 hrs 

18 lur 

18 hrs 

48 hrs 

48 hrs 

48 hrs 

40 h-s 

111 hrs 

72 hs 

fRESHMATER SPECIES 

Llxo 

LCM 

Lcm 

LC50 

LC50 

LCM 

Lao 

lx50 

LCM 

LCM 

l.c.50 

LC50 

h-3 

2,m 

2,oofJ 

1,650 

Calms, l t al. 1978 

Colrns, et al. 1978 

Calms, et al. 1978 

Calms, l t al. 1978 

blrnc, et al. 1978 

9,300 Rehuoldt, ut al. 1973 

&xl Calms, et al. 1976 

m Calms, at al. 1976 

3,m 

2,400 

1,000 

300 

210 

Calms, et al. 1978 

Calms, et al. 1978 

Calrn.5, et al. 1978 

Calms, ot al. i978 

Calrnr, et al. 1978 

Ratwro 

u30 67.7 Ylnner 4 Farrell, 

1976 

B-49 
Table 6. Kant Inud) 

spmclas 

cw=.-fb 

Osp(nIa * 

CllMlO#rWl, 

Daphnla magna 

Cladoceran, 

Dophn Is mgna 

Cladoceron, 

Daphnlo ragna 

Ctadocsran. 

Daphnla raqna 

c I bldwardll, 

Oaphn I a mgnd 

C I adocoran, 

Daphnla aagoa 

Cladoceran, 

_Ddpha I Q mdgna 

C ladoceran, 

Oaphn I a s 

Cladoceran, 

L)a_yhn to magna 

C ladoceran, 

Daphnta magna 

C ladO4MNI. 

Daphnla magna 

c I adoceran l 

Oaphnla s 

C Iadoceran, 

Oaphn la mdqna 

IhNat locr 

48 hrs 

48 tus 

40 hl-s 

48 hrs 

48 trs 

1116, cyclb, 

Llte cycle 

Lit8 cycle 

Llf6 cycle 

life cycle 

Life cyclu 

Llfu cycle 

Lltu cycle 

l-2 IYS 

Et tect 

LC50 

LC50 15 C) 

lmo (IO C) 

LC50 (I5 C) 

LC50 (23 Cl 

Huauced numbr ot 

young pr aluced 

fbduced mmbur of 

young pr cxiuced 

Reduced producf lvlty 

Reduced productlvlty 

Reduoed product I VI ty 

Reduced producf I vl ty 

Raduced product I v I ty 

Reduced number ot 

young pratuced 

Lcm 

Result 

OrQto 

60 

90 

70 

40 

I 

IO 

IO 

21.1 

26.2 

a.2 

lat.2 

49 

10 

80.5 

Retwonca 

Bleslnger 4 

ChrIstensen. I972 

Cdlrns, u,t 01. 197tl 

Gilrns, ut al. 1978 

~IIrllL, et 41. 19118 

Ulnnor, et dl. 1977 

Wlnrier, ot ~1. l-)77 

Btualnyor A 

Chrlstmwn, 1972 

bflnrwr, et ‘11. 1377 

Wlmar , tit 01. I977 

Winner, et IAl. 1977 

Winner & tcw-rol I, 

1976 

Adeuti 6 lkkirout Vdn 

ZIJI, 1972 

Wlnnur 6 Ior r-4 I, 

1976 
Table 6. Kant Inued~ 

Species 

C I adocer dn, 

Da phn I a magna 

C IaWan, 

l%e!!!alwgns 

C hkceran, 

Oophla mugno 

C I adwxran , 

Daphn lo maqns 

C I atieran, 

Oophnlo mqno 

C I adoceran, 

Oophnla lsqna 

Cladoceran, 

Oaphnla magna 

C I ado-ran, 

Osphnlo garvulo 

C I adocwm, 

Oaphnla parvula 

C I adoceran, 

Daphnla porvulo 

C Iodaceran, 

Oaphnla pulex 

C Iotieron. 

Daphnla pulex 

Cladoceran, 

Oaphnlo pulex 

Durst Ion 

72 hrs 

72 hrs 

72 tars 

72 b-s 

72 hrs 

29 hrs 

24 hrr 

72 hrvs 

R tYs 

Llte cycle 

72 hs 

72 hrs 

life cycle 

Result 

Ettect &I/l) 

LC50 

LCSO 

LC50 

lC50 

LC50 

Mudlan survival tlm 

LC50 

LC50 

LC50 

Reduced productlvlty 

LC50 

LC50 

Reduced product I vl ty 

00.8 

85 

81.5 

01.4 

85.3 

12.7 

BQ 

57 

72 

49 

54 

86 

49 

Referewe 

Winner 6 Farrul I, 

1976 

Wlnnw & Farrel 

1976 

Winner 4 F&rut 

1976 

Winner 4 Farrel 

1976 

Ylnner A Fcurel 

1976 

Andrew, et al. 1917 

BrIngnan 4 Kuhn, 1917 

Ylnner 6 Farrel I, 

1976 

Wlnnw & Farret I, 

1976 

Winner 4 Farrel I, 

1976 

Wlnnw- 6 Farrel I, 

1976 

Winner 6 Farrel I, 

I916 

Winner 6 Farrell, 

1976 
Cl-M, 

oaklIly. pub* 

Cl&&CUM, 

Daphnlm pulu 

Cl-M, 

04phl4 pulrx 

C ladmoran, 

Dsphnlo Pulex 

c I adocrran , 

Daphnla Jwllcsrls 

C I adoceran, 

Uaphnla $ullcarls 

C I sdoceren, 

Daphnla pullcarla 

Clsdocnran, 

Daphnls pullcarla 

Cladacoran, 

Daphnle pullcarla 

C I adocersn , 

oaphnla pul Icarlo 

C I a&wan, 

Osphnla pullcarla 

C I abcersn, 

Oaphnis pul lcarla 

Cladoceren, 

Oaphnla pullcarla 

Clsdoceran, 

Oaphnla ~llcarla 

oumtlon 

48 hr 

I hrs 

48 h-s 

48 hrs 

40 IN-S 

48 hrs 

43 hrs 

40 hs 

40 lus 

48 hs 

4a hrs 

40 hs 

40 hrs 

18 hs 

Elfed 

Lc50 (5 Cl 

Rrullt 

hwl, Rmtwencm 

70 Calms, et al. 1978 

Lcw (IO C) 60 Calrnr, at al. 1978 

Lc50 (I5 C) 20 Calms, et 41. 1978 

Lc50 (25 C) 5.6 Calms, et aI. 1978 

LC50 (Tot I4 q/l) 55.5 Llnd, et al. 

Manuscr I pt 

LC50 (1cx.z I3 mg/l) 53.3 Llad, et al. 

Manuscrlpt 

Lc50 (Taz I3 q/l) 53.3 Llnd, ut al. 

Martuscr Ipt 

LC50 (Ta: 28 q/l) 97.2 Llnd, et al. 

Mamscr I yt 

LC50 (TOC 34 mg/l) I99 Llnd, et al. 

Manurer I pt 

LC50 (TCC 34 19/l, 627 Llnd, et al. 

Manuscr I pt 

LC50 (TOC 32 ag/l, 213 Llnd, et al. 

Manuscr I pt 

Lc50 (TOC 32 q/l, I65 Llnd, et al. 

Manuscr I pt 

Ii30 (Ta: 12 mg/l) 35.5 Llnd, ut al. 

Manuscr I pt 

LC50 (TOC I3 q/l) 78.8 Llnd, et al. 

Cbnuscrlpt 

B-52 
Table 6. Llhntlnwdl 

Swles 

Cladoceran. 

Dspbel~~f lcar la 

ClrOourw. 

Oa+bl~~l lcarla 

Clwlocmran, 

Daphnla pl lcarla 

CIbdocfu-an, 

Daphnla pl Icarla 

C I adocaran, 

Dsphnla pullcarla 

Cladoceran, 

Uaphnla iublqua 

Scud, 

Gmw-~s lacustr Is 

MaYi IY. 

Lphtmerulla subvarla 

Wf IY. 

tpharerel la sand16 

stonet ly. 

Pteronarcys callfornlca 

Caddlsf ly, 

Hydropsyche bettenl 

Mldye, 

Tanytarsus dlsslmllls 

Crayf Ish, 

Orconectes rustlcus 

Rot I f er , 

Phi lodIm acutlcwnls 

Duratlan 

4fl kc 

40 tus 

48 hrs 

48 hrs 

40 fKs 

Life cycle 

% hrs 

48 hrs 

I4 days 

I4 days 

14 days 

IO days 

I7 days 

48 hrs 

Result 

Ef forA wf/l) 

LC50 (TOC 28 mgg/l) II3 

LC50 (TOC 25 mg/l) 76.4 

LC50 (TCC I3 q/l) 04.7 

LC50 (TCC 21 y/l) I84 

LC50 (TOC 34 mg/l) 240 

Reduced productlvlty 49 

LC50 J,!@fJ 

LC50 320 

LC50 kwmo 

LC50 IO, IOO13,900 

501 survival 32,000 

LC50 16.3 

Survival of 125 

newly hdtched young 

LC50 1,m 

Rd weace 

Llnd, et al. 

Mamscr Ipt 

Llnd, et al. 

f4anuscr I pt 

Llnd, et al. 

Manuscr I pt 

Llnd, et al. 

Manuscr I pt 

Llnd, et al. 

Manuscr Ipt 

Winner & Fsrrel I, 

1976 

kbf3ker & Laufln, 

1964 

Warnlck b t&II, I%9 

tihr Ing, 1976 

Mhr Ing, 1976 

Ywnlck 4 tioll, 1969 

Andeison, et al. 19Ml 

tfubshmn, I%1 

Calms, et al. 1918 

B-53 
Table 6. GoatInud) 

SpUl~ 

fwlfw, 

Phi lodlns acut lcornls 

Rotltu, 

Phllodlna acutluwnls 

Rotlfer, 

Phflodlna acutlcornlr 

Rotlfer, 

Phi lodlna acutlcwnls 

coho 5alIyy1, 

Oncorhynchus hlsutch 

Coho salmon, 

Oncorhynchur klsutch 

coho salmon, 

Oncorhynchus klsutch 

coho SalmxI. 

Oncorhynchus klsutch 

Coho saIlon, 

Oncorhynchus kfsutch 

coho salmm, 

Oncorhynchus klrutch 

coho salmon, 

Oncorhynchus klsutch 

cdl0 Mlmon, 

Oncorhynchus klsutch 

coho =I-, 

Oncorhynchus k I rutch 

coho salmon, 

Oncorhynchus klsutch 

Duretlon 

48 hrs 

JB hrs 

43 lus 

40 hrs 

46 lx-s 

30 days 

n hf-s 

72 hrs 

R frs 

72 hrr 

72 hrs 

72 hrs 

72 hs 

72 bra 

Ef hct 

LC50 

LC50 

LC50 

Lcw 

Reduced surv I val 

on transfer to 

seawater 

LC50 

LC50 

LC50 

LC50 

LC50 

LC50 

LCM 

LC50 

LCbO 

RemIt 

QNl/l) 

1,200 

1,130 

l,oo(-J 

950 

30 

280 

370 

I90 

480 

440 

460 

480 

560 

Ref ereeu 

Calms, et al. 1918 

Calms, et sl. 1978 

Calms, et al. I978 

Calms, et al. I918 

Lorz 4 WPherson, 

1976 

Holland, et al. IWO 

tblland, et al. I960 

HOI land, et al. I%0 

Hollsnd, et al. I%0 

fblland, et al. I%0 

HOI land, et al. I%0 

HOI land, et al. I%0 

Holland, et al. 1960 

tbl land, et al. 1%0 

B-54 
Table 6. Kaatleumd) 

Sprlu 

cob0 safm, 

Oncwhyncbus kl sutch 

colbo YlIp*, 

Ontxrw klsutch 

cd0 ~lrn, 

oacuhyndrus k lrutch 

cdm salam, 

Chcorhyncfwr klsutch 

soclmym salnm, 

Oncorhynchus aerke 

Chfnook salUn, 

Oncorhynchus tshawytscha 

Chfnook salon, 

Oncwhynchus tshawytscha 

ChinOoft salwa~ fslsvlnJ, 

Oncorhynchus tshamytscha 

Chlnook salrwr (sfevln), 

Oncorhynchus tshawytscha 

ChInook salm IsrfrupJ, 

Ollcorhynchur tshauytrcha 

Chlnooh salvn fsrlrup), 

Oncorhynchus tshaaytscha 

ChInooh ralun Iparr), 

Oncahynchus tshaytscha 

Chfnooft saIlron tparr), 

Oncwhynchus tshawytscha 

Chfnodc salvwr fsmolt), 

Oncorhynchus tshauytscha 

Dwatlon 

72 IKS 

72 hr 

72 fur 

72 fur 

24 h-s 

5 days 

ia days 

200 h-5 

2Do fus 

zoo hrs 

200 MS 

200 frs 

MO hrs 

200 ffrs 

Ettmct 

LC50 

LC50 

LCSO 

LCM 

Slgrlf lcant cfban94 

in uxtlcostmrlod 

fstr4ssJ 

LCSO 

Reduced urvlval and 

grouth of sac fry 

LCM 

LCIO 

LCM 

LCIO 

LC50 

LCIO 

LC50 

Result 

cl&r I 

780 

5to 

520 

480 

64 

I78 

21 

20 

I5 

I9 

J4 

30 

I7 

26 

Ratwwcw 

tilland. et al. 1960 

HOI land, et al. I960 

Holland, et al. I%0 

Holland, et al. I960 

Donaldson & Dye, 1975 

Holland, et al. I%0 

Hazel & Melth, l9Xl 

Chapman, 1978 

Chapron, 1978 

-pun, I978 

Chapran, 1978 

chapMn, 1978 

Chaplkm, 1978 

Chapman, 1978 

B-55 
Table 6. UkmtIru*d) 

N 

chinook vlwn (molt), 

Oncorhynchus tshimytscha 

ChInook salmon, 

Omxuhynchus tshsrytscha 

Ralnbou trout, 

Salm qalrdnerl 

Halnbou trout, 

Salvo qalrdnerl 

RaInhow trout, 

Salr, Qalrdnerl 

Halnbw tr out, 

Salm qalrdnerl 

Halnbou trout, 

&3lao y~lrdnerl 

Ra lnbow trout, 

Salm q~lrdnerl 

Ralnbou trout, 

Sala qalrdnerl 

Ralnbow trcwt, 

Salmo galrdner I 

Ralnboa trout falevln), 

Salvo qalrdnerl 

ftalnbou trout falevln), 

Salm qalrdnerl 

RaInbow trout (swlaruy), 

Salem qdlrdner I 

Ralnbw trout fswlm-up), 

Sd Ire yd I I- Jner I 

ouratlon 

mo hrs 

72 fus 

96 hrs 

% hrs 

% hrs 

2 hrs 

7 days 

21 days 

IO days 

7 days 

I86 hrs 

I66 hrs 

200 b-s 

mo lus 

Result 

Effwt crqI1, 

LCIO 

LC50 

LC50 

LC50 

LCSO 

Oeprtrssed 01 factory 

response 

LC50 

&dlan perfod of 

survival 

Depressed feed Ing 

rate snd grouth 

kdlan period of 

wrvl val 

LC50 

LC IO 

LC50 

LCIO 

I0 

I90 

516# 

309’ 

Ill’ 

a 

44 

40 

75 

44 

26 

I9 

I7 

9 

ReferChapMn, 1978 

HOI land, I960 

tkmuth b Sprague, 

1970 

tiorwth 4 Sproyue, 

1978 

tiouarth 6 Sprayuu, 

1970 

tkua, et al. 1976 

Lloyd, I%1 

Graode, 1966 

Lett, et al. 1916 

Lloyd, l%l 

Chap-, In press 

Chapaan, In press 

Chapakin, In putis 

Chapniul, In prt&Ll 

3-36 
Table 6. collt lewd) 

Species 

RaInbo* trout (Parr), 

Salm galrdner I 

Ralnbou trout (parr), 

Slrlgpr(rdnwl 

RaInbaa trout (molt). 

Salt aslrdnerk 

RaInbar trout (molt), 

Salm galrdnerl 

RaInbar trout (molt), 

Sala galrdnerl 

Ralnbou trout (smelt), 

Salm qalrdner I 

Ralnbou troui (fry), 

Salvo qalrdnerl 

Rainbow trout (fry), 

Sa Iw, gal rdner t 

RaInbow trout (fry), 

Salvo galrdnerl 

Ralnbou trout (fry), 

Sala qalrdwl 

Rain& trout (fry), 

Sallo qalrdnerl 

RaInboa trout (fry), 

Saluo qalrdner I 

Ralnbou trout (fry), 

Salr, qalrdnerl 

RaInbar trout (fry), 

Salr, qalrdnerl 

lhwatlon 

200 hrs 

200 hrs 

mo hrs 

mo hrs 

>I0 days 

I4 days LC50 

lhr Avol dance beha v lor 

24 fws IL50 

24 hi-s LC50 

24 frs Lcm 

96 hrs 

% hrs 

40 hrs 

% hrs 

Effect 

LC50 

cc10 

Lc50 

LCIO 

Threshold lE50 

LC50 (tIeId) 

LC50 

LC50 IfIeld) 

LC50 

Result 

kI/IJ 

15 

Reference 

Chapman, In press 

8 Chapatn, In pruss 

21 Chapman, In press 

7 Chapran, In press 

94 Fcgels A Sprague, 

1977 

870 Calamarl 4 Marchettl, 

1973 

0.1 folur, 1976 

9SO Calms, et al. I978 

430 Calms, et al. 1973 

I50 Calms, et al. 1978 

253 hle, 1977 

2s*680 Lett, et al. 1976 

70 Cala*arl a Marchettl, 

1975 

250 Goett1, et al. I972 

a-57 
Tabla 6. (COdIMd) 

SIWCIW 

Ralabcu trout (try), 

Salc ~lrdnwl 

Rslnbor trout (fry), 

salrp g8lcdnwI 

Ralnba tfft:fry), 

Salmo ga 

RaInbar trout, 

Salmo galrdnerl 

Rslnbom trout, 

Sala galrdnerl 

Ralnbou trout, 

Salm galrdnwl 

Rslnbou trout, 

Sallo galrdnerl 

Ralnbw trout. 

Salmo galrdnerl 

Ralntw trout, 

Salmo galrdnerl 

As lnbw trout, 

Salr, qalrdnerlRalnbw trout, 

Salrr, galrdner I 

Ralnbw trout, 

Salao galrdfhwl 

Ra lnbw trout, 

Salr*, galrdnerl 

Halntmu trout, 

Salru gnlr4nurl 

Durrt Ion 

24 hr 

24 brs 

72 trs 

,I5 days 

>I5 cbys 

,I5 days 

>I5 days 

>I5 days 

>I5 Qays 

40 hrs 

48 hrs 

40 hrs 

72 hrs 

4a nrs 

Effect 

lc50 

LC50 

Threshold iE50 

Threshold LC50 

Threshold Lc50 

Threshold LC50 

Threshold LC50 

Threshold LIZ50 

Lc50 

LCSO 

LC50 

Lcxl 

LC!m 

ROSUH 

!rp/l 

140 

I30 

500 

I9 

54 

48 

78 

I8 

% 

750 

I50 

\,I00 

270 

RdUUU4 

shau 6 flroun, 1974 

Sbau & Brorn, l9?4 

Brown, et al. 1974 

Ml I ler 4 McKay, 1380 

Mll ler & McKay, I980 

Ml I ler 4 McKay, 1380 

Mll ler I ClcK~y, I380 

WI ler & McKisy, 1980 

Mll ler 6 McKay, 1980 

&own, I%8 

Eroun & Dslton, 1970 

Cope, 1966 

Lloyd, \%\ 

tiurlluI~t 6 Varulyku, 

I%4 

B-Si3 
Table 6. uhntlnuui) 

Spuler 

Atlantic salmon, 

Salmo salar 

-- 

Atlantlc 5almo0, 

J?J=-= 

AiIaMlc salroo, 

salr, salsr 

-- 

At lant Ic Lo Imoa, 

Salm salsr 

-- 

Brwn trout, 

Sallo trutta 

-- 

Brook trout, 

SalvelInus fontlnalls 

crook trout, 

Salve1 lnus tontlnal I5 

tkook trout, 

SalvelInus tontlnalls 

Stonerol ler, 

Carpostonla ancmalw 

Goldtlsh, 

Carass lus auratus 

Coldfls), 

Carasslus auratus 

GoldfIsh, 

Carars I us W&U5 

Golden 5hlner. 

Noiemlgonlus cry5oleucas 

Golden shiner. 

Notmlgonlu5 crysolatcas 

Golden shiner, 

Notmlgonlus crysoleucas 

ourstIoa 

7 days 

7 days 

21 days 

21-30 tu-s 

21 days 

24 Ius 

21 days 

33? days 

% hrs LCSO 

24 lrs LC50 

24 hrs LC50 2,900 Calms, ut al. 1978 

24 hrs LC!xJ 

24 tars LC50 

24 bus 

24 b-5 

RuU1t 

Etlect (W/l) RetuUWX 

lnclplent lethal 48 

level 

Sprague, 1964 

Inclplent lethal 32 Sprague & &msay, 

level I%5 

MadIan period ot 40 Grande, I%6 

5urvIval 

Medlan perlod ot 

5urvlval 

50 Zltko 6 Carson, 19/b 

Medlan period ot 

wrvlval 

45 Grade, l96h 

SIgnIt Icant change 

In cough rate 

9 Drumond, et al. 1973 

Slgnlf lcant change5 

In blood chmlstry 

23 MLKIR, st al. 1970 

Slgnlflcmt changes 

In blood chumlstry 

17.4 McKlr, et al. 1970 

1,400 Gerklar, et til. 1976 

2,700 CaIrna, et al. 1978 

1,510 Calms, et al. 1978 

330 Calrn5, et al. 1918 

LC50 230 Calrns, et al. 1978 

LC50 270 Cdlrns, et al. I978 

B-59 
Table 6. K-oat Inued) 

Result 

(W/l) 

t1,400 

brat Ion 

96 hrs 

Effect 

LC50 

Reference 

Geckler, at Gil. I916 

Species 

Sir lped shiner. 

Hotrop chrysocepha 1~5 

Strlpmd Miner, 

No)rop chryrocepha les 

Strlped shiner, 

Roiropls chrysocephales 

Strlped shInor, 

Motropls chrysocephales 

Str lped shlnmr, 

Notropls chrysocephales 

Strlped shiner, 

Notr opls chyysocephales 

% hrs LC50 16,ooO Geckler, et al. I976 

% hrs LCSO 3,400 Geckler, et al. l97b 

% hrs Lcx 4,m Geckler, ut al. 1976 

96 hrs LC50 5.ooo Gckler, et al. I916 

96 hrs DecrtMbrt blood 

osmolarlty 

2,5oQ 

48 hs LC50 (21 tests) 750- 

21,ooo 

Gxklrr, al al. 1976 

96 hrs LC50 (6 tests) l,laoM,W 

Ceckler, el dl. 1976 

96 hrs LC50 (21 tests) l,600- 

21,000 

8rungs, et al. 1976 

(650 

23,600 

740- 

13,ooo 

4x8 

B I untnose minnow, 

Plwphales notatus 

bluntnose l lnnw, 

Plrephales notatus 

fathead rlnnw, 

Plmephaltrs prorelas 

96 hrs 

%.hrs 

Fathead minnow, LC50 (36 test;s, Geckler, el al. 1976 

Plmephales JJrmel~5 

Fathead l lmww, Lc50 (7 tests) Geckler, et dl. 1976 

Plmephales prcmelas 

Fathead rlnnor, 

Plmephales prorelas 

fathead rlnnou, 

Plmephaler prorelas 

% hrs LC50 (T(r: - I2 

edI) 

LC50 (TOC = I3 

WI) 

Llnd, et al. 

Manuscr I pt 

Llnd, et ai. 

Manuscr I pt 

96 hrs 516 

B-68 
Tab10 6. soatlw8d) 

Spulms 

Fathead l lnnw, 

Plaephales prcmelar 

Fathoad &mor, 

w8w F-las 

fmw ‘&au, 

~prcmelas 

Fathad l lnmw, 

Plmmphslor fbroular 

fathead l lnaw, 

P Im@ubl~s prKcrrlas 

FatMad l lnnou, 

Ptmephales prmlas 

fathead rlnnca, 

PI*ephales prcuelas 

Creek chub, 

Semtl lus atrmculatus 

Creek chub, 

Seatllus atrmculatus 

Bran bul Ihead, 

lctalurus nobulosus 

Channrl catt I rh, 

lctalurus punctatus 

Chsnnel ottIs>, 

Ictalwus punctatus 

Channel catt I sh, 

lctalurus punctatus 

Channel catflsh, 

Ictalurus pwrctatus 

Durat Ian 

% b-5 

% hrs 

96 hrs 

% IN-S 

96 hrr 

96 hrs 

Llte cycle 

96 IKS 

96 hrs 

% hrs 

94 tars 

24 hrs 

24 hrs 

24 lrs 

Effect 

lC50 (TOC - 36 

*4/l) 

LC50 (TOC - 28 

Is/l) 

LC50 (TOC - I5 

*g/l) 

LC%l (TOC - 34 

41) 

LC50 (TCC - 30 

WI) 

LCBO (TW - 30 

WI) 

aNonlc Ilalts 

Lcm 

LC!jo 

LCW 

Decrmsd blocd 

osaolwlty 

L&m 

Lcm 

Lcm 

Rwult 

(Pa/l, 

1.586 

1,129 

550 

I.001 

2,050 

2.336 

66I20 

ll,mo 

1.100 

ll,Wo 

2,5M 

1,730 

2,a 

3,100 

Refwuwm 

Llnd, et dl. 

Manuscr Ipt 

Llnd, et al. 

Mbnuscr Ipt 

Llnd, r? ~1. 

Manuscr I p: 

Llnd, at al. 

Manuscr I pr 

Llnd, et al. 

M8nuscrIpt 

Llnd, et al. 

Manuscript 

fkungs, et al. 1976 

ekler, et al. 1976 

Geckler. et al. 1976 

l%ckler, et al. 1976 

LOUIS A LwIs, 1971 

Calms, et al. IY?B 

Calms, et al. 1978 

Calms, et al. 1978 

B-61 
Table 6. Kontlrued) 

Result 

(p!J/l) 

680 

E,ttect 

lC50 

Uurat Ion uetarence 

IO cbys 

% hrs 

SlMlClU 

Fl*#lJ. 

rarkw) t lorldatl 

Wosqultot Irh, 

Gemburls attlnls 

WJPY, 

Pcacl I I4 retlcula?a 

Ralnbom darter, 

Eiheosi4ma caeruleur 

Aslnbou darter, 

Eiheosttma cserulew 

RaInbow dzu tor, 

tthwslw caerutauur 

Johnny dater, 

Ltheostema nlgrunl 

Orangethroat barter, 

E theostoma spactabl le 

Orangethrclat darta-, 

6 theostoma spectabl le 

Orangethroat darter, 

Etheostora spectabl le 

Orangethroat dafter, 

E theostcma spactabl le 

Rock bass. 

Adlopl I tes relpastr Is 

Elluegll I. 

Lepollls wxrochlrus 

Mluaglll, 

Lepculs aacrochlrus 

t 

7 

els & Spraguu, 

I9 7 

LC50 1750 ag/l 

turbldlty) 

LC50 

75,ooo Yal len, et til. 1957 

24 hr* 1,250 Mln lcuccl , 1971 

96 hrs LCM Geckler, et al. 1976 

96 hrs LC50 bckler, et CII. 1976 

% hrs 

96 hrr 

96 hrs 

LC50 Geckler, ul dl. I976 

LC50 6,000 Gackler, et dl. 1916’ 

LCM 9.800 Geckler, ut ~81. I916 

96 lws Lc50 7.900 Geckler, al di. 1976 

96 hrs LCQ >,400 (;trckltW, tit d,1. lYl6 

% tus LCSO 5, mo Guckler, et dl. lg?b 

% hrs 

24-36 hrs 

LC50 1,432 Llnd, et dl. 

Mmuscr I pi 

Al tertd oxygen OViara, 1971 

consuqt Ion rates 

LC50 

300 

411 Iv5 2,800 uq-m, I%6 

3-62 
Table 6. mMbtlnuod) 

Spec I es 

Bluegill, 

Lepomis macrochlrus 

8lWBlU 

l~~ochlrus 

BlWl~ I, 

Lepo~lr mcrochlrur 

Bluaglll, 

L-1 5 macro& I rus 

Colonial hydrold, 

Clllpanularla tloxuosa 

Colonial hydrold, 

~ampaaularle tlexuosa 

Colonial hydrold, 

E Irene vlrldula 

Polychaete wora, 

Clrrlforrla splrabrtia 

Polychaete worm, 

Phyllodoce naculsta 

Polychaoto uora, 

fleanthes armaceodentata 

Pol ycheete WI, 

Neanthes arenaceodntata 

Bay seal lop, 

Argopecten lrradians 

say scallop, 

Argopacten lrradlans 

kerlcan oyster (larva), 

Crassostrea vlrglnlca 

Duration 

96 hrs 

96 hrs 

% hrs 

% hrs 

11 days 

14-21 days 

26 days 

9 days 

28 days 

20 days 

42 days 

I19 days 

I2 days 

Etfect 

LCSO 

LC50 

LC50 

LCSO 

SALTWATER WECIES 

Growth rate 

lnhlbltlon 

Enzyme InhIbItIon 

Growth rate 

lnhlbltlon 

50% mortal I ty 

50% aorta1 Iiy 

50% mortality 

501 moriallty 

EC%, growth 

loo% mortality 

MS rortallty 

Result 

crdl) 

16,000 

17,ooo 

740 

1,800 

lo-13 

1.43 

30-60 

40 

80 

44 

100 

5.8 

5 

46 

Reterence 

Geckler, et al. 1976 

Geckler, et al. 1976 

Tram, 1956 

Turnbull. et al. 1954 

Stebblng, 1976 

Mcwe A Stebblng, 

1976 

Karbe, 1972 

Wllanovlch, tit al, 

1976 

McLusky 1 Phi I I Ips, 

1975 

Pesch 4 Worgan, 1978 

Pusch 6 Morgan, 1978 

U.S. EPA, 1980 

U.S. WA, 1980 

Calabrase, et al. 

1977 

B-63 
Table 4. aontlnued) 

-It 

!yp/l) 

a32 

ournt loa 

Black Zion*, 4 days 

ueckodl I 

Red ahIp% 

HDllotls rutescubr 

hrthur quahaug (Iwva) 

blucmarIn aoqenarla 

s&t slml Iod clam, 

5 afmnarla 

Musse I, 

Mytl lus edul Is 

Channeled whelk, 

Fiusycon canallculatum 

kid snail, 

Nasser lus cbsoletus 

Calanold ccbpepad, 

Acart la clausl 

-- 

Calanold copepod, 

Acartla tonsa 

-- 

QWW. 

Metrldla pacltlcs 

-popDd, 

Phlalldaum sp. 

Calanold copepod, 

Acartle tonsa 

-- 

CopePod, 

Euchaeta aar lna 

Erred 

llIrtopathologlcal 

glll l bwulltlms 

Hlrtopatholaglcal 

gIlI l bMwulltl~ 

50% w-tallty 

Reteruce 

Mwtln, at al. 1971 

4 lklys ,32 Wtln, at al. 1977 

a-10 days 

71 days 

30 Calebre6e, l t al. 

I977 

Shuster 4 Prlngle, 

I%6 

Elrlar, 1977 

53s un-tal Ity 25 

7 days 50$ oortallty 35 

1 days 

77 days 

sol mortality Scott 4 Ma&r, 1972 

50s mortal lty 470 Better & Yevlch, 1915 

3 days Decrease In oxygen 

consumpt ICNI 

50% mortality 

IO0 Maclnnes 6 Ttburberg, 

I973 

2 days 34-82 Mwa I taw 

AposlololKlu IOU, 1978 

Sosnouskl, et sl. 

1979 

Raave, et al. 1976 

6 days 50s mortallty 9-73 

24 h-s 

24 hrs 

24 Ius 

24 lus 

lc50 I76 

Lao 34 Reeve, et al. 1976 

lx50 104-31 I fbeve, et sl. 1976 

IX50 I88 Reeve, et al. 1976 

B-64 
Tablw 6. woatlaud~ 

Speclos 

W-pod, 

Undlnula vulqarls 

gep&y’~ 

Rot1 fu, 

&acblonus pllcatllls 

ctenophore, 

Wnerlopsls ucrodyl 

Ctenophore, 

Pleurobrachla pl leus 

Larval annol Ids, 

Mlxed speclaa 

Chaetognat h, 

Sayltta hlsplda 

Shrlep, 

Euphausla pacltlca 

CopePod. 

Labldocera scott I 

Aaerlcan lobster, 

-us amm-lcMus 

Coral-met achlnold, 

Echlnorretra mtbael 

Sea urchin, 

Arbacla punctulata 

Sea urchin, 

Paracentrotus I Ivl bus 

-1cw, 

Fundulus hetamclltus 

ouratlon 

24 lus 

24 h-s 

24 hrs 

24 lu-s 

24 lrs 

24 h-s 

24 hs 

24 hs 

24 lus 

I3 days 

4 days 

4 days 

21 days 

Rmsult 

litted h/l 1 

LC50 192 

LC50 40 

LC50 100 

LCM 17-29 

Ia0 33 

LC50 89 

LC50 43-460 Ueuve, et al. I916 

ImQ 14-30 

Lc50 I32 

50% mortal Ity 56 

Supprerslon ot 

larval skeletal 

dav*loprent 

20 

56Y docrease In 

spera mtlllty 

300 

Retardat Ion ot 

gouth ot pluteal 

larvae 

IQ-20 

tllstopathologlcaI 

I es Ions 

600 

Rotwonce 

Reeve, et al. I976 

Reeve, et al. 1976 

f&eve, et al. 1976 

Reeve. et al. 1976 

f&eve, et al. 1976 

Reeve, et al. 1976 

Uewe, et al. 1916 

Reeve, et al. 1976 

McLeese, 1974 

lies I Inga, 1976 

young & Nelscm, 1974 

aougls, 1965 

Gardner A la Hoche, 

I973 

B-65 
spadu 

-b=hog, 

PfldJgu~ betuocl I tus 

Mloatlc rl Iverslda, 

baldlo mmldls 

-- 

Paclflc herrIng (fwryo), 

Clupea harwqus pllssl 

Pacltlc brrlng (Iuva), 

Clupea harengur pallasl 

Atlmtlc aeflhaden, 

Brevooftls tyrannus 

Spot, 

1 elostmus x.anlhuc us 

At Iant Ii croaker, 

MIcropagan undulate 

Pint Ish, 

Laqodon rhcnboldoa 

Plslce, 

Pleuronectes platessa 

Y Inter t lounder. 

PS8Udop l8UWW3Ci8S 

amerICMU5 

Alga, 

Lamlnerls hyperborla 

Durst loa 

4 days 

4 days 

6 hays 

2 days 

14 days 

I4 dqa 

I4 days 

14 days 

4 days 

I4 days 

28 days 

50s l ortal 

50s -till 

50s llKu-talliy 

IQ 

IQ 

50s lnortallty 

501 mtallty 

HlstopaiholoyIc~l 

les Ions 

Result 

tPQ/l, 

600 

Gardner b LoHocht,, 

1973 

610 Engel, et al. 1976 

160 Engel. et al. 1916 

210 Qel, et al. 1916 

I50 Lngol, et ,al. 1976 

750 Wmard, et al. 1975 

I60 Baker, 1963 

tttwt 

Enzyme InhIbItIon 

HlstopatholoyICaI 

IOSlOWi 

InCIplent LC50 

lnClpl8nt LC50 

Grath decrease 50 Hopkins d Krtln, 1971 

l Olssolv8d Copper; no other medsuremfmt reported 

3-66 
REFERENCES 

Adema, D.Y.M. and A.M. Degroot-Van Zijl. 1972. The influence of copper on 

the water flea Daphnia magna. TN0 Nieuws. 27: 474. 

Anderson, 3.G. 1343. The apparent thresholds of toxicity to Oaphnia magna 

for chlorides of various metals when added to Lake Erie water. Trans. Am. 

Fish. Sot. 78: 96. 

Anderson, R.L, et al. 1980. Survival and growth of Tanytarsus dfssimilis 

(Chironomidae) exposed to copper, cadmium, zinc, and lead. Arch. Environ. 

Contam. Toxicol. 9: 329. 

Andrew, R.W. 1976. Toxfcity Relationships 

Waters. &: Toxicity to 6fota of Metal Forms 

Cormr. Windsor, Ontario, Canada. p.127. 

to Copper Forms in Natural 

in Natural Water. Int. Joint 

Andrew, R.W., et al. 1977. Effects of inorganic complexing on toxicity of 

copper to Daphnia magna. Water Res. 11: 309. 

Arthur, J.W. and E.H. Leonard. 1970. Effects of copper on Gamnarus pseudolinnaeous, Physa Integra, and Campeloma decisum in soft water. Jour. Fish. 

Res. Board Can. 27: 1277. 

8aker, J.T.P. 1969. Histological and electron microscoofcai observations 

on copper poisoning in the winter flounder (Pseudopleuronectes americanus). 

Jour. Fish. Res. 8oard. Can. 26: 2785. 

B-67 
3drtlett, L., et al. 1974. Effects of cxoer, .zjflc, and :aCm~ .m ;n 

Selanastrgm caoricornutum. Water Res. 8: 179. 

3enoit, D.A. 1975. Chronic effects of copper on survival, growth, and reproduction of the bluegill (Lepomis macrochirus). Trans. Am. Fish Sot. 

104: 353. 

Betxer, 5.8. and P.P. Yevich. 1975. Copper toxicity in Busycon canaliculatun l.. 8101. Bull. 148: 16. 

-- 

Bfesfnger, K.E. and G.M. Christensen. 1972. Effects of various fletals on 

survival, growth, reproduction, and metabolism of Oaphnia magna. Jour. Fish 

Res. Board Can. 29: 1691. 

Birdsong, C.L. and J.W. Avavit, Jr. 1971. Toxicity of certain chemicals to 

juvenile pompano. Prog. Fish. Cult. 33: 76. 

Birge, W.J. and J.A. Black. 1979. Effects of Copper on Embryonic and Juvenile Stages of Aquatics Animals. &: J.O. Nriagu (ed.), Copper in the 

Environment. J. Wiley and Sons, New York. 

Eougis, P. 1965. Effect of copper on growth of the pluteus of the sea urchin (Paracentrotus lividus). C.r. hebd. Seanc. Acad. Sci., Paris. 

260: 2929. 

Bringmann, G. and R. Kuhn. 1959. Comparative water-toxicology 

tlons on bacteria, algae, and Daphnids. Ges. Ind. 80: 115. 

invest iga- 
Srjqgmann, C. and ?. Kuhn. 1377. Conditions of tCXiCity #Jf dater-s3\>bie 

substances against 3aphnia magna. Z.f, WasseT und Abwasseriorschung. 

10: 151. 

Brown, B.T. and B.M. Rattigan. 1979. Toxicity of soluble copper and other 

metal ions to Elodea canadensis. Environ. Pollut. 19: 303. 

Brown, V.B. 1968. The calculations of the acute toxicity of mixtures of 

ooisons to rainbow trout. Water Res. 2: 723. 

Brown, V.M. and R.A. Oalton. 1970. The acute toxicity to rainbow trout of 

mixtures of copper, phenol, zinc, and nickel. Jour. Fish. Biol. 2: 211. 

born, V.M., et al. 1974. Aspects of water quality- and toxicity of copper 

to rainbow trout. Water Res. 8: 797. 

8rungs, W.A., et al. 1973. Acute and long-term accumulation of copper by 

the brown bullhead (tctalurus nebulosus). Jour. Fish Res. 8oard Can. 

30: 583. 

bungs, W.A., et al. 1976. Acute and chronic toxicity of copper to the 

fathead minnow in a surface water of variable quality. Water Res. 10: 37. 

Buikema, A.L., et al. 1974. Evaluation of Philodina acutacornis (rotifera) 

as a bioassay organism for heavy metals. Water Res. Bull. 10: 648. 

B-69 
Buikema, A.L., et al. 1977. Rot'fer sensitivity '0 combinations of inorganic water PO1 lutants. Bull. 92 - Virginia Mater Resour. ?es. Center, 

Blacksburg, Virginia. 

Cabejszek, I. and M. Stasiak. 1960. Studies on the influences of some 

metals on water biocenosis employing Oaphnia magna. Rozniki Panst. Zakl. 

Hig, ilarsar. 11: 303‘ 

Cairns, J., et al. 1978. Effects of temperature on aquatic organism sensitivity to selected chemicals. 3~11. 106 - Virginia Water Resour. Res. 

Center, Blacksburg, Virginia. 

Cairns, J., et al. 1979. Invertebrate response to thermal shock following 

exposure to acutely sub-lethal concentrations of chemicals. Arch. Hydriobiol. 77: 162. 

Calabarese, A., et al. 1973. The toxicity of heavy metals to embryos of 

the American oyster Crassostrea virginica. Mar. 8iol. 18: 162. 

Calabrese, A., et al. 1977. Survival and growth of bivalve 1 arvae under 

heavymetal stress. Mar. 6iol. 41: 179 

Calamari, 0. and R. Marchetti. 1973. The toxicity of mixtures of metals 

and surfactants to rainbow trout (Salmo gairdneri Rich.), Water Res. 

7: 1453. 

s-70 
Calanari, 0. and q. Marchetti. 2975. Predicted and observed acute toxicity 

of copper-and ammonia to rainbow trout (Salma gairdneri i7icfr.). Prog. Water 

Tech. 7: 569. 

Chakoumakos, C., et a?. 1979. The toxicity of copper to rainbow and cutthroat trouts under different conditions of alkalinity, pH and hardness. 

Env. Sci. Tech. 13: 213. 

Chapman, G.A. 1978. Toxicities of cadmium, copper and zinc to four juvenile stages of chinook salmon and steelhead. Trans. Am. Fish Sot. 107: 841. 

Chapman, G.A. and J.K. McCrady. 1977. Copper Toxicity: A Question of 

Form. 2: Recent Advances in Fish Toxicology, a Symposium. EPA 

600/3-77-085. U.S. Environ. Prot. Agency, p. 132. 

Chapman, G.A. and D.G. Stevens. 1978. Acute lethal levels of cadmium, copper and zinc to adult male coho salmon and steelhead. Trans. Am. Fish Sot. 

107: 837. 

Chapman, G.A., et al. Effects of water hardness on the toxicity of metals 

to Daphnta mapna. (Manuscript). 

Chynoweth, D.P., et al. 1976. Effect of Organic Pollutants on Copper Toxicity to Fish. & foxlc4ty to Biota of Metal Forms in Natural Water. Int. 

Joint Corm., Windsor, Ontario, Canada. p. 145. 

8-71 
Clendenning, K.A. and W.J. North. 1959. Effects of ilastes on the Giant 

kelp, Macrocystis pyrifer. In: E.A. Pearson, (ed.), Proc. 1st Int. Conf. 

Waste Oisposal in the Yarine Environment. Berkeley, California. 

Connor, P.M. 1972. Acute toxicity of heavy metals to some marine larvae. 

Mar. Pollut. Bull. 3: 190. 

Cope, 0.8. 1966. Contamination of the freshwater ecosystems by pesticides. dour. Aopl. Ecol. 3 (Suppl.): 33. 

Donaldson, E.M. and H.M. Oye. 1975. Cortfcosteriod concentrations in sockeye salmon (Oncorhynchus nerka) exposed to law concentrations of capper. 

Jour. Fish Res. Board Can. 32: 533. 

Drumnond, R.A., Ct al, 1973. Some short-tam jndfcatots of sublethal effects of copper on brook trout, Salvelinus fontlnalis. Jour. Fish Res. 

Board Can. 30: 698. 

Eisler, R. 1977. Acute toxicities of selected heavy metals to the softshell clam, Mya arenaria. Bull. Environ. Contam. Toxicol. 17: 137. 

Elder, J.F.. and A.J. Horne. 1973. Copper cycles and CuSo4 algjcidal 

capacity in twu California lakes. Environ. Manage. 2: 17. 

Engel, O.'r(., et al. 1976. Effects of copper on marine eggs and larvae. 

Environ. Health Perspect. 17: 287. 

0-72 
Erickson, s.;. 1972. Toxicity of coo[;er to Thallassiosira pseudofiana 'I0 

unenriched inshore seawater. Jour. Phycology. 34: 318. 

Erickson, S.J., et al. 1970. A screening technique for estimating copper 

toxicity to estuarine phytoplankton. Jour. 'dater Pollut. Control Fed. 42, R 

270. 

Fogels, A. and J.3. Sprague. 197?. Comparative short-term 

zebrafish, flagfish, and rainbow trout to five poisons includ 

reference toxfcants. Water Res. (GA.) 11: 811. 

tolerance of 

ing potential 

Folmer, L.C. 1976. Overt avofdance reaction of rainbow trout fry to nine 

herbicfdes. Bull. Environ. Cont. Toxicol. 15: 509. 

Gachter, R., et al. 1973. Complexing capacity of the nutrient medium and 

its relation to inhibition of algal photosynthesis by copper. Schweit. 

Zeits. fur Hydra?. 35: 252. 

Gardner, G.R. and G. LaRoche. 1973. Copper induced lesfons in estuarine 

teleosts. Jour. Fish. Res. Board Can. 30: 363. 

Geckler, J.R., et al. 1976. Validity of laboratory tests for predicting 

copper toxicftj in streams. EPA 600/3-76416. U.S. Environ. Prot. Agency. 

Goettl, J.P., et al. 1972. Water pollution studies. Colorado Fish. Res. 

Rev. No. 7, 36, Dir. Game, Fish. Parks, Fort Collins, Colorado. 

B-73 
Grande, M. 1966. Effect of cooper and zinc on salmonid fishes. Adv. 'AatetPollut. Res. 1: 97. 3rd Conf. yunich. 

Hale, J.G. 1977. Toxicity of metal mining wastes. Bull. Environ. Contam. 

Toxicol. 17: 66, 

Hara, T., et al. 1976. Effects of mercury and copper on the olfactory response in rainbow trout, Salmo qairdneri. Jour. Fish. Res. Board Can, 

33: 1568. 

Hazel, C.R. and S.J. Meith. 1970. Bioassay of king salmon eggs and sac fry 

in copper solutions. Calif. Fish Game. 36: 121. 

Herbert, D.W.M. and J.M. Vandyke. 1964. The toxicity to fish of mixtures 

of poisons. II. copper - amnonia and zinc - phenol mixtures. Ann. Appl. 

8101. 53: 415. 

Heslinga, G.A. 1976. Effects of copper on the coral-reef echinoid Echinometra mathael. Mar. Biol. 35: 155. 

Holland, G.A., et al. 1960. Toxic effects of organfc and inorganic pollutants on young salmon and trout. State of Washington - Dep. Fish. Res. 

Bull. 5: 223. 

Hopkins,. R. and J.M. Kain. 1971. The effect of marine pollutants on 

Lamfnarea hyperboria. Mar. Pollut. Bull. 2: 75. 

3-74 
doming, Y.3. 3nd T.J. Neiqeisel. 1979. 

bluntnose minnow (Pimephaies notatus Raf 

Toxicol. 8: 545. 

Chrcfl i 

inesoue) 

Howarth, R.S. and J.8. Sprague. 1978. Cooper lethality to rainbow trout in 

waters of various hardness and pH. Water Res. 12: 455. 

HuSshnan, J.9. 1967. Effects of copper on the crayfish Crconectes rusticus 

(Girard): I. Acute toxicity. Crustaceana. 12: 33. 

Hughes, J.S. 1971. Tolerance of Strfped Bass, Motone saxitalis (Walbaum) 

Larvae and Fingerlings to Nine Chemicals Used in Pond Cultures. In: Proc. 

24th Ann. Conf. S.E. Assoc. Game Fish. Comn. p.431. 

Hughes, 3.5. 1973. Acute toxicity of thirty chemicals to striped bass 

(Morone saxitalis). Presented at Western Assoc. State Game Fish. Comm., 

Salt Lake City, Utah. 

Jackim, E. 1973. Influence of lead and other metals on aaminolevulinate 

dehydrase activity. Jour. Ffsh. Res. Board Can. 30: 560. 

Johnson, M. and J.H. Gentile. 1979. The acute toxicity of copper, cadmium, 

and mercury to larval American lobster Homarus americanus. Environ. Contam. 

Toxicol. 22: 258. 

G-75 
Jones, L.H., et al. 1976. Some effects of Salinity on the toxicity of copper to the polychaete Nereis diveriscolor. Estuarine Coastal Mar. Sci. 

4: 107. 

Karbe, L. 1972. Marine hydroiden als testorganismen zur prufung der toxizitat von abwasserstoffen. Dfe wfrkung van schwemetallen auf 'kolonien von 

Eirene viridula. Mar. Biol. 12: 315. 

Lett, P.F., et al. 1976. Effect of copper on some aspects of the bioenergenetics of rainbow trout. Jour. Fish. Res. Board Can. 33: 1335. 

Lewis, M. 1978. Acute toxicity of copper, zinc, and manganese in single 

and mixed salt solutions to juvenile longfin date, Agosia. chrysogaster. 

Jour. Fish Bfol. 13: 695. 

Lewis, 5.0. and W.M. Lewis. 1971. The effect of zinc and copper on the osmolarity of blood serum of channel catfish, Ictalurus punctatus Raf., and 

golden shiner, Noternfgonius crysoleucas Mitchell. Trans. Pm. Fish. Sot. 

100: 639. 

Lind, O., et al. Regional copper-nickel study. Aquatic toxicology progress 

report. (Manuscript). 

Lloyd, R. 1961. The toxicity of mixtures of zinc and copper sulphates to 

rainbow trout (Salmo qafrdntrl R.). Ann. Appl. Biol. 49: 535. 

9-76 
Lam, H.Y. and 8.P. McPherson. 1976. Effects of copper or zinc in fresh 

water or the adaptation to sea water and ATPase activity and the effects of 

copper on miqatoty disposition of coho salmon. Jour. Fish. Res. Board Can. 

33: 2023. 

MacInnes, J.R.. and F.P. Thurberg. 1973. Effects of metals on the behavior 

and oxygen consumotdon of the mud snail. Mar. Poll&. Bull. 4: 1895. 

Majori, L. and F. Petronfo. 1973. Marine pollution by metals and their accumulation by biological indicators (accumulation factor). Rev. Int. Oceanogr. Med. Tomes XXXI. 

Martin, M., et al. 1977. Copper toxicity experjments in relation to abalone deaths observed In a power plant's cooling waters. Calif. Fish. Game. 

63: 95. 

McKim, J.M. and O.A. Benott. 1971. Effects of long-term exposures to copper on survival, growth, and reproduction of brook trout (Salvelinus fontinalis). Jour. Fish. Res. Board Can. 38: 655. 

McKim, J.M., et al. 1970. Changes in the blood on brook trout (Salvelinus 

fontfnalis) after short-term and long-term exposure to copper. Jour. Fish. 

Res. Board Can. 27: 1883. 

McKIm, J.M., et al. 1978. Metal toxicity to embryos and larvae of eight 

species of freshwater fish. - II. Copper. Bull, Environ. Contam. Toxicol. 

19: 608. 

e-77 
UcLeese, 3.i. 1374. Tzxicjty Of scooper at two temperatures 3r.d :nree 

salinities to the American lobster (IJomarus americanus), dour. Fish. ?es. 

goard Can. 31: 1949. 

McLusky, O.S. and C.N.K. Phillips. 1975. Some effects of copper on the polychaete Phyl:odoce maculata. Estuarine Coastal Mar. Sci. 3: 103. 

MI ! accv: c,. , 

.h CO t ., ., et al. 1976. Uptake of cupper by the polychaete Cirrifornria spirabranchia in the presence of dissolved yellow organic matter of 

natural origin. Estuarine Coastal Mar. Sci. 4: 585. 

Miller, T.G. and W.C. McKay. 1980. The effects of hardness, alkalinity and 

pH of test water on the toxicity of copper to rainbow trout (SdlmO qairdneri). Water Res. 14: 129. 

Fcinicucci, 0.0. 1971. Flow effects in aquatic bioassays the toxicity of 

copper at various flow rates to the guppy, Lebistes reticulatus. Ph.D. 

Thesis. Univ. of Michigan. 

Moore, M.N. and A.R.O. Stebbing. 1976. The quantitative cytochemical effects of three metal ions on the lysosomal hydrolase of a hydroid. Jour. 

Var. Viol. Assoc. 56: 995. 

Moraitou4postolopoulou. 1978. Acute toxicity of copper to a copepod. 

Yar. Poll. Sull. 9: 278. 

B-78 
Fount, 0.1. 1968. Chronic toxicity of cooper to fathead nrinnows (?i;reohales Dromelas Rafinesquej. Water Res. 2: 215. 

Mount, 0.1. and C.E. Steohan. 1969. Chronic toxicity of copper to tne fathead .Tinnow (Pimephales promelas) in soft water. Jour. Fish. Res. Board 

Can. 26: 2449. 

Nebeker, A.V. and A.R. Gaufin. 1964. Bioassays to determine pesticide toxicity to the amphipod crustacean (Gamnarus lacustrfs). Proc. Utah Acad. 

Sci. 41: 64. 

Nehring, R.B. 1976. Aquatic insects as biotogical mon 

pollution. Bull. Environ. Contam. Toxicol. 15: 147. 

itors of heavy meta 

O'Hara, J. 1971. Alterations in oxygen consumption by bluegills exposed to 

sublethal treatment with copper. Water Res. 5: 321. 

Okazaki, R.K. 1976. Copper toxicity in the Pacific oyster Ctassostrea 

gigas. Bull. Envir. Contam. Toxicol. 16: 658* 

Patrick, R., et al. 1968. The relatfve sensitivity of diatoms, snails, and 

fish to twenty CORW~ constituents of industrial wastes. Prog. Fish,-Cult. 

30: 137. 

Pesch, C.E. and 0. Morgan. 1978. Influence of sediment in copper toxicity 

tests with polycfraete Neanthes arenaceodentata. Water Res. 12: 747. 

B-79 
?hil?ips, O.J.H. 1375. The common nussel Yytilus edulis as an indicator of 

pollution by zinc, cadmium, lead and copper. I. Effects of environmental 

variables on uptake of metals. "ar. Viol. 38: 59. 

Pickering, Q.H. and C. Henderson. L966. The acute toxicity of some heavy 

metals to different species of warmwater fishes. A+ Water Pollut. Int. 

Jour. 10: 453. 

Pickering, Q.H., et al. 1977. Effect of exposure time and copper concentration on reproduction of the fathead minnow (Pimephales promelas). Water 

Res. 11: 1079. 

Reeve, W.R., et al. 1976. A Controlled Environmental Pollution Experiment 

(CEPEX) and Its Usefulness in the Study of Larger Marine Zooplankton under 

Toxic Stress. In: P.M. Lockwood fed.), Effects of Pollutants on Aquatic 

Organisms. Cambridge, Univ. Press, New York. p. 145. 

Rehwoldt, R., et al. 1971. Acute toxicity of copper, nickel, and zinc ions 

to some Hudson River fish species. 8~11. Environ. Contam. Toxicol. 6: 445. 

Rehwoldt, R., et al. 1972. The effect of increased temperature upon the 

acute toxicity of sane heavy metal ions. Bull. Environ. Contam. Toxicol. 

8: 91. 

Rehwoldt, R., et al. 1973. The acute toxicity of some heavy metal ions toward benthic organisms. Bull. Environ. Contam. Toxical.. 10: 291. 

B-80 
?ice, DA,, Lr. and F.L. Yarrison. 1977 I Copper sensitiviry of S3~;~i:: 

herring, C!upca harmgus pallasi, during its early life .history. Fish. 2es. 

Bull. 76: 347. 

Riley, J.?. and I. Roth. 1971. The distribution of trace elements in some 

species of phytoplankton grown in culture. Jour. Yar. Biol. Assoc. 51: 53. 

Rosko, J.J. and J.W. Rachlin. 1975. The effect of copper, zinc, cobalt and 

manganese on the growth of the marine diatom Nitzschia closterium. 8~11. 

Torrey Bot. Club. 102: 100. 

Rosko, J.J. and J.iJ. Rachlin. 1977. The effect of cadmium, copper, mercury 9 zinc and lead on cell division, growth and chlorophyll d content of 

the chlorophyte Chlorella vulgaris. Bull. Torrey Bat. Club. 104: 226. 

Saifullah, S.M. 1978. Inhibitory effects of copper on marine dinoflagellates. Mar. Viol. 44: 299. 

Sakaguchi, T., et al. 1972. Uptake of copper by Chlorella regularis. Nippon Nog. Kag. Kaishi. 51: 497. 

Sauter, S., et al. 1976. Effects of exposure to heavy metals in selected 

freshwater fish, toxfcity of copper, cadmium, chromium and lead to eggs and 

fry of seven fish species. EPA 600/3-76-105. U.S. Environ. Prot. Agency. 
Saward, a., et 31. :975. ExQer'Rental stlldies on tye effects of copoer on 

3 narine food chain, Mar. 8iol. 29: 351. 

Scott, D.M. and C.!4. Major. 1972. The efcect of copper (II) on survival, 

pespiration, and heart rate in the comnon blue mussel, Mytilus edulis. 

Eiol. 81~11. 143: 679. 

Shaw, T.L. and V.H. Grown. 1374. The toxicity of some forms of copper to 

rainbow trout. Water Res. 8: 377. 

Shuster, C.N., Jr. and 8.H. Pringle. 1968. Effects of trace metals on estuarine molluscs. Proc. 1st MidAtlantic Ind. Waste Conf., Nov. 13-15, 1967. 

Shuster, C,N., Jr. and 0.H. Pringle. 1969. Trace metal accumulation by the 

American eastern oyster, Crassostrea virginica. Proc. Natl. Shellfish. 

Assoc. 59: 91. 

Sosnowski, S.L. and J.H. Gentile. 1978. Toxicological comparison of 

natural and cultured populations of Acartia tonsa to cadmium, copper and 

mercury. Jour. Ffsh. Res. Board Can. 35: 1366. 

Sosnowski, S.L., et al. 1979. The effect of nutrition on the response of 

field populations of the calanoid copepod Acartia tonsa to COQQer. Water 

Res. 13: 44% 

Soear, p. 1977. Cooper accumulation kinetics and lethal tolerance in relation to fish size. Y.S. Thesis. Concordia Univ., Montreal, Canada. 
Sorsgue, d.3. 1964. Lethal :oncevtra:ions of cooDer 3~d zirc for jo~,ng Itlantjc salmon. dour. Fish, Res. Soard Can. 31: 17. 

Sprague, J.B. and B.A. Ramsay. 1965. Lethal levels of mixed copper-tire 

solutions for juvenile salmon, Jour. Fish. Res. Board Can. 22: 425. 

Stanley, 8.A. 19?4. Toxicity #2f be3aiy metals and salts to euras 

;nilfoil (Myriophyllm spicatus L.). Ai-ch. Environ. Contan. Toxic01 

an water2: 33i. 

Stebbing, A.R.D. 1976. The effects of low metal levels on a clonal hydroid. Jour. Mar. Biol. Assoc. 56: 977. 

Steemann-Melsen, E. and H. Bruun-Laursen. 1976. Effect of CuC04 on the 

photosynthesis rate of phytoplankton in four Danish lakes. Oikos. 27: 239. 

Steemann-Nielsen, E. and L. Kemp-Nielsen. 1970. Influence of de 

concentrations of copper on the growth of Chlorella pyrenoidosa. 

Plant. 23: 828. 

leter 

Phys 

i ous 

iol. 

Steemann-Nielsen, E. and 5. tlium4ndersen. 1970. Copper ions as poison in 

sea and in freshwater. Mar. 8iol. 6: 93. 

Stokes, P. and T.C. Hutchinson. 1976. Cooper Toxicity to Phytoplankton, as 

Affected by Organic Ligands, Other Cations and Inherent Tolerance of Algae 

to Copper. &: Toxicity to Biota of Vet31 Furms in Natural Water. Int. 

Joint Corm., Windsar, Ontario, Canada. 3. 1591 
c3r~uell, S.V. 3rd C. qenderson. :960. Toxicity of :ess common -et-Z:s '3 

fjshes. !nd. 'rlastes. 5: 12. 

-rama, E.8. 1954. The toxicity of copter to the common bluegill (Lepomis 

machrocnirus Rafinesaue). Notulae Natur. No. 257. p. 1. 

'sai, C. and J.A. McKee. 138C. Acute toxicity to goldfish of mjxtures of 

chloramines, copper, and linear a:%ylate sulfonate. Trans. Am. Fish. Sot. 

lC9: 132. 

Turnbull, Ii., et al. 1954. Toxicity of various refinery materials to 

freshwater fish. Ind. Eng. Chem. 46: 324. 

U.S. E?A. 1980. Unpublished Laboratory data. Environ. Res. Lab.-Narragansett, Rhode Island. 

Ualbridge, C.T. 1977. A flow-through testing procedure with duckweed, 

ILemna minor L.). EPA 60013-77-108. U.S. Environ. Prot. Agency. 

-- 

Wallen, I.E., et al. 1957. Toxicity to Gambusia affinis of certain pure 

chemicals in turbid waters. Sew. Ind. Wastes. 29: 695. 

Warnick, S.L. and H.L. Bell, 1969. The acute toxicity of some heavy metals 

to different species of aauatic insects. Jour. Water Poll. Control Fed. 

41: 280. 
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 variable concentrations. 

From 1955 to 1958 the annual United States production of recoverable copper was about 900,000 metric tons. By 1975, the production 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). 

Human exposure to copper can occur from water, food, and air, 

and through direct contact of tissues with items that contain copper. 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. 

Schroeder, et al. (1966) place considerable emphasis on drinking water as a source of copper. They reported that the mean values 

of copper in human livers (56 cases) from Dallas, Denver, and Chicago varied from 410 to 456 μg/g of ash, and that the mean value 

C-1 
from Miami was 578 μg/g of ash1. The municipal water supplies of 

these cities each provided relatively hard potable waters with measured hardness ranging from 75 to 125 mg/l. On the other hand, 143 

human livers from seven cities with relatively soft waters ranging 

from 10 to 60 mg/l had mean levels of copper varying from 665 to 816 

μg/g of ash. Of the cases from soft water areas, 37.1 percent had 

hepatic copper of 700 or more μg/g of ash, compared with only 14.3 

percent of the samples from the hard water cities. Of the 56 individuals from three cities with the hardest water, only two showed 

such high values. Unfortunately no studies were made of cities 

with very hard water. 

lie in the ability of calcium or magnesium ions in hard water to 

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 

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. 

1 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 Flowing through Copper Pipes ah 

Item w/1 

Spring water, Brattleboro, Vermont, mountain 

Municipal water, soft, Brattleboro 

Brook, inlet to reservoir 

Reservoir, lake 

water, main end 

Hospital, at tap 

cold, running 30 min 

hot, running 30 min 

cold, standing 12 hr 

cold, standing 24 hr 

Spring water, soft, private houses, Brattleboro, 

Vermont, at tap 

No. 1 from spring, unpiped 

running 30 mfn 

cold, standing 24 hr 

hot, standing 24 hr 

No. 2 

No. 3 

Well water, private houses, Windham County, at tap 

No. 4, hard 

No. 5, hard 

No. 6, hard 

No. 7, hard, at well 

at tap 

No. 8, soft 

1.2= 

16 

55 

150 

170 

440 

550 

730 

2.8' 

190 

1,400 

1,460' 

1,240 

75 

36 

4.4c 

40 

4= 

36' 

278 

'Source: Schroeder, et al. 1966. 

b Water 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 

evaporating L liter water. 

c-3 
Zadjiznarkos (:367), on the csntrary, sugqested c,hat drinking 

water may be only a minor source of copper. He reported that the 

mean drinking water concentration of copper is 0.029 mg/l, which 

could nean a daily intake of 58 pg 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 difference in location. However, it is difficult to pinpoint local CODper concentrations in drinking water sources, since the only readily 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 individual, 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/l [U.S. Department of Health, Education and Welfare (U.S. HEW), 19701. The highest concentration 

reported was 8,350 ug/l; a little over 1 percent of the samples exceeded the drinking water standard of 1 mg/l. 

The 1 mg/l copper standard was established not because of toxicosis but because of the taste which develops with higher levels 

of copper in the water (U.S. HEW, L970). It is most commonly exc-4 
ceeded in soft water that is acidic in nature; however, it is rare 

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 Adm., 1968) l For this reason, regulatory aqenties have not treated copper in public water supplies as a siqnificant problem. In New York City, Copper is intentionally added to 

the water suPPlY to maintain a concentration of 0.059 mq/l 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 COppet concentration to cause acute copper 

toxicosis (see Acuter Subacute, and Chronic Toxicity section); however, because of taste problems, modern equipment does not contain 

copper conduits. 

The national impact of a water-borne contribution of copper is 

df f f icult to detect, predict, or evaluate because information is 

either absent or irretrievable. The current trend for recycling 

warta (animal wastes, sewage solids and liquids, channel dredging, 

and indurtrial warts) to the land offers very real possibilities 

that inbrlancw in organisms may unwittingly be created, because 

much wastes are comaonly high in trace element concentration0 

T)Ieu trace l Lraents my directly alter crop production and indirwtly affmt the conrumer (Patterson, 1971). 

Anotbae source of copper in water is the use of copper sulfate 

to control alga.. Some idea of the distribution of copper sulfate 

WY be Wind fra th work of Button, et al. (1977), who applied 

9rrnufar CoPPer sulfate to the surface of Koover Reservoir, FrankC-S 
lin County, Ohio. Soluble and particulate cupric copper concentrations at several depths were measured by atomic absorption spectrophotometry 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 qms of copper sulfate per square meter were 

added to the surface. Most of the copper sulfate was dissolved in 

tke first 1.7s 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 qms 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 vq/q to 

as high as 400 pg/q (McCance and Widdowson, 1947; Schroeder, et al. 

1966). fln an "as-cooked and as-served" basis, calves' liver, oysters, and many species of fish and green vegetables have recently 

been classed as unusually good source3 of copper (more than 100 ~q 

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 feeding to swine diets that are high (up to 250 pq/q) in copper in order 

to increase daily weiqht 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 ugnoo b 

calories 

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 

=39 Yolk 

Egg white 

Dried skimmed milk 

Whole milk, dairy 1 

Whole milk, dairy 2 

Butter, salted 

Mean 

3.33 

0.48 

137.05 

1.12 

1.70 

0.81 

0.58 

0.51 

3.40 

694 

100 

27,410 

38 

85 

4'1 

42 

297 

1.49 167 

11.00 

0.42 

0.83 

5.30 

3.90 

3.72 

0.95 

7.13 

1.99 

3.92 

2.44 

1.70 

2.39 

0.26 

0.12 

3.92 

L.76 

769 

34 

21 

441 

130 

260 

384; 

99 

249 

70 

460 

63 

cii 

49 

‘Source: Schroeder, et al. 1966 

bdaloric values of foods from R.A. McCance and E.M. Widdowson, 

1947 

V.I. - indicates that the sample came from St. Thomas, Virgin 

Islands. 

c-7 
TABLE 2 (cont.) 

Copper in Foods 

Item w/g ug/loo b 

calories 

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, Macfntosh 

Mean, excluding coconut seed 0.82 

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 

70 

410 

181 

75 

i:: 

1.0:: 

663 

32 

1,487 

143 

453 

187 

600 

70 

470 

257 

40 

205 

344 

350 

567 

929 

362 

86 

265 

100 

278 

182 

c-a 
TABLE 2 (cont.) 

Copper in Foods 

Item u9/9 ug/loo b 

calories 

Grains and cereals 

Wheat seed 

Wheat, whole 

Wheat germ 

Wheat head, chaff and stalk 

Bread, white 

Bread, whole wheat 

Oats, whole 

Corn, No. 1 

Corn, No. 2 

Rye, No. 1 

Rye, No. 2 

Rye, dry, flour 

Benzene extract 

Residue 

Barley 

Buckwheat 

Rice, brown, U.S. 

Rice, Japanese, polished 

Bengal gram, India, 1 

Bengal gramr fndia, 2 

Grapenuts 

Millet 

Doughnut, cream filled 

Mean, excluding grapenuts and extracts 

1.09 

2.48 

0.1s 

0.14 

0.19 

0.63 

0.40 

0.46 

0.65 

0.92 

4.12 

4.20 

10.82 

1.87 

3.83 

8.21 

0.47 

3.04 

4.23 

0.56 

14.95 

2.34 

2.32 

2.02 

33 

75 

2: 

ii 

19 

27 

123 

124 

106 

227 

13 

1:: 

16 

415 

67 

66 

58 

C-9 
TXBLE 2 (car.:. 

Copper in Foods 

Item ug/lOO b 

calories 

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 

Chili powder 

Thyme, ground 

Bay leaves (laurel) 

Cloveu, whole 

Ginger, ground 

Ginger, root, V.I. 

Car away seeds 

Vinegar, cider 

Yeast, dry, active 

Molasses 

Sugar, refined 

Yean 

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 

34 

28 

24 

25 

274 

14 

36 

60 

19 

9 

58 

233 

131 

231 

370 

211 

234 

235 

a5 

14 

c-10 
TABLE 2 (cont.) 

Copper in Foods 

Item u9/9 ,&loo b 

calories 

Beverages 

Gin, domestic 

Vermouth, French 

Vermouth, Italian 

Whiskey, Scotch 

whiskey, Bourbon 

Brandy, California 

Bitters, Angocltura 

Wine, domestic, red 

Beer, canned 

Cola 

Grape juice 

Orange drink, carbonated 

Orange juice, packaged 

Coffee, dry, ground 

Coffee, infusion 

Tea, infusion 

Mean, excluding dry coffee 

Miscellaneous 

Chocolate bar, Hershey 

Ice cream, vanilla 

Gelatin, Knox 

Purina laboratory chow 

Aspirin, Squibb 

Saccbar in 

0.03 

0.88 

0.38 

0.35 

0.18 

0.45 

0.75 

0.28 

0.38 

0.38 

0.90 

0.20 

0.89 

2.35 

0.22 

0.31 

0.44 

0.70 

0.29 

3.87 

15.61 

3.12 

5.43 

E 

148 

c-11 
up to 400 to 600 ug/g in the liver. However, Swine will raGidly 

eliminate copper once it is removed from the diet. Sheep also acdumulate 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. 19781. 

Animal and industrial wastes (including sewage solids) commonly 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 Lf the 

yield of crops were reduced or if copper were increased in feed 

products (NILS, 1977). 

The National Academy of Science (1977) noted that the consumption 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 sugarr and honey rarely contain more 

than 0.5 pg copper/g. The nonleafy vegetables and most fresh 

fruits and refined cereals generally contain up to 2 ug/g. Cheese 

(except mental), 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), 19731. 

The refining of cereals for human consumption results in significant losses of copper, although this loss is not so severe as 

it is for iron, manganeser and zinc. Levels of copper in wheat and 

wheat products are given in Tables 3 and 4. 

c-12 
TABLE 3 

Mineral Content of Known Wheats, the Flours Milled from them 

and the Products Prepared from the Flours a& 

Number 

Of 

Samples 

Moisture Ash 

Q 0 (Wper 

PS/S 

Wheat, common hard 

Flour, Baker's patent 

Bread, sponge-dough 

Bread, continuous-mix 

Wheat, common soft 

Flour, soft patent (cake)= 

Cake 

Flour, straight-gradec 

Cracker 

Flour, cut-off (cracker) 

Cracker 

Wheat, Durum 2 10.7 2.03 + 0.01 

Semolina 2 14.7 0.83 T 0.01 

Warcaroni 2 9.6 0.82 z 0.01 

5 

z 

S 

11.0 1.87 + 0.10 

13.9 0.49 Ti 0.03 

36.3 3.39 T 0.19 

35.3 3.42 z 0.30 

10.6 

11.9 

22.8 

11.4 

1::: 

4.5 

1.73 + 0.17 

0.42 T 0.03 

2.71 7 0.11 

0.50 T 0.05 

3.42 T: 0.50 

0.71.T 0.04 

3.09 z 0.34 

5.1 + 0.5 

1.9 7 0.2 

2.3 'i 0.3 

2.0 z 0.2 

4.5 -t 0.5 

1.6 7 0.3 

0.8 T 0.1 

1.6 T 0.2 

1.6 T 0.1 

2.6 + 0.1 

2.4 z 0.1 

4.8 + 0.1 

2.2 T 0.1 

2.5 5 0.1 

%ource: Zook, et al. 1970 

b Mean and standard deviation, dry weight basis. 

'Includes two flours prepared by air classification. 

C-13 
TABLE 4 

Mineral Content of Consumer Products Purchased in Ten Cities a& 

Product 

Total Producers Sampled 

Sample8 Per Model 

Collected Total city city Hoi sture Ash Copper 

No. No. Range No. 0 0 P9/9 

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 

I’$ 

28 

38 

7 l-3 

6 4-6 

3 2-3 

26 2-8 

9.5 l.as + 0.07 

8.0 1.87 T 0.12 

4.8 3.78 + 0.17 

37.8 3.87 i 0.12 

37 

17 

34 

20 

8 

19 

3-9 

;I; 

1-s 

l-4 

3-4 

35.8 

36.7 

33.6 

21.9 

9.8 

12.9 

3.23 t 0.12 2.1 t 0.2 

3.10 T 0.13 2.3 + 0.3 

2.85 ri 0.08 2.5 + 0.2 

2.61 i 0.20 1.7 T 0.2 

4.28 T 0.26 1.6 T 0.2 

0.56 ‘i: 0.03 1.8 + 0.2 

5.3 + 0.2 

6.1 T 0.4 

4.7 7 0.3 

5.1 T 0.5 - 

“Source: Zook, et al. 1970 

b Mean and standard deviation, dry weight basis. 

c-14 
Schroeder, et al. (1966) have suggested that since copper DCcurs 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 copper from food appeared to be 2 to 2.5 my 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 pg/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 suggested 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 adequdte to provide 2 mg of copper 

per day (Klevay, 1977; Klebay, 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 
drinks, water, and snacks, suggesting that food subjected to modern 

processing and preparation methods may be znuch 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 mq 

of copper per day. 

Engel, et al. (1967) conducted studies on young girls which 

indicated that 2 P’; coppet/ cf die t was adequate for good nutrition. Petering, et al. il971) mention that the copper content of 

hair appears to be related to the age of the individual and suggest 

that the need for copper may differ between the sexes. 

Because of the essentiality of copper, the copper balance in 

newborn infants has been examined (Cave11 and Widdowson, 1964). It 

was noted that breast milk ranged from 0.051 to 0.077 mg/lOO ml and 

that total copper intakes of the babies ranqed from 0.065 to 0.1 

w/Wday l In the first week of life, some infants 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 bioconcentrationlfactor (BCF) 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 concerning food intake to calculate the amount of cooper 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 
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 estuarine fish and shellfish is 6.5 g/day (Stephan, 1980). The per capita consumption of bivalve molluscs is 0.8 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 BCF Reference 

Bay scallop, 

Argopecten irradianr 

3,310 

Bay scallop 

Argopecten irradians 

4,160 

American oyster, 

Crassoetrea virginica 

28,200 

American oylter, 20,700 

Crassostrea virginica 

Northern quahaug, 

Mercenaria mercenaria 

Soft shelled clafll, 

Mya arenaria 

MusselF 

Mytilus edulis 

Mussel, 

Mytilus edulfs 

Mussel, 

Mytilus galloprovincialis 

88 

3,300 

208 

Shuster and 

Wingle, 1969 

Shuster and 

Pringle, 1969 

Shuster and 

Pringle, 1968 

Shuster and 

Pringle, 1968 

Zaroogian, 1978 

108 Zaroogian, 1978 

90 Phillips, 1976 

800 MajOri and 

Petronio, 1973 

Zaroogian, 1978 

Zaroogian, 1978 

c-17 
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 organisms 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 copper 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 

Copper has 

trial substance 

power plants. 

not been considered a particularly hazardous indusbecause 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 exposure to copper sulfide and copper oxide dust, both of which are insoluble (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 240 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 zis a result 

of the welding of copper structures (McCord, 1960). 

C-18 
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 mg/m3 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 pg/m3 in 

rural and urban communities, respectively (Natl. Air Pollut. Control Admin., 1968). Even near copper smelters, where high levels 

(1 to 2 ug/m3) are reached, the dose of metal that would be acquired 

through inhalation of ambient air would comprise only about I percent 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 medical 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 hemodialysis may be the membranes fabricated with copper* the 

copper tubing, or the heating coils of the equipment. Copper stopcocks 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 monkey 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 (Yjor, 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, sometimes 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 contraceptive measure (NAS, 1977). Analysis of IUDs that have been in utero _Ifor months to years shows that about 25 to 30 mq of copper are lost 

each year. Some of the metal is excreted with endometrial secretions. 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. 

2 Acknowledgement is made of the courtesy of the late Dr. Far1 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 
Much of the information on copper absorption in humans has 

come from studies of patients with Wilson’s disease. studies conducted with these patients using radioactive copper indicate that 

about one-half of the copper in the diet is not absorbed but is excreted directly into the feces. The average absorption in these 

individuals has been reported to be approximately 40 percent 

(Sternlieb, 1967; Strickland, et al. i972a). Investigations by 

Cartwright and Wintrobe (1964a) indicated that the daily intake of 

copper in Wilson’s disease patients was 2 to 5 mq, of which 0.6 to 

1.6 mq were absorbed, 0.5 to 1.2 mq were excreted in the bile, 0.1 

to 0.3 mg passed directly into the bowel, and 0.01 to 0.06 mg appeared 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; Bearn and Runktl, 1954, 1955; Beckner, et al. 1969; Bush, et 

al. 1955; Jensen and Ramin, 1957). 

Estimates of the amount of the copper that is actually absorbed by normal individuals vary considerably and must be considered inconclusive. The values obtained have ranged from as low as 

15 percent ta 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 confounded 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 excreted in the bile. Most of the values that have been obtained with 

normal subjeats lsuqqest that 40 to 60 percent of the dietary copper 

is absorbed (Van Ravenstcyn, 1944: Cartwright and Wintrobe, 1964a; 

Bush, et al. 1955; Matthews, 1954: Weber, et al. 1969: Strickland, 

et al. 1972a,b; Sternlieb, 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 interfere with copper absorption, including competition for binding 

sites as with zinc, interactions with molybdenum and with sulphates, 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 transported in the plasma. Approximately 80 percent of the absorbed 

copper is bound in the liver to metallothionein. The remaining 

copper is incorporated into compounds such as cytochrome-c-oxidase 

or is sequestered by lysosomes (Bearn and Kunkel, 1954, 1955) l 

Little information is available concerning absorption of copper 

into the lymphatics, although in pathological conditions this may 

be significant (Trip, et al. 19691. 

c-22 
Several studies have been conducted on humans and laboratory 

animals concerning absorption of copper as a result of the use of 

copper IUDs. 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 retained, it would result in amounts of copper similar to those retained 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 womenr 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 wfth or without copper. No significant difference 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 chotion and the decidua of the pregnant women with IUDs in 

place did notdiffer from the levels noted in pregnant women without IUDs. Apparently, the long-term use of copper-containing IUD3 

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- Thef c result8 [ndfatr ~ 

copper l[uD affect&! the Sectetory @*domettfupt b 

ut not: - Q-wllc ative endometr Lun. 

In another study, fstaclf 

contains both copper and zinc, 

als if they had had low strmn 

section. Rowewes, 

uppeg limits of normal values. *t3 sig*~ffWR statfrtfat, fl* 

ence wad; found between the IerM level* Of capprn bfar, r) N 

tnsettion ot the IU& 

It has been sugg+atsd that diaktic ra+a w tw ar)lllr, 

of th. r?IWttirt f fbrolytic ACttVttp QtWWkt.8 JLlllm r) m 
Distribution 

The amount and distribution of copper in body tissues varies 

with sexr ager and the amount of copper in the diet. Copper content 

of fat-free tissues of most animals ranges upward from about 2 

w/g l 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 (Cartwright and Wintrobe, 1964a,b: Smith, 1967; Schroeder, et al. 1966). 

Some tissues are very high in copper, e.g., the iris and the choroid of the eye , which may contain as much as 100 ~g/gm (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 musculature, and the remaining one-third is dispersed in other tissues. 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: Sumino, et al. 1975; Sass-Kortsak and Bearn, 1978). 

The relatively high percentage of liver copper is related to the 

liver’s function as a storage organ for conper and a8 the only site 

for the synthesis and release of ceruloplasmin, the most abundant 

copper protein in the blood. 

In the brain, the striatum 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. clther 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). Rowever, 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 nut:iticnal status. They found that the 

mean concentration of copper in hair samples was 31 2 23 vg/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/lOO ml of blood. The amount of copper in blood serum can range 

widely from S ug/lOO ml to 130 pg/lOO ml. In practically all species, copper deficiency is first manifested by a slow depletion of 

body copper stores, including the blood plasma, eventually resulting 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 copperr 

a labile pool and a stable pool, which contain approximately 40 and 

60 percent respectively, of the copper in the blood (Bush, et al. 

195s). Ceruloplasmin represents the predominant portion of cooper 

in the serum pool. There appears to be little or no interchange 

between ceruloplasmin 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/lOO 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 arr.cunt 

of copper f 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). 

Chex, a% 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 copper of the whole body (Widdowson and Spray, 1951). A newborn infant 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 Zondek, 

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 120year-old healthy children, but 

by five months of age the serum concentration of copper is approximately the same as in older children. Ther.e is no difference between 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 
Hetabolism 

The copper content of red blood cells remains remarkedly constant, but the plasma copper is subject to striking changes asgociated with the synthesis and release of ceruloplasmin, which fs 

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 applicability to humans is uncertain. Evans (1973) and others have reviewed this subject (Mann and Keilin, 1938t 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 almo8t entirely due to 

the increased synthesis of ceruloplasmin (Henkin, et al. 1972; 

Markowitz, et al. 1955; 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 assooiated with estrogen, since either sex receiving estrogen shows an increase in copper level of the plasma (Elsner and Hornykiewicz, 1954: Gault, et 

al. 1966: Humoller, et al. 1960: Russ and Raymunt, 1956). 

The use of oral contraceptives causes a marked increase in 

serum copper lavels 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 
There are two inherited diseases that represent abnormal copper metabolism, Menkes' disease and Wilson’s disease. Yenkes' disease is a progressive brain disease caused by an inherited sexlinked recessive trait. It is often referred to as the “kinky 

hair” disease or "steely hair" disease (Danks, et al. 1972). The 

primary characteristic of Menkes' disease appears to be a diminished ability to transfer copper across the absorptive cells of the 

intcstinalmucosa (Danks, et al. 1972, 1973). The general symptoms 

of the disease are similar to those observed in animals suffering 

from copper 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 “hepatolent fcular degeneration, a 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 intestinal excretion of copper, and occurrence of Kayser-Fleischer 

rings due to excessive accumulation of copper around the cornea. 

If therapy witb d-penicillamine is instituted during the early 

phases of Wflronls disease, it can assure a normal life expectancy, 

especially when accompanied by a low-copper diet (Deias, et 31. 

1971: Sternlieb and Scheinberq, 1964, 1968; WaSshe, 1956). 

Other abnormalities of copper metabolism are primarily associated with low levels of copper. Ayoocupremia, which is defined as 

c-29 
80 'Jg or less of copper/100 ml (Cartwright and Wintrobe, 1964a), 

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). HYPOcupremia can also result from malabsorption that occurs during a 

small bowel disease (Sternlieb and Janowitz, 1964). 

Hypercupremia, abnormally hiqh levels of copper, occurs with a 

number of neoplasms (Delves, et al. 1973; Herring, et al. 1960; 

Goodman, et al. 1967; Janes, et al. 1972). Elevated serum copper 

levels occur in psoriasis (Kekki, et al. 1966; Molokhia and Portnoy, 1970). 

It is well recognized that copper is necessary for the utilization of iron. Much of this work has been done in animals, and the 

subject is well covered by Underwood (1977). It appears that ceruloplasmin is essential for the movement of iron from cells to plasma (Osaki, et al. 1966). Reticulocytes from copper-deficient animals can neither pick up iron from transferrin normally nor synthesize heme from ferric iron and protoporphyrin at the normal rate 

(Williams, et al. 1973). 

The ratio of copper to other dietary components, e.q.# zinc, 

iron, sulfate, and molybdenum, may be almost as important a3 the 

actual level of copper in the diet in influencing the metabolic 

response of mammalian species (Smith and Largon, 1946). The cardiovascular disorder "falling disease", reported by Bennetts, et 

al. (1942), is associated with a copper deficiency in cattle. Similar conditions have been observed in pigs and chicken3 (O'Dell, et 

al. 1961; Shields, et al. 1961). In this disorder the elastic tisc-30 
sue of major blood vessels Is deranged, markedly reducing zhe tensile strength of the aorta. This appears to be associated with a 

biochemical lesion, the reduced activity of lysyl oxidase, a copper-requiring enzyme necessary for elastic tissue formation and 

maintenance (Hill, et al. 1967). 

Evans has discussed the metabolic disorders of copper metabolism including nutriticnal disorders, inborn order errors of proper 

homeostasis, and disorders due to the lack of copper-requiring enzymes (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 nay relate to ischemic 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 whic.h has been associated with increased susceptibility to ischemic heart disease (Allen and Klevay, 

1978a,b; Petering, 1974; Lei, 1978; Klevay, et al. 1977). In a 

different context, Barman (1970) has suggested that copper in the 

diet in excess of needs may result in free radicals that cause adverse effects fn the cardiovascular system. 

Excretion 

It has been noted that perhaps 40 percent of dietary copper is 

actually absorbed (Cartwright and Wintrobe, 1964a). These estimates are largely based on the difference between oral intake and 

c-31 
fecal excretion. S’rinary excretion of copper ?Lays 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 reabsorbed 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 excretion in normal subjects, the evidence for quantitative values of 

copper excretion by this route is fragmentary. Cartwr ight and Wintrobe (1964a) suqqest that 0.5 to 1.2 mq per day is excreted in the 

bile. This is in reasonable accord with the report (Frommer, 1974) 

that excretion was approximately 1.2 mq/day in ten control subjects. 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 mq/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 approximates 1 mq 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. Estimates range from 10 to 60 ug/day and average 18 ug/day (Cartwright 

and Wintrobe, 1964a; Zak, 1958). It is possible, of courser that 

copper may be reabsorbed from the kidney tubules (Davidson, et al. 

1974). 

C-32 
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 flow, but an average value of 0.11 f 0.07 mg per 

period seems reasonable (Ohlson and Daum, 1935; Leverton and Binkley, 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 ceruloplasmfn, 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 Uliary 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. 

c-33 
EFFECTS 

Acute, Subacute, and Chronic Toxicity 

Copper toxicity produces a metallic taste in the mouth, nausea, vomiting, epigastric pain, diarrhea, and depending on the 

severity, jaundice, hemolysis, hemoglobinuria, hematuria, and oliguria. 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. Hemolysis occurs at high copper levels. A high level in the blood can 

also result from absorption through the denuded skin, as when applied to burns, because of dialysis procedures, or because of exchange 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 copper 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 quantic-34 
ties of ionic copper generally protect the patient from the serious 

systemic toxic effects which include hemolysis, hepatic necrosis, 

gastrointedtinal 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 from 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 vinegah 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 drinkdispensing machines overnight, the copper content of the first 

drink of the day may be increased enough to cause a metallic taste, 

nausear 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 comr 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 93OC at night. The family used hot water for all 

c-35 
cooking and beverages. After two rr,ontfis, 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 pg/lOO ml, compared to a 

normal range of 164 2 70 ug/lOO ml. Analysis of water in the home 

found 350 pg/l of copper in the cold water and 790 ug/l of copper in 

the hot water. Cold and hot water levels in the hospital were 40 

and 300 ug/l, respectively, and in North London the values were 80 

and 160 ug/l. 

Walker-Smith and Blomfield (1973) treated the male infant described in the preceeding paragraph, who had received high levels 

of copper from contaminated water over a period of three months, 

with d-penicillamine and prednisolone. The infant made a slow recovery. The method of Eden and Green (1940) was used to determine 

copper levels. It is possible that the infant was exhibiting Wilson's disease and responded to the appropriate treatment. 

Eden and Green (1940) reported on a male infant 'who received 

high levels of copper frosn contaminated water ingested over a period of three 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 copper content develops a surface scum due to the formation of insoluble copper compounds). 

Chronic toxicity has been studied in animals, and there appears 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 pg 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 pg/g in the diet of swine. Toxicosis does develop with hypochromic microcytic anemia, jaundice, and marked increases in the 

liver and serum copper levels as well as serum aspartate amino 

transferase. These signs of copper toxicosis in swine can be eliminated by including an additional 150 pg 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 pg/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 an& 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. 

c-37 
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 (Gunningham, 1931). 

It is well known that with ruminant animals, molybdenum and 

sulfate interact with the copper. Cooper 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 TAlOO 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 l:l,OOO lowered the 

most active concentration of the triose reductone to 1 mM from 2.5 

to 5 ref. 

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 mutagenic 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 essential for mutagenicity. 

In the Acute, Subacute, and Chronic Toxicity section, it was 

pointed out that the dietary levels of zinc and iron are as imporC-38 
tant as the level of copper in determining the toxic level of 

copper . 

Teratoqenfcfty 

There is very little evidence in the literature to suggest 

that copper has a teratoqenic effect in either animals or humans. 

Mutagenicity 

No data were found to suggest that copper itself has a mutagenic 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). 

Carcinoqeniclty 

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 Italyr exposed to copper sulfate sprays 

mixed with lime to control mildew, developed qranulomas in the 

liver and malignant tumors in the lung (Pimental and Menezes, 1975; 

Villar, 1974). Because of the route of expoaure, 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 investigators 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 (Xuratsune, et al. 1974; Lee and 

c-39 
Fraumeni, 1969; Yilham and Strong, 1974; Tokudome and Kuratsune, 

1976). 

Some studies have reported that, with the development of various tumors, the copper content in both blood and the tumor tissue 

is likely to increase, although this is not always the case (Pedrero and Kozelka, 1951; Dick, 1953; Kline, et al. 1971: Wahal, et 

al. 1965). Kowever, 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 metastatic 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 between the tumor and copper as a causative agent. 

Workers in Hong Kong (Fang, et al. 1977) have been investigating 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 
In 3ummaryl it must be stated that evidence for the oncolcgical effects of copper, even at high concentrations, is essentially 

nonexistent. With the exception of the references cited, there 

appear to be 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 ewen,tial role in the functioning of many enzyme systems. 

c-41 
CRITERION FORMULATION 

Existing Guidelines and Standards 

Far more attention has been given to the problems of copper 

deficiency than to the problems of excess copper in the environment. The 1 mg/l 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/l, 2 mg/l and 

1.5 mg/l of copper. The choice of 1 ppm as a level that was organoleptically 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/m3 of air. The standard for copper fume was changed 

in 1975 to 0.2 mg/m3 (Gleason, 1968: Cohen, 1974). 

As indicated below, the Food and Nutrition Board of the National 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 0.5-0.7 4- 6 1.5-2.0 

0.5-1.0 0.7-1.0 7-10 2.0-2.5 

l-3 1.0-1.5 ll-Adult 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 ranqa from 6 to 8 mg 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 considered an adequate nutritional intake (Klevay, et al. 1977; Diem and 

Lentner, 1970; Robinson, et al. 1973; Schroeder, et al. 1966; WHO, 

1973; Cartwright and Wfntrobc, 1964a). 

The average concentration of copper in United States water 

systems is approximately 134 &l with a little over 1 percent bf 

the samples taken exceeding the drinking water standard of 1 mg/l 

(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 mq/l (W.S. HEM, 1970). 

In 1966, the National Air Sampling Network found airborne copper concentrations ranging from 0.01 to 0.257 ug/m3 in rural and in 

urban communities, respectively. Levels of copper as high as 1 to 

2 yg/m3 werm found near copper smelters, but this was not considered hazardous (Natl. Air Pollut. Control Admin., 1968; Schroeder, 

1970). 

c-43 
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 periods of tine have dissolved copper into the vended liquids. 

Other groups that may be at risk are medical patients suffering from Wilson's disease and those patients who are being treated 

with copper-contaminated fluids in dialysis or by means of parenteral alimentation. These are medical instances in which the copper content of the materials used should be carefully controlled. 

There is also a reasonable likelihood that exposure to elevated levels of copper (ca. 1.0 ppm) from community drinking water 

may be a contributory factor in the precipitation of acute hemolysis in individuals with a glucose-6-phosphate dehydroqenase 

(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 humane were found to be.markedly more sensitive to 

several indicators of oxidant stress as measured by increases in 

methemoglobin. levels and decreases in the activity of red cell 

acetylcholineeteraea indicating that susceptibility to copperinduced oxidative stress is associated with the presence of low red 

cell G-6-PD activity (Calabrese and ?4oore, 1979; Calabrese, et al. 

1980). 

c-44 
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 focd prcduct that was excessively high in copper. The Committee also raised the question of exposure to copper 

from intrauterine contraceptive devices (IlJDs), but subsequent reports have failed to demonstrate any abnormal accumulation of copper because of the use of these devices. 

Basis and Derivation of Criterion 

Copper is an essential dietary element for humane 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 conjunction with such constituents as zinc, iron, and ascorbic acid. The 

minimum level meeting requirements for copper intake in intravenous 

feeding is 22 vg copper/kg body weight (Vilter, et al. 1974). 

The short biological half-life of copper and the homeostasis 

that exists in humane 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 current dietary and environmental situations. 

c-45 
Although acute and chronic levels Of intake may occur, there 

are no data that adequately define these Levels. It has been suggested that intakes above 15 mg of copper per day may produce observable 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, arsenic, 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/l 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 criterion of 1.0 mg/l are based on organoleptic effects (U.S. LlEW, 1970) 

and are not toxicological assessments, the consumption of fish and 

shellfish is not considered as a route of exposure. 

C-46 
REFERENCES 

Adelstein, S.J., et al. 1956. Metalloenzymes and myocardial infarction. 1. The relation between serum copper and ceruloplasmin 

and its catalytic activity. New England Jour. Med. 255: 105. 

Allen, K.G.D. and L.M. Klevay. 1978a. Cholesterol metabolism in 

copper-deficient rats. Life Sci. 22: 1691. 

Allen, K.G.D. and L.M. Rlevay. 1978b. Chalesterolemfa and cardiovascular abnormalities in rats caused by copper deficiency. Atherosclerosis. 29: 81. 

Barber, R.S., et al. 1978. The value of virginiamycin (eskalfn) 

as a feed additive for growing pigs in diets with or without a high 

copper supplement. Jour. Anim. Prod. 26: 151. 

Bearn, A.G. 1953. Genetic and biochemical aspects of Wilson's 

disease. Am. Jour. Med. 15: 442. 

Bearn, A.G. and H.G. Kunkel. 1954. Localization of Cu 64 in serum 

fractions following oral administration: an alteration in Wilson's 

disease. Proc. Sot. Exp. Biol. Med. 85: 44. 

Bearn, A.G. and H.G. Runkel. 1955. Metabolism studies in Wilson's 

disease using Cu 64 

. Jour. Lab. Clin. Med. 45: 623. 

c-47 
Beckner, W.M., et al. 1969. External gamma scintillation counting 

of 67 Cu over the liver and other sites in patients with Wilson's 

disease, family members and controls. Jour. Yucl. Med. 10: 320. 

Bennetts, H.W., et al. 1942. Studies on copper deficiency of cattle: The fatal termination ('falling disease’). Aust. Vet. Jour. 

18: 50. 

Benoit, D.A. 1975. Chronic effects of copper on survival, growth, 

and reproduction of the bluegill (Lepomis macrochirus). Trans. Am. 

Fish. Sot. 104: 353. 

Beutler, E. 1972. Glucose-6-phosphate Dehydrogenase Deficiency. 

2: J.B. Stanbury, et al. teds.), The Metabolic Basis of Inherited 

Disease. McGraw-Hill, New York. p. 1358. 

Bezruchko, V.I. 1976. Copper content and ceruloplasmin activity 

in the blood serum of oncological patients. Aktual. Probl. Onkol. 

Med. Radiol. 6: 149. Chem. Abstr. 89: 4261~. (Rus.) 

Bloomfield, J. 1969, Copper contamination in exchange transfusions. Lancet- 1: 731. 

Bloomfield, J., et al. 1971. Potential hepatotoxicity of copper 

in recurrent hemodialysis. Arch. Intern. Med. 128: 555. 

C-48 
Bowness, J.M. and R.A. Yorton. 1952. Distribution of copper and 

zinc in the eyes of fresh water fishes and frogs. Occurrence of 

metals in melanin fractions from eye tissues. Biochem. Jour. 

51: 530. 

Bowness, J.M., et al. 1952. Distribution of copper and zinc in 

mammalian eyes. Occurrence of metals in melanin fractions from eye 

tissues. Biochem. Jour. 51: 521. 

Bremner, I. 1974. Heavy metal toxicities. Q. Rev. Biophys. 

7: 75. 

Bruckmann, G. and S.G. Zondek. 1939. Iron, copper and manganese 

in human organs at various ages. Biochem. Jour. 33: 1845. 

Burch, R.E., et al. 1975. Newer aspects of the roles of zinc, 

manganese and copper in human nutrition. Clin. Chem. 21: 501. 

Bush, J.A., et al. 1955. Studies on copper metabolism. XVI. 

Radioactive copper studies in normal subjects and in patients with 

hepatolenticular degeneration. Jour. Clin. Invest. 34: 1766. 

Button, R.S., et al. 1977. Copper dispersal in a water supply 

reservoir. Water Res. 11: 539. 

Calabrese, E.J. and G.S. Moore. 1979. Can elevated levels of copper in drinking water precipitate acute hemolysis in G-6-PD deficient individuals? Med. Hypotheses. 5: 493. 

c-49 
Calabrese, E.J., et al. 1980. LOW glucose-G-phosphate dehydrogenase (G-6-PD) activity in red blood cells and susceptibility to copper-induced oxidative damage. Environ. Res. 21. 

Cartwright, G.E. 1950. Copper Metabolism in Kuman Subjects. &: 

W.D. McElroy and B. Glass (eds.), A Symposium on Copper Metabolism. 

Johns Hopkins Press. Saltimore. p. 274. 

Cartwright, G.E. and H.M. Wintrobe. 1964a. Copper metabolism in 

normal subjects. Am. Jour. Clin. Nutr. 14: 224. 

Cartwright, G.E. and M.M. Wintrobe. 1964b. The question of copper 

deficiency in man. Am. Jour. Clin. Nutr. 15: 94. 

Cartwright, G.E., et al. 1956. Studies on copper metabolism. 

XVII. Further observations on the anemia of copper deficiency in 

swine. Blood. II: 143. 

Cavell, P.A. and E.M. Widdowson. 1964. Intakes and excretions of 

iron, copper and zinc in the neonatal period. Arch. Dis. Child. 

39: 496. 

Chatterji, S.K. and H.D. Ganguly. 1950. Copper in human urine and 

feces. Ind. Jour. Med. Res. 38: 303. 

Chez, R.A., et al. 1978. Amniotic fluic, copper and zinc concentrations in human pregnancy. Obstetrics Gyn. 52: 125. 

c-50 
Chuttani, A.K., et al. 1965. Acute copper sulphate poisoning. 

Am. Jour. Med. 39: 849. 

Cohen, J.M., et al. 1960. Taste threshold concentrations of metals in drinking water. Jour. Amer. Water Works Assoc. 52: 660. 

Cohen, S.R. 1974. A review of the health hazards of copper exposure. Jour. Occup. Med. 16: 621. 

Consolazio, C.F., et al. 1964. The trace mineral losses in sweat. 

U.S. Army Med. Reg. Nutr. Lab. Rep. No. 284: 1. 

Crampton, R.F., et al. 1965. Observations on the mechanism of 

absorption of copper by the small intestine. Jour. Physiol. 

178: 111. 

Cumings, J.N. 1948. The copper and iron content of brain and liver 

in the normal and in hepato-lenticular degeneration. Brain. 

71: 410. 

Cunningham, I.J. 1931. Some biochemical and physiological aspects 

of copper in animal nutrition. Biochem. Jour. 25: 1267. 

D'Amico, R.J. 1959. Mineral Production in the United States. g: 

Minerals Yearbooks for 1958. U.S. Dep. Interior. Bur. Mines. 

c-51 
Daniels, A.L. and 0.9. Wright. 1934. Iron and copper retentions 

in young children. Jour. Nutr. 8: 125. 

Danks, D.M., et al. 1972. Menkes' kinky hair syndrome. An inherited defect in copper absorption with widespread effects. Pediatrics. 50: 188. 

Danks, D.M., et al. 1973. Menkes' kinky hair disease: further 

definition of the defect in copper transport. Science. 179: 1140. 

Davenport, S.J. 1953. Review of literature on health hazards of 

metals. I. Copper. U.S. But. Mines Inf. Circ. No. 7666. U.S. 

Government Printing Office, Washington, D.C. 

Davidson, I.W.F., et al. 1974. Renal excretion of trace elements: 

chromium and copper. Proc. Exp. Biol. Med. 147: 720. 

Deiss, A., et al. 1970. Hemolytic anemia in Wilson's disease. 

Ann. Intern. Med. 73: 413. 

Deiss, A., et al. 1971. Long term therapy of Wilson's disease. 

Ann. Intern. Med. 75: 57. 

De Jorge, F.B., et al. 1964. Studies on copper metabolism. III. 

Copper contents of saliva of normal subjects and of salivary glands 

and pancreas of autopsy material. Clin. Chim. Acta. 9: 148. 

C-52 
Delves, H-T., et al. 1973. Copper and zinc concentration in the 

plasma of leukaemic children. Br. Jour. Haematol. 24: 525. 

Dick, A.T. 1953. The contro1 of copper storage in the liver of 

sheep by inorganic sulfate and molybdenum. Austr. Vet. Jour. 

29: 233. 

Diem, K. and C. Lentner, feds.1 1970. Composition of Foods. Cocumentia Geigy. Scientific Tables. 7th ed. Geigy Pharmaceuticals, 

Division of Ciba-Geigy Corp., Ardsley, N.Y. 

Earl, C.J. 1961. Anatomical Distribution of Copper in Human 

Brain. In: J.M. Walshe and J.N. Cumings (eds.), Wilson's Disease. 

Some Current Concepts. Blackwell, Oxford. p. 18. 

Eden, A.A. and H.H. Green. 1940. Micro-determination of copper in 

biological material. Biochem. Jour. 34: 1202. 

Elsner, P. and 0. Hornykiewicza. 1954. Die beeinflussbarkeit der 

p-polyphenoloxydase-aktivitat des menschliehen blutserums durch 

sexualhormone. Arch. Gynakol. 185: 251. 

Engel, R.W., et al. 1967. Copper I manganese, cobalt, and molybdenum balance in pre-adolescent girls. Jour. Nutr. 92: 197. 

Evans, G.W. 1973. Copper homeostasis in the mammalian system. 

Physiol. Rev. 53: 535. 

C-53 
Evans, G.W. 1977. Yetabolic disorder s of copper ?tetabolism. Tidv. 

Nutr. Res. 1: 167. 

Evans, G.W., et al. 1973. Copper and zinc binding components in 

rat intestine. Clin. Res. 21: 867. 

Federal Water Quality Administration. 1968. Water quality criter ia. Rep. Natl. Tech. Adv. Comm. to the Secretary of the Interior, Washington, D.C. 

Fong, L.Y.Y., et al. 1977. Zinc and copper concentrations in tissues from esophageal cancer patients and animals. Trace Subs. 

Environ. Health. 11: 184. 

Fontenot, J.P., et al. 1972. Effects of feeding different levels 

of broiler litter to ewes for long periods of time on performance 

and health. Virginia Polytechnic Inst. State Univ. Res. Div. Rep. 

No. 145: 33. 

Forbes, G. 1947. Poisoning with a preparation of iron, copper and 

manganese. Br. Med. Jour. 1: 367. 

Frommer, D.J. 1974, Defective biliary excretion of copper in Wilson’s disease. Gut. 15: 125. 

Gault,: M.H.; et al. 1966. Serum ceruloplasmin in hepatobiliary 

and other disorders: significance of abnormal values. Gastroenterology. 50: 8. 

c-54 
Gipp, W.F., et al. 1974. Effect of dietary copper, iron and ascorbic acid levels on hematology, blood and tissue copper, iron and 

zinc concentrations and 64Cu and " Fe metabolism in young pigs. 

Jour. Nutr. 104: 532, 

Gleason, R.P. 1968. Exposure to copper dust. Am. Ind. Hyg. 

Assoc. Jour. 29: 461. 

Gollan, J.L. 1975. Studies on the nature of complexes formed by 

copper with human alimentary secretions and their influence on copper absorption in the rat. Clin. Sci. Molec. Med. 49: 237. 

Gollan, J.L. and D.J. Deller. 1973. Studies on the nature and excretion of biliary copper in man. Clin. Sci. 44; 9. 

Goodman, S.I., et al. 1967. Bypercupremia in a patient with multiple myeloma. Jour. Lab. Clin. Med. 70: 57. 

Gubler, C.J., et al. 1953. Studies of copper metabolism. IX. The 

transportation of copper in blood. Jour. Clin. Invest. 32: 405. 

Hadj imarkos, D.M. 1967. Effect of trace elements on dental 

caries. Jour- Fed. 70: 967. 

Harman, D. 1970. Atherogenisis in Minipigs: Effect of Dietary Fat 

Unsaturation and Copper. z: R.J. Jones ted.), Athersclerosis. 

Proc. 2nd Int. Symp. Springer-Verlag, New York. 

c-55 
Henkin, R.I., et al. 1971. Maternal-fetal metabolism of copper 

and zinc at term. Am. Jour. Obst. Gynecol. 110: 131. 

Henkin, R.I., et al. 1973. Changes in total, nondiffusible and 

diffusible plasma zinc and copper during infancy. Jour. Ped. 

82: 831. 

Herring, W.B., et al. 1960. Trace metals in human plasma and red 

blood cells. A study of magnesium, chromium, nickel, copper and 

zinc. II. Observations of patients with some hematologic diseases. 

Am. Jour. Clfn. Nutr. 8: 855. 

Hill, C.H., et al. 1967. Role of copper in the formation of elastin. Fed. Proc. 26: 129. 

Ffoltzman, N.A., et al. 1966. Copper intoxication. Report of a 

case with observations on ceruloplasmin. New England Jour. Med. 

275: 347. 

Hooper, S.B. and B.S. Adams. 1958. Copper poisoning from vending 

machines. Pub. Health Rep. 73: 910. 

Hui, K., et aI, 1977. Analysis of copper in brain by the massspectrometric integrated-ion-current procedure. Neuro Chem. Res. 

2: 495. Chem. Abstr. 88: 3409OM. 

C-56 
Humoller, F.Lor et al. 1960. Enzymatic properties of ceruloplasmin. Jour. Lab. Clin. Med. 56: 222. 

Hunt, C.E., et al. 1970. Copper deficiency in chicks: Effects of 

ascorbic acid on iron, copper, cytochrome oxidase activity, and 

aortic mucopolysacchar ides. Br. Jour. Nutr. 24: 607. 

Ivanovich, P., et al. 1969. Acute hemolysis following hemodialysis. Trans. Am. Sot. Artif. Intern. Organs. IS: 316. 

Jacob, R.A., et al. 1978. Hair as a biopsy material. V. Hair 

metal as an index of hepatic metal in rats: copper and zinc. Am. 

Jour. Clin. Nutr. 31: 477. 

Janes, H.M., et al. 1972. Trace metals in human osteogenic sarcoma. Mayo Clin. Proc. 47: 476. 

Jensen, W.N. and 8. Xamin. 1957. Copper transport and excretion 

in normal subjects and in patients with Laennec’s cirrhosis and 

Wilson's disease: A study with Cu 64 

. Jour. Lab. Clin. Med. 

49: 200. 

Kartar, S. ana A.R. Chowdhury. 1977. Release of copper ions from 

an intra vas copper-wire contraceptive device. Ind. Jour. Physiol. 

Pharmacol. 21: 387. 

C-57 
Kekki, M., et al. 1966. Serum ceruplasmin-bound copper and noncetuloplasmin-bound copper in uncomplicated psoriasis. Jour. Invest. Dermatol. 47: 159. 

Klein, L.A., et al. 1974. Sources of metals in New York City waste 

water. Intern. Water Pollut. Control Fed. 46: 2653. 

Kleinbaum, 8. 1963. Votubergehendt hypoproteinamine mit hypocupramie und eisenmangclanemie bei dystrophen sauglingen. Ztschr. 

Kinderheilk. 88: 29. 

Klevay, L.M. 1977. The role of copper and zinc in cholesterol 

metabolism. Adv. Nutr. Res. 1: 227. 

Klevay, L.M., et al. 1977. United States diets and the copper requirement. Fed. Proc. 36: 1175. 

Kline, R.D., et al. 1971. Effects of copper, molybdenum and sulfate on performance, hematology and copper stores of pigs and 

lambs. Jour. Anim. Sci. 33: 771. 

KoPP I J.F. and R.C. Kroner. 1968. Trace metals in waters of the 

United States: = five-year summary of trace metals in rivers and 

lakes of the United States, October 1, 19620September 30, 1967. 

U.S. Dept. Inter., Fed. Water Pollut. Cmtrol Admin., Cincinnati, 

Ohio. 

C-58 
Kuratsune, Mar et al. 1974. Occupational lung cancer among ccpper 

smelters. Int. Jour. Cancer. 13: 552. 

Lahey, M.E., et al. 1953. Studies on copper metabolism. VII. 

Blood copper in pregnancy and various pathologic states, Jour. 

Clin. Invest. 32: 329. 

Larsson, B., et al. 

trium in diabetic 

15: 711. 

1977. 

women 

Fibrinolytic activity of the endomeusing copper IUDs. Contraception. 

Lee, A.M. and J.F. Fraumeni, Jr. 1969. Arsenic and respiratory 

cancer in man. An occupational study. Jour. Natl. Cancer Inst. 

42: 1045. 

Legutko, L. 1977. Serum iron and copper levels in acute lymphoblastic leukemia in children. Polish Tyg. Led. 32: 225. Chem. 

Abstr. 88: 168175b. (Pal.) 

Lei, K.Y. 1978. Oxidation, excretion and tissue distribution of 

260~~ C cholesterol in copper-deficient rats. Jour. Nutr. 

108: 232. 

Leverton, R.M. and E.S. Binkley. 1944. The copper metabolism and 

requirement of young women. Jour. Nutr. 27: 43. 

c-59 
Lewis, K.O. 1973. The nature of the copper complexes in bile and 

their relationship to the absorption and excretion of copper in 

normal subjects and in Wilson's disease. Gut. 14: 221. 

Lyle, W.H., et al. 1976. Haemodialysis and copper fever. Lancet. 

2: 1324. 

Majori, L. and F. Petronio. 1973. Marine pollution by metals and 

their accumulation by biological indicators (accumulation factor). 

Rev. Intern. Oceanoqr. Med. Tomes XxX1. 

Mallory, F.B. and F. Parker, Jr. 1931. Experimental copper poisoning. Am. Jour. Pathol. 7: 351. 

Mann, P. and D. Keilln. 1938. Haemocuprein and hepatocouperin, 

copper protein compounds of blood and liver in mammals. Proc. R. 

sot. London B-126: 303. 

Markowitz, H., et al. 1955. Studies on copper metabolism. XIV. 

Copper I ceruloplasmin and oxidase acitivity in Sara of normal human 

subjects, pregnant women, and patients with infection, hepatolentitular degeneration and the nephrotic syndrome. Jour. Clin. Invest. 34: 1498. 

Hatthews, W.B. 1954. The absorption and excretion of radiocopper 

in hepatolenticular degeneration (Wilson's disease). Jour. Neurol. 

Neurosurg. Psychiat. 17: 242. 

C-60 
McCabe, L-J-I et al. 1970. Survey of community water Supply systems. Jour. em. Water works Assoc. 62: 670. 

McCance, R.A. and E.M. Widdowson. 1947. The Chemical Composition 

of Foods. Chem. Pub. Co., New York. 

McCord, C.P. 1960. Metal fume fever as an immunological disease. 

Ind. Med. Surg. 29: 101. 

McMullen, W. 1971. Copper contamination of soft drinks from bottle pourers. Health Bull. (Edinburgh) 29: 94. 

Mertz, W. Institute of Nutrition. U.S. Dept. of Agric., Beltsville, Md. (personal communication). 

Milham, S., Jr. and T. Strong. 1974. Human arsenic exposure in 

relation to a copper smelter. Environ. Res. 7: 176. 

Mjor, I.A., et al. 1977. Biologic assessment of copper-containing 

amalgams. Int. Dental Jour. 27: 333. 

Molokhia, M.M. and B. Portnoy. 1970. Neutron activation analysis 

of trace elements in skin. V. Copper and zinc in psoriasis. Br. 

Jour. Dermatol. 83: 376. 

Mondorf; A.W., et al. 1971. Coeruloplasmin. Teil I: Die Biochemie des Coeruloplasmins. Teil 11: Der Einfluss von Ostroqenen 

auf den coeruloplasminqehalt des Serums. Klin Wochnschr. 49: 61. 

C-61 
Morell, A.G., et al. 1961. Copper Binding Protein of Human Liver. 

z: J.M. Walsh and J.N. Cumings feds.), Wilson's Disease. Some 

Current Concepts. Blackwell Sci. Publ. Ltd., Oxford. p. 36. 

Murakimi, A., et al. 1978. A fundamental study of copper-T (intrauterine device). Nippon Funin Gakkai and Zasski. 23: 28. 

Chem. Abstr. 88: 1647752. (Gap.) 

National Academy of Science. 1977. Copper. Nedfcal and biologic 

effect3 of environmental pollutants. National Research Council, 

Washington, D.C. 

National Academy of Science. 1980. Food and Nutrition Board. 

National Air Pollution Control Administration. 1968. Air quality 

data from the National Air Surveillance Networks and contribution 

of State and local networks, 1966 ed. NAPCA Publ., APTD-68-9. 

U.S. Government Printing Office, Washington, D.C. 

NRC - 42 Committee on Swine Nutrition. 1974. Cooperative regional 

studies with growing swine: the effects of vitamin E and levels of 

supplementary copper during the growing finishing period on gain, 

feed conversion, and tissue copper storage in swine. Jour. Anim. 

sci. 39: 512. 

C-62 
NusSaum, M.J. and A. Zettner. 1973. The content of calcium, magnesium, copperr iron, sodium, and potassium in amniotic fluid from 

eleven to nineteen weeks' gestation. Am. Jour. Obstet. Gynecol. 

115: 219. 

Oakes, B.W., et al. 1976. Human copper deficiency: ultrastructural studies of the aorta and skin in a child with Menkes' syndrome. Exp. Mol. Pathol. 25: 82. 

O'Dell, B.L., et al. 1961. Connective tissue defect Fn chicks resulting from copper deficiency. Proc. Sot. Exper. Biol. Med. 

108: 402. 

Ohlson, M.A. and K. Daum. 1935. A study of the iron metabolism of 

normal women. Jour. Nutr. 9: 75. 

Ohtake, M. 1977. Serum, zinc, and copper levels in healthy Japanese infants. Tokyo Jour. Exp. Med. 123: 265. Chem. Abstr. 

88: 350243. 

Okuyama, M., et al. 1977. Study on copper level in endometrium of 

women using copper IUDs. Osaka-Shiritsu Diagaku Xgaku Zasshi. 

26: 53. Chem. Abstr. 89: 85133F. (Jap. 1 

Omura, H., et al. 1978. Mutagenic action of triose reductone and 

ascorbic acid on Salmonella typhimurium strain TAlOO. Jour. Nutr. 

Sci. Vitaminol. 24: 185. 

C-63 
Oreke, T., et al. 1972. Systemic absorption of intrauterine CODper. Science. 177: 358. 

Osaki, S., et al. 1966. The possible significance of the ferrous 

oxidase activity of ceruloplasmin in normal human serum. Jour. 

Biol. Chem. 241: 2746. 

Osborn, S.B., et al. 1963. Uptake of radioactive copper by the 

liver. A study of patients with Wilson's disease and various control groups. Clin. Sci. 24: 13. 

Oster, G. and M.P. Salgo. 1977. Copper in mammalian reproduction. 

Adv. Pharmacol. Chemother. 14: 327. 

Patterson, J.B.E. 1971. Metal toxicities arising from industry. 

Trace elements in soils and crops. ?IMSO Ministry Agrfc. Fish. 

Food, London Tech. Bull. 21: 190. 

Pedrero, E. and F.L. Rozelka. 1951. Effect of various pathological conditions on Cu content of human tissues. A.M.A. Arch. 

Pathol. 52: 447. 

Pennsylvania Morbidity and Mortality Weekly Reports. 1975. Acute 

copper poisoning, Drinks that are stored in copper-lined cocktail 

shakers or vessels can have the same effect. 24: 99. 

C-64 
Petering, H.G. 1974. The Effect of Cadmium and Lead on Copper and 

Zinc Metabolism. In: W.G. Hoekshra, et al. (eds.), Trace Element - 

Metabolism in Animals-2. University Park Press, Baltimore. 

p. 311. 

Petering, H.G., et al. 1971. Trace metal content of hair. I. Zinc 

and copper content of human hair in relation to age and sex. Arch. 

Environ. Health. 23: 202. 

Phillips, D.J.H. 1976. The common mussel Mvtilus edulis as an 

indicator of pollution by zinc, cadmium, lead and copper. I. Effects of environmental variables on uptake of metals. Mar. Biol. 

38: 59. 

Pimental, J.C. and F. Marques. 1969. 'Vineyard sprayer's lung': A 

new occupational disease. Thoras. 24: 670. 

Pimental, J.C. and A.P. Menezes. 1975. Liver granulomas containing copper in vineyards sprayer’s lung. A new etiology of hepatic 

granulomatosis. Am. Rev. Respir:. Dis. 111: 189. 

Porter, H. 1951. Copper excretion in the urine of normal individuals and of patients with hepatolenticular degeneration (Wilson's 

disease). Arch. Biochem. Biophys. 31: 262. 

Quijada, S., et al. 1978. Fertility inhibition by intra-oviductal 

insertion of copper beads in rabbits. Contraception. 17: 553. 

C-65 
Roberts, R.R. 1956. Hemolytic anemia associated with copper sulfate poisoning. Miss. Doctor. 33: 292. 

Robinson, M.F., et al. 1973. Metabolic balance of zinc, copper, 

cadmium, iron, molybdenum and selenium in young New Zealand women. 

Br. Jour. Nutr. 30: 195. 

Russ, E.M. and J. Raymunt. 1956. 

serum copper and ceruloplasmfn. 

92: 465. 

Influence of estrogens on total 

Proc. Sot. Exp. Biol. Med. 

Salmon, M.A. and T. Wright. 1971. Chronic copper poisoning presenting as 'pink' disease. Arch. Dis. Child. 46: 108. 

Sass-Kortsak, A. and A.G. Beatn. 1978. Hereditary Disorders of 

Copper Metabolism [Wilsonls disease (hepatolenticular degenetation) and Menkes' disease (kinky-hair or steely-hair syndromejl. 

In: J.B. Stanbury, et al. (eds.), Metabolic Basis of Inherited Disease, 4th ed. McGraw-Eill, New York. p. 1098. 

Scheinberg, I.B. 1961. Proc. Fed. Am. Sot. Exp. Biol. 20: 

10: 179. 

Scheinberg, I.K. and D. Gitlin. 1952. Deficiency of ceruloplasmin 

in patients with hepatolenticular degeneration (Wilson's disease) l 

Science. 116: 484. 

C-66 
Scheinberg, I.H. and I. Sternlieb. 1969. Metabolism of Trace Yetals. In: B.R. Bondy (ea.), Duncan's Diseases of Metabolism, Vol. 

2, Endocrinology and Nutrition. 6th ed. W.D. Saunders Co., Philadelphia. 

Scheinberg, I.R., et al. 1954. The concentration of copper and 

ceruloplasmin in maternal and infant plasma at delivery. Jour. 

Clin. Invest. 33: 963. 

Schorr, J.B., et al. 1958. Studies of serum ceruloplasmin during 

early infancy. Am. Jour. Dfs. Child. 96: 541. 

Schroeder, H.A. 1970. A sensible look at air pollution by metals. 

Arch. Environ. Health. 21: 798. 

Schroeder, H.A., et al. 1966. Essential trace metals in man. Copper. Jour. Chronic Dis. 19: 1007. 

Seeling, W., et al. 1977. The trace elements, chromium, manganese, copper and zinc in fetal liver tissue, Jour. Perinatal Med. 

38: 55. 

Shaw, J.C.L. 1973.. Parenteral nutrition in the management of sick 

low birth rate infants. Pediatric Clin. N. Am. 20: 333. 

Shields, G.S., et al. 1961. Studies on cooper metabolism. XXXI. 

Erythrocyte copper. Jour. Clin. Invest. 40: 2007. 

C-67 
Shuster, C.N., Jr. and B.H. Pringle. 1968. Zffects of trace netals on estuarine molluscs. Proc. First Mid-Atl. Indus. Waste 

Conf., NOV. 13-15, 1967. p. 285. 

Shuster, C.N., Jr. and B.H. Pringle. 1969. Trace metal accumulation by the American eastern oyster, Crassosstrea virginica. PKOC. 

Natl. Shellfish. Assoc. 59: 91. 

Smith, 8. 1967. The distribution of antimony, arsenic, copper and 

zinc in human tissue. Jour. Forensic Sci. Sot. 7: 97. 

Smith, J.C., Jr. and E.D. Brown. 1976. Effects of Oral Contraceptive Agents on Trace Element Metabolism: A Review. G: A.S. Prasad 

and D. Oberleas teds.), Trace Elements in Human Health and Disease. 

Academic Press, New York. 2: 315. 

Smith, S.E. and E.J. Larson. 1946. Zinc toxicity in rats: antagonistic effects of copper and liver. Jour. Biol. Chem. 163: 29. 

Spillane, J.D., et al. 1952. Amino-aciduria and copper metabolism 

in hepatolenticular degeneration. Jour. Clin. Pathol. 5: 16. 

Starcher, B.C. 1969. Studies on the mechanism of copper absorption in the chfck, Jour. Nutr. 97: 321. 

Stephan, C.E. 1980. Memorandum to J. Stara. U.S. EPA. July 3. 

C-68 
Sternlieb, I. 1967. Gastrointestinal copper absorption in Tan. 

Gastroenterology. 52: 1038. 

Sternlieb, I. and H.D. Janowitz. 1964. Absorption of copper in 

malabsorption syndromes. Jour. Clin. Invest. 43: 1049. 

Sternlieb, I. and 1-H. Scheinberg. 1964. Penicillamine therapy 

for hepatolenticular degeneration. Jour. Am. Med. Assoc. 

189: 748. 

Sternlfeb, I. and I.H. Scheinberg. 1968. Prevention of Wilson's 

disease in asymptomatic patients. New England Jour. Med. 

278: 352. 

Sternlfeb, I., et al. 1961. The incorporation of copper into 

ceruloplasmin in viva: Studies with copper 64 

-- and copper 67 

. Jour. 

Clin. Invest. 40: 1834. 

Sternlieb, I., et al. 1962. The ,unfqueness of ceruloplasmin in 

the study of plasma plaamin proteinsynthesis. Trans. Assoc. Am. 

Physicians. 75: 228. 

Sternlieb, I.# et al. 1973. Lysosomal defect of hepatic copper 

excretion in Wilson's disease (hepatolenticular degeneration) l 

Gastroenterology. 64: 99. 

C-69 
Strickland, G.T., et al. 1972a. Absorbtion of copper in homozygotes and heterozygotes for Wilson's disease and controls: Isotope 

tracer studies with 67Cu and 64cu. Clin. Sci. 43: 617. 

Strickland, G.T., et al. 1972b. Turnover studies of copper in 

homozygotes and heterozygotes for Wilson’s disease and controls: 

Isotope tracer studies with 67cu . Clin. Sci. 43: 605. 

Sumino, R., et al. 1975. Heavy metals in normal Japanese tissues. 

Amounts of 15 heavy metals in 30 subjects. Arch. Environ. Health. 

30: 487. 

Suttle, N.F. and C.F. Mills. 1966. Studies of the toxicity of copper to pigs. 2. Effect of protein source and other dietary components on the response to high and moderate intakes of copper. Br. 

Jour. Nutr. 20: 149. 

Tamaya, T., et al. 1978. Effect of copper IUD on the human endometr ium. Nippon Funin Gakkai and Zasski. 23: 24. Chem. Abstr. 

88: 164776A. (Jap. 1 

Tatum, H.J. 1974. Copper-bearing intrauterine devices. Clin. 

Obst. Gynecol.. 17: 93. 

Thornton, I., et al. 1966. Geochemical reconnaissance and bovine 

hypocuprosis in County Limerick, Ireland. Irish Jour. Agric. Res. 

5: 280. 

c-70 
Tipton, I.H. and M.J. Cook. 1963. Trace elements in human tissue. 

II. Adult States. Health Phys. 9: 103. 

Tokudome, S. and M. Kuratsune. 1976. A cohort study on mortality 

from cancer and other causes among workers at a metal refinery. 

Int. Jour. Cancer. 17: 310. 

Tompsett, S.L. 1934. The excretion of copper in urine and faeces 

and its relation to the copper content of the diet. Biochem. Jour. 

28: 2088. 

Trip, J.A., et al. 1969. The state of copper in human lymph. 

Clin. Chim. Acta. 26: 371. 

Underwood, E.J. 1977, Trace Elements in Buman and Animal Nutrition, 4th ed. Academic Press, New York. 

U.S. Bureau of Mines. 1976. Copper. Commodity data summaries. 

1976. An up-to-date summary of 95 mineral commodities. U.S. 

Dept. Inter., Washington, D.C. 

U.S. Department of Health, Education and Welfare. 1970. Significance of national findings. Publ. Health Serv. Environ. Health 

Serv. Bull. Water Hyg. Community Water Supply Study. Washington, D.C. 

c-71 
U.S. EPA. 1980. Seafood consumption data analysis. Stanford Research Institute International, Menlo Park, Calif., Final Report, 

Task 11. Contract No. 68-01-3887. 

Vallee, B.L. 1952. The time course of serum copper concentrations 

of patients with myocardial infarctions. Metabolism. 1: 420. 

Van Ravensteyn, A.H. 1944. Metabolism of copper in man. Acta Med. 

Stand. 118: 163. 

Villar, T.G. 1974. Vineyard sprayer's lung: Clinical aspects. 

Am. Rev. Respir. Dis. 110: 545. 

Vilter, R.W., et al. 1974. Manifestation of copper deficiency in 

a patient with systemic sclerosis on intravenous hyperalimentation. 

New England Jour. Med. 291: 188. 

Voelker, R.W., Jr. and W.W. Carlton. 1969. 

acid on copper deficiency in miniature swine. 

30: 1825. 

Effect of ascorbic 

Am. Jour. Vet. Res. 

Wahal, P.K., et al. 1965. Renal complications in acute copper 

sulphate poisoning. Ind. Pratt. 18: 807. 

Waldmann, T.A., et al. 1967. Measurement of gastrointestinalprotein loss using ceruloplasmin labeled with 67 copper. Jour. Clin. 

Invest. 46: 10. 

C-72 
Walker, W.R. 1977 I The couper bracelet story: Some aspects of the 

role of copper in the inflammatory disease. Chem. Austr. 44: 247. 

Walker, W.R., et al. 1977. Profusion of intact skin by a saline 

solution of bfs (glycinato) copper (II). Bioinorganic Chem. 

7: 271. 

Walker-Smith, J. and J. Bloomfield. 1973. Wilson's disease or 

chronic copper poisoning? Arch. Dis. Child. 48: 476. 

Walsh, F.M., et al. 1977. Acute copper intoxication. Pithophysiology and therapy with a case report. Am. Jour. Dis. Child. 

131: 149. 

Walshe, J.M. 1956, Penicillamine, a new oral. therapy for Wilson’s 

disease. Am. Jour. Med. 21: 487. 

Weber, P.M., et al. 1969. Gastrointestinal absorption of copper: 

Studies with 64cu, g5 Zr, a whole body counter and the scintillation 

camera. Jour. Nucl. Med. 10: 591. 

Widdowson, E.M. and J.W.T. Dickerson. 1964. Chemical Composition 

of the Body. Et C.L. Comar and F. Bronner teds.), Mineral Metabolism: An Advanced Treatise. Academic Press, New York. p. 1. 

Widdowson; E.M. and C.M. Spray. 1951. Chemical development & 

utero. Arch. Dis. Child. 26: 205. 

c-73 
Widdowson, E.M., et al. 1951. The chemical ccmpasitiDn of the 

human body. Clin. Sci. 10: 113. 

Williams, D.M., et al. 1973. Mitochondrial iron metabolism. Fed. 

Proc. 32: 924. 

World Health Organization. 1973. Trace elements in human nutrition. Tech. Rep. Ser. No. 532. Rep. WHO Expert Comm. World Health 

Organ., Geneva. 

World Metal Statistics. 1974. Copper. 27: 33. 

Zak, B. 1958. Simple procedure for the single sample determination of serum copper and iron. Clin. Chim. Acta. 3: 328. 

Zarooqian, G. 1978. EPA Environmental Research Lab, Narragansett, 

Rhode Island. (In preparation). 

Zook, E.G., et al. 1970. Nutrient composition of selected wheats 

and wheat products. VT. Distribution of manganese, copper, nickel, 

zinc, magnesium, lead, cadmium, chromium and selenium as determined 

by atomic abaorbtion spectroscopy and calorimetry. Cereal Chem. 

47: 720. 

c-74