Element Concentrations 

Toxic to Plants, 

Animals, and Man

G F 0 L 0 G I C A L S U R V E Y B I I. I. F T IN

Element Concentrations 

Toxic to Plants, 

Animals, and Man

* By LARRY P. GOUGH, HANSFORD T. SHACKLETTE, and 

ARTHUR A. CASE

GEOLOGICAL SURVEY BULLETIN 1466

An appraisal of the toxicity hazard 

to plants, animals, and man from 

natural and manmade element 

concentrations of environmental concern

UNITED STATES GOVERNMENT PRINTING OFFICE, WASHINGTON : 1979
UNITED STATES DEPARTMENT OF THE INTERIOR 

CECIL D. ANDRUS, Secretory

GEOLOGICAL SURVEY 

H. William Menard, Director

Library of Congress catalog-card No. 79-66277

For sale by the Superintendent of Documents, U.S. Government Printing Office

Washington, D.C. 20402 

Stock Number 024-001-03201-5
CONTENTS

Introduction ............................................................................................................................ 1

Aluminum .............................................................................................................................. 4

Antimony ................................................................................................................................ 7

Arsenic .................................................................................................................................... 8

Beryllium .............................................................................................................................. 11

Boron ...................................................................................................................................... 13

Bromine .................................................................................................................................. 14

Cadmium .............................................................................................................................. 15

Chlorine ................................................................................................................................ 17

Chromium .............................................................................................................................. 19

Cobalt .................................................................................................................................... 20

Copper .................................................................................................................................... 22

Fluorine ................................................................................................................................ 24

Iodine ...................................................................................................................................... 27

Lead ........................................................................................................................................ 28

Lithium .................................................................................................................................. 31

Manganese ............................................................................................................................ 33

Mercury ................................................................................................................................ 35

Molybdenum ........................................................................................................................ 36

Nickel .................................................................................................................................... 38

Selenium ................................................................................................................................ 40

Silver ...................................................................................................................................... 44

Sulfur .................................................................................................................................... 46

Thallium ................................................................................................................................ 49

Tin .......................................................................................................................................... 51

Uranium ................................................................................................................................ 52

Vanadium .............................................................................................................................. 55

Zinc ......................................................................................................................................... 56

Other elements that possibly present a toxicity hazard .......................................... 59

Barium .......................................................................................................................... 59

Germanium ................................................................'.................................................. 59

Magnesium .................................................................................................................. 60

Rubidium ...................................................................................................................... 61

Tellurium ...................................................................................................................... 61

Titanium ........................................................................................................................ 61

Tungsten .........................................................................................^.....,....................... 62

Zirconium ..................................................................................................................... 63

Rare earth elements (lanthanides) ................................................................................ 63

Cerium .......................................................................................................................... 64

Lanthanum .................................................................................................................. 64

Dysprosium, gadolinium, holmium, neodymium,

praseodymium, samarium, terbium, and thulium ............................................ 64

Erbium, europium, and lutetium ............................................................................ 65

References cited .................................................................................................................. 65

Appendix .............................................................................................................................. 78

ni

ELEMENT CONCENTRATIONS TOXIC 

TO PLANTS, ANIMALS, AND MAN

By LARRY P. GOUGH, HANSFORD T. SHACKLETTE, and 

ARTHUR A. CASE

INTRODUCTION

Investigators have long recognized the importance of certain elements, commonly called "minerals," in the diet of humans and animals 

and in the soil that supports plants, in that these elements are essential for the life or optimum health of the organisms. Deficiencies of 20 

to 24 elements in animals and man (Frieden, 1972) and of 13 to 18 

elements in plants (Epstein, 1965) have been recognized. At the same 

time, an understanding of the responses of these organisms to the 

insult of toxic concentrations of these and other elements also has been 

of interest. More recently, concern has arisen regarding the effects of 

an organism's exposure to the more subtle chronic and subchronic 

concentrations of certain elements that industrial and other human 

activities are releasing into the environment.

Many studies of element toxicities have been made, and reports of 

these studies are scattered through the biological, medical, geological, 

and other literature. The present requirement for preparing environmental impact statements before certain types of industrial and other 

operations are undertaken necessitates that judgments be made regarding the potential health effects, if any, of elements that may be 

released into the environment by these operations. Although these 

judgments may be outside the fields of the physical and biological 

scientists who must predict environmental impacts that are likely to 

occur, certain valid estimations can be made inadequate information is 

available. The purpose of this outline is to provide some specific data on 

the known toxicity levels of certain elements that may reach potentially dangerous concentrations in the environment. We have limited 

our emphasis to toxic levels that are acquired by organisms through 

absorption, ingestion, and inhalation; intravenous, subcutaneous, intramuscular, or intraperitoneal injections of toxic elements can hardly 

be considered of environmental concern. We have given but little 

emphasis to the effects of occupational exposure to hazardous chemical 

compounds.
2 ELEMENT CONCENTRATIONS TOXIC TO PLANTS, ANIMALS, AND MAN

Much has been written on the toxicities of some elements such as 

lead, mercury, and selenium, and our chief task with these elements 

was that of selecting the most useful reports to include. For some other 

elements, reports of toxicities are few and often in obscure publications. The elements selected for this discussion are those that may be 

environmentally important and especially those for which we have 

quantitative data. Some of the information in this outline is from 

unpublished data in our files; most statements, however, are identified 

by reference citations.

The elements are presented alphabetically by their common English 

names. We have divided the notes on each element into three parts 

plants, animals, and man and classified associated toxicities under 

natural and man-induced conditions, where appropriate. References to 

the toxicities of a few elements of possible environmental concern are 

inadequate for an evaluation to be made of their hazard. These elements are grouped near the end of this report, and a general discussion 

is given of the available information on each element.

Concentrations of elements generally are presented as parts per 

million (ppm), although other methods of expressing concentrations 

may be quoted. In some instances units such as mg/kg of body weight, 

jumoles/L, ju,g/m3 , parts per billion (ppb), or percent provide a clearer 

concept for a given example, and converting them to ppm was considered to be unnecessary. A part per million is 10~4 percent and a part 

per billion is 10~7 percent.

It will be noted in this report that many of the elements are essential 

for plants or animals, yet are toxic under certain conditions (Wallace, 

Romney, Alexander, and Kinnear, 1977). The toxicity of an element 

depends, first of all, on its chemical form. For example, chlorine in the 

elemental form (a gas) is highly toxic, whereas chlorine compounds 

may be relatively harmless, as is sodium chloride (common salt). 

Conversely, elemental arsenic is not toxic, although some arsenical 

compounds are highly toxic. Many reports do not specify the chemical 

form of an element when discussing its toxicity. It can be assumed for 

most of these reports that, under the specified natural or experimental 

conditions, the element existed in an undetermined compound and 

that only the total concentration of the element was known. For most 

reports in which the basis for expressing concentrations of an element 

in plant or animal tissues is not specified, a dry-weight basis can be 

assumed.

The toxicity of a substance is also determined by the dosage that is, 

the amount (in relation to body weight or to the growth medium) and 

the frequency and duration of administering the substance to the 

organism. The duration of specified dosages of toxic elements was not 

given by some investigators, including Bowen in table 7.4 of his 1966
INTRODUCTION 3

paper. Some reports define the minimum lethal dose (MLD); that is, the 

amount of a substance that kills the organism in one dose. In reports 

that relate toxicity to body weight of the experimental animals, "live" 

or "wet" weight of the animal is commonly used. Amounts of an element in relation to body weight are expressed as ingested amounts, 

unless otherwise noted. The term "LD50" means that the specified dose 

is lethal to 50 percent of the experimental organisms. Quantities of 

total diets given are based on a one-day consumption, unless otherwise 

stated.

Tb be toxic, an element must be "available" to the plants or 

animals that is, it must exist in a form that can enter tissues of the 

organism either in solution (generally aqueous), as a gas, or (uncommonly) as a solid; or it must emit ionizing radiation. Tbtal amounts of a 

toxic element in the environment are not relevant to an adequate 

estimation of the toxicity hazard that may be present unless it can be 

shown that the element exists in, or is likely to assume, an available 

form under the environmental conditions in which it occurs.

The toxicities of elements resulting from ionizing radiation are not 

discussed in this report. Although these elements may be of primary 

concern in some environmental studies, an adequate appraisal of their 

impact on plants, animals, and man is beyond the scope of this report. 

Exposures of organisms to natural occurrences of radiation levels 

significantly higher than those found in the normal environment are 

not common, and the effects of these exposures have been but rarely 

noted. Because the areas where these radiation levels are found generally are very limited in extent, the mobility of the larger animals 

reduces their period of exposure to this radiation. We have reports of 

the effects of naturally occurring radiation only for plants. The studies 

by Shacklette of bog bilberry (1962a) and of fire weed (1964) that grew 

over a near-surface uranium (pitchblende) deposit demonstrated conspicuous morphological changes that were attributed to genetic modification caused by radiation. In later reports by Steere (1974; 1977, p. 

426), the evolution of a new species of moss (Coscinodon arctolimnia) at 

the same pitchblende deposit noted above was suggested to be ". . . the 

end result of a progressive series of multiple mutations induced by 

natural radioactivity over a period of thousands of years." These are 

the only reports that we have of the influence of naturally occurring 

radiation on morphological, and perhaps genetic, changes in plants.

Experimental studies by Cannon (1957) demonstrated that morphological changes in native plant species (prince's plume, among 

others) could be induced by "salting" natural soils with radioactive 

agents. The extensive experimental studies of the effects of radiation 

from radioactive isotopes on many kinds of organisms, and the increased body burdens of radioactivity in native plants, animals, and
4 ELEMENT CONCENTRATIONS TOXIC TO PLANTS, ANIMALS, AND MAN

man caused by radioactive fallout from nuclear explosions, are not 

reviewed in this report.

Some types of landscape disturbance may result in a deficiency of 

certain elements that are essential to organisms in low, but toxic in 

high, concentrations. Amounts of these elements that are nutritionally required for the major classes of organisms cannot be generalized 

because they are highly dependent on characteristics of different 

species. Therefore, we have only noted the essentiality of an element, 

or lack thereof, for the larger classes of organisms, following the 

generally accepted concepts of essentiality for the element. The list of 

essential elements is subject to change because the metabolic role of 

the trace elements is continually being reappraised by experimental 

studies. Moreover, the definition of essentiality depends on the views of 

the investigators, which range from a strict concept that only growth 

and reproduction are required to broader concepts that include optimum health and growth of the organism. Generally accepted criteria 

for determining essentiality of an element for animals were given by 

Underwood (1958, p. 34) as follows: "(1) Repeated demonstration of a 

significant growth response to dietary supplements of the element and 

this element alone; (2) development of the deficiency state on diets 

otherwise adequate and satisfactory, i.e., containing all other known 

dietary essentials in adequate amounts and proportions and free from 

toxic properties; and (3) correlation of the deficiency state with the 

occurrence of subnormal levels of the element in the blood or tissues of 

animals exhibiting the response." The same principles can be applied 

to determining essentiality of an element to plants and other organisms. A method of determining whether an element is essential or 

nonessential in human tissues was proposed (Liebscher and Smith, 

1968) based on essential trace elements having a "normal" distribution 

of concentrations and nonessential trace elements having a "lognormal" distribution, but the validity of this method has not been fully 

tested.

Gough and Shacklette (botanists) of the U.S. Geological Survey 

prepared this report with the assistance of Case (clinical veterinarian, 

toxicologist) of the School of Veterinary Medicine, University of 

Missouri Columbia.

ALUMINUM

[Nonessential for plants and animals]

Plants

Under natural conditions Because aluminum is abundant in most 

soils, toxicity is largely dependent on the exchangeable amount present due to low soil pH. Only small quantities of soluble aluminum
ALUMINUM 5

were found by Magistad (1925) in soils that had pH values between 4.7 

and 7.8. Pierre (1931, p. 193-194) stated, in discussing his experiments, 

"It will be noted that the concentrations of aluminum in the soil 

solutions are in most cases very small, even at low pH values. ... As 

was to be expected it was found that the greater the hydrogen-ion 

concentration of a particular soil, the greater is the concentration of 

aluminum in its displaced soil solution." For instance, in Gory silt loam 

he found 5.7 ppm aluminum in the soil solution at pH 4.43, but only a 

trace of aluminum at pH 6.00. Agronomists have demonstrated that 

varieties of cultivated species vary greatly in their aluminum tolerance. Foy and others (1967) reported that aluminum-sensitive wheat 

and barley cultivars apparently mobilize soil aluminum, and thereby 

increase its availability, by lowering the pH of the rhizosphere. Because of aluminum toxicity, certain crops cannot be grown on some 

naturally acid soils without applications of lime. In contrast, some 

plants are known as "aluminum accumulators" and may contain as 

much as 37 percent aluminum in ash.

Under man-induced conditions Susceptibility to aluminum 

poisoning differs widely among plant species. McLean and Gilbert 

(1927) classified 12 crop plants according to their sensitivity to aluminum in culture solutions as follows: sensitive (depressed by 2 ppm 

aluminum) barley, beet, lettuce, and timothy; intermediate (depressed by 7 ppm) cabbage, oats, radish, rye, and sorghum; and tolerant (depressed by 14 ppm) corn, redtop, and turnip. Wallace and 

Romney (1977) reported, "The threshold concentration of Al for toxicity was about 20 /Ltg/g in rice shoots and about 30 /ug/g in soybean 

leaves. The solution level necessary for these concentrations was 8 /Ltg 

Al/ml. Plant concentrations which caused severe toxicity were 70 //.g 

Al/g plant with 81 /xg Al/ml solution. Most Al remained in roots, but 

leaves contained more than did stems of soybeans." Acidic mine spoil 

and drainage waters may be suspected of causing aluminum poisoning 

in some native and cultivated plants. 

Animals

Under natural dietary conditions We have no reports of animal 

toxicity attributed to naturally occurring aluminum in the environment. Bentonite, kaolin, A12(S04)3 , A12 03 , and A1(OH)3 have been used 

as growth stimulants for rabbits, chickens, sheep, cattle, and hogs 

without adverse effects as long as they composed no more than 1-2 

percent of the diet (Sorenson and others, 1974). It seems very unlikely 

that grazing animals, even those that consume a relatively large 

proportion of their diet as soil (such as sheep and horses), would ever 

achieve these concentrations naturally. Several investigators have 

reported that aluminum is a specific root poison for many species and 

that the poisoned roots are unable to translocate the element to other
6 ELEMENT CONCENTRATIONS TOXIC TO PLANTS, ANIMALS, AND MAN

parts of the plant (Pratt, 1966a); therefore there seems to be little 

likelihood that grazing animals are affected by these plants. On the 

other hand, sweetleaf, an aluminum accumulator (Robinson and Edgington, 1945), is a preferred browse shrub for horses and cattle (Small, 

1933); yet no toxicity symptoms in these animals have been reported as 

due to aluminum. However, Hutchinson (1943) concluded that this 

plant, reported to contain 2.4 3.5 percent aluminum in dry matter, 

could not constitute the sole diet of these animals because of the 

inhibitory effect of aluminum on phosphorus metabolism.

Under man induced dietary conditions Acute toxicity studies involving laboratory animals were reviewed by Sorenson and others (1974). 

These authors gave the LD50 for A12 (SO4)3 administered orally to mice 

as 6.2 g/kg and for A1C13 as 3.85 g/kg. Further, the LD50 for A1(NO3)3 

 9H2O to rats was given as 0.26 g/kg. Chronic toxicity results in 

several phosphorus-metabolism imbalances including excretion of 

phosphorus, decreased incorporation of phosphorus into phospholipids, 

and a drop in ATP and a rise in ADP levels in blood. Sorenson and 

others (1974) reported that 150 mg of AlCl3/kg/day fed to rats will result 

in the expression of these imbalances. They also reported that concentrations of aluminum in excess of 1.5 /ng/ml in the environment of 

rainbow trout fingerlings were lethal to some. Bowen (1966) listed 200 

mg A13+ in a 10-g/day dry-weight diet (20,000 ppm) as being toxic to 

rats, whereas 220 mg (22,000 ppm) was lethal. 

Man

Aluminum poisoning in humans appears to be rare. Smith (1928) 

reported that ingestion of 150 mg of aluminum per day is without 

obvious effects on normal humans; 200 mg may, however, give rise to 

mild catharsis, which increases with the dose. Sorenson and others 

(1974) reported that 5.5 mg of aluminum per kilogram of body weight 

in food and drink does not cause adverse effects in humans, probably 

because the aluminum is usually in the less-toxic colloidal form. Regarding absorption of inhaled airborne aluminum, Hutchinson (1943, 

p. 252) wrote, "The fact that all investigators have found aluminum in 

the bile indicates that some of the aluminum present in the faeces, as 

well as in the urine, has been involved in a metabolic cycle. It is 

conceivable that this aluminum has in part entered the blood stream 

through the pulmonary epithelium, but if such a mode of entry were 

generally important significant negative balances would have been 

reported wherever balance sheets have been made." A number of 

observations indicate that high concentrations of aluminum may be 

toxic to the nervous system (Crapper and others, 1973). These authors 

analyzed the brains of persons who died with Alzheimer's disease (a 

disease occurring after the age of 40 and producing progressive dementia) and found concentrations of aluminum similar to those in the
ANTIMONY 7

brains of experimental animals that had been injected with 150-225 

/u,g aluminum, as aluminum chloride, and that as a result had developed neurological symptoms similar to those of Alzheimer's disease 

in humans. Pulmonary fibrotic reactions to inhaled silica and certain 

aluminum-containing compounds can result in silicosis, aluminosis, 

aluminum lung, and bauxite pneumoconiosis (Sorenson and others, 

1974).

ANTIMONY

[Considered nonessential for plants and animals]

Plants

Under natural conditions Brooks (1972) listed toxicity to 

plants as moderate; we have found, however, no reported cases of 

natural poisoning. Shacklette (1965b) reported that a birch tree growing over, and having root contact with, mercury, antimony, and arsenic 

minerals in Alaska contained 50 ppm antimony in the ash of stems, yet 

the tree exhibited no symptoms of toxicity. Samples of 27 trees and 

shrubs that grew over this deposit, but which were not proven to have 

root contact with these minerals, contained 7 50 ppm antimony in 

stem ash without evidence of toxicity to the plants, even though the 

soil contained as much as 95 ppm antimony (Shacklette and others, 

1978). Brooks (1972) reported 1 ppm as the concentration in plant ash. 

Soils were reported by Brooks (1972) to contain 0.5 ppm only half the 

value he reported in plants which suggests that plants concentrate 

this element above the levels in soils. The studies in Alaska cited above 

do not support this view, nor did Lisk (1972), who gave the plants/soil 

antimony ratio as 0.01. In analyses of 863 soil samples from throughout 

the conterminous United States, one sample was found to contain 500 

ppm antimony; all other samples contained less than 150 ppm (the 

lower detection limit of the analytical method that was used) 

(Shacklette and others, 1971). The single high value was attributed to 

contamination of the sampling site by fluorspar mine tailings.

Under man-induced conditions We have no reports of experimental studies of the toxicity to plants caused by this element. 

Animals

Under natural dietary conditions Because of the low concentrations of antimony believed generally to occur in plants, toxicity to 

animals from plant sources is unlikely. Sittig (1976) reported, however, 

that marine animals concentrate antimony in their muscle tissue, and 

that studies had indicated certain levels in this tissue that were toxic 

to some fish.

Under man-induced dietary conditions Sea birds were killed in the 

Irish Sea in 1969 in a massive disaster, the cause of which was unknown but suspected to be ocean dumping of industrial wastes.
8 ELEMENT CONCENTRATIONS TOXIC TO PLANTS, ANIMALS, AND MAN

Holdgate (1971) reported that livers of the dead birds contained concentrations of antimony ranging from 40 to 400 ppm, and Tucker (1972) 

stated that the 400 ppm that was found could be considered the approximate lethal threshold. Extremely low concentrations of antimony in 

feed were shown by experiments to shorten the life span of small 

mammals (Schroeder, 1974a). 

Man

Under normal environmental conditions There seems to be little 

danger to man from concentrations of antimony that are commonly 

encountered in natural materials. The levels in foodstuffs, however, 

are not well established.

Under the effects of contamination by industrial operations Exposure 

to antimony dust can cause irritation of nasal passages, eyes, and 

lungs. Ingestion of 100 mg is fatal (Schroeder, 1974a). Occupational 

exposure to antimony ore, elemental antimony, and antimony oxides 

has been implicated in a lung disease (pneumoconiosis), whereas exposures to antimony trisulfide have been associated with cardiovascular 

changes (Sittig, 1976). This writer reported further (p. 7), "There is no 

evidence that antimony is carcinogenic, teratogenic, or a mutagen."

ARSENIC

[Considered nonessential to plants and animals]

Plants

Under natural conditions Although the free element is not considered poisonous, some of its compounds are extremely so (Liebig, 

1966). Brooks (1972) stated that the toxicity of this element to plants 

was severe. It was reported (Embleton and others, 1976) that >5 ppm 

(dry matter) arsenic in the leaf tissue of Navel and Valencia oranges is 

probably an excessive amount. The arsenic in normal soils ranges from 

<1 to 40 ppm (Underwood, 1971); within this range, damage to plants is 

not expected, and the arsenic content of most species is low (<10 ppm; 

arsenic in the leaf tissue of Navel and Valencia oranges is probably 

based on dry weight). Soils in the vicinity of some heavy-metal deposits 

may contain much more arsenic, and Douglas-fir growing in such soils 

may contain as much as 8,200 ppm in ash (Warren and others, 1968).

Under man-induced conditions The toxicity to plants of certain 

arsenic compounds, principally sodium arsenite and arsenic trioxide, 

is so great that these compounds were used as herbicides for many 

years. Arsenic compounds such as calcium arsenate, lead arsenate, 

and cupric arsenite (Paris green) formerly were widely used as insecticides. The long-term use of these materials in agricultural practice 

accounts for most recorded cases of plant toxicities. The National 

Research Council (1977a) reported from the literature that leaves of
ARSENIC 9

fruit trees displaying toxicity symptoms (shot-holing and defoliation) 

had arsenic concentrations of 2.1-8.2 ppm; normal leaves, 0.9-1.7 

ppm. The toxicity depends on the concentration of soluble, not total, 

arsenic in soils. Damage to alfalfa and barley was proportional to the 

concentration of soluble arsenic; if above 2 ppm, marked damage to the 

plants occurred (Vandecaveye and others, 1936). Soils "salted" with 

500 ppm sodium arsenate and allowed to come to equilibrium for 1 

month were toxic to all vegetable crops tested, whereas, at 10, 50, and 

100 ppm, crops survived (National Research Council, 1977a). Studies of 

unproductive, old orchard soils in the Yakima Valley, from which apple 

trees had been removed, revealed 3.4-9.5 ppm of readily soluble arsenic in the top 15 cm of soil. In Missouri, orchard soils with total arsenic 

levels above 100 ppm were considered to be highly contaminated (Hess 

and Blanchar, 1977). These authors also found that most of the arsenic 

was near the soil surface (upper 20 cm). Arsenic is introduced into the 

environment as an air pollutant from burning coal, and from smelters 

and refineries (Underwood, 1971), but we have no reports of damage to 

plants from these sources of arsenic. 

Animals

Under natural dietary conditions Examples of toxicity of arsenic to 

animals under natural conditions are believed to be uncommon. 

Grimmett (1939) investigated livestock poisoning in a valley of New 

Zealand and found that soils and muds contained as much as 1.9 

percent arsenic; water from springs, streams, and surface depressions 

varied from a trace to 13 ppm of arsenic; and pasture grasses contained 

2.8-6.9 ppm (dry weight) arsenic. He concluded that the danger to 

stock was not from the arsenic in the forage, but from that in the mud 

or water which might be ingested.

Under man-induced dietary conditions There is probably little 

danger of arsenic poisoning from feeding plants and plant products to 

animals. In fact, four organic arsenic compounds (arsenilic acid, 

4-nitrophenylarsonic acid, 3-nitro-4-hydroxyphenylarsenic acid, and 

arsenobenzene) are used as growth stimulants for pigs and poultry 

(Underwood, 1971). Selby and others (1974), however, reported the 

death of several cattle that grazed in pastures contaminated by high 

arsenic in the soil (probably the result of drainage from a refuse heap 

suspected of containing arsenic residues). Further, Case (1974) stressed that numerous reports in the literature emphasize the danger of 

allowing sheep or cattle to graze in orchards sprayed with arsenicals. 

Trivalent compounds (arsenites) are far more toxic than the pentavalent forms (arsenates). Case (1974) reported the following lethal oral 

dosages of sodium arsenite for sheep: for 1 of 48, 2 g; for 4 of 30,3 g; for 

14 of 15, 4 g. In addition, he stated that all sheep given 1 g of lead 

arsenate per day for 6 days died within 6 to 94 days. The National
10 ELEMENT CONCENTRATIONS TOXIC TO PLANTS, ANIMALS, AND MAN

Research Council (1977a) stated that, in general for most animals, the 

lethal oral dose is 1 25 mg/kg of body weight as sodium arsenite. The 

96-hour LD50 for mice and rats is 11.2 ppm arsenite in the diet, whereas 

it is 112 ppm for arsenate. Schroeder and Balassa (1966) reported that 

arsenic deactivates enzymes with thiol groups and acts as an antagonist of iodine and selenium.

Man

Under natural dietary conditions Water is the most common natural material causing arsenic poisoning. Amounts in excess of 0.05 mg/L 

in drinking water constitute grounds for rejection (U.S. Public Health 

Service, 1962). Wyllie (1937) reported illness and one fatality in a farm 

family that used water from a deep well having 0.4-10 ppm arsenic (as 

As2O3). Large beds of FeAsS occurred about 16 km from this well. 

Water from shallow wells near this farm were free of arsenic. Borgono 

and Greiber (1971) reported that prolonged consumption (12 years) of 

water high in arsenic (0.8 ppm) produced cutaneous lesions in over 30 

percent of the inhabitants of a city in Chile. Foods of plant origin 

contain so little arsenic that toxicity to humans is unlikely. Seafood 

contains much more arsenic maximum values reported (fresh 

weight) follow: oysters, 10 ppm; mussels, 120 ppm; prawns, 174 ppm; 

and shrimp, 42 ppm (Underwood, 1971). This author stated further that 

the amounts of arsenic ingested daily in the food are greatly influenced 

by the amounts and proportions of seafoods included in the diet.

General notes on toxicity Inhalation of high levels of arsenic released from powerplants and smelters may pose health problems. 

Friberg (1975) reported that coal from Czechoslovakia containing 

1,000-1,500 g of arsenic/ton of coal was responsible for the release of 

0.5-1.0 ton of arsenic per day into the atmosphere from a powerplant. 

Elemental arsenic is not toxic (Schroeder and Balassa, 1966), whereas 

most compounds of this element are highly toxic (Stecher, 1968). 

Schroeder and Balassa (1966) reported that mountaineers in Syria and 

the Alps have been known to consume large quantities of native 

arsenic ("arsen"), believing that it promotes endurance at high altitudes. The minimum fatal dose of arsenous oxide for man was given 

as 0.06-0.18 g by Monier-Williams (1949). This author also stated that 

the British Royal Commission set maximum limits of 1.4 ppm arsenic 

for solid foods and 0.14 for liquid foods including beverages. This limit 

for foods seems unrealistic, in view of the arsenic content of seafoods 

listed above. Thomas (1973) gave 5-50 mg/kg body weight as the 

probable lethal dose for an adult; Bowen (1966) listed as toxic 5-50 mg 

As(lll) or As(V) in a 750-mg/day dry-weight diet (7-67 ppm) and as 

lethal, on the same basis, 100-300 mg (133-400 ppm), duration not 

given. The National Research Council (1977) gave the average esti-
BERYLLIUM 11

mated fatal dose of arsenic trioxide as 125 mg. (For a 70-kg man, this is 

equivalent to about 1.4 mg/kg of body weight).

BERYLLIUM

[Considered nonessential for organisms]

Plants

Under natural conditions The toxicity of beryllium to plants is 

given as severe by Brooks (1972). The geometric mean for beryllium in 

847 samples of U.S. soils was reported to be 0.6 ppm with a range of <1 

to 7 ppm (Shacklette and others, 1971). Only a small proportion of this 

total amount, however, is actually available for absorption by plants. 

Beryllium often substitutes for aluminum in secondary.clay minerals. Further, it will displace divalent cations in the exchange complex 

and become strongly fixed in the soil. Beryl (beryllium aluminum 

silicate, the important beryllium-bearing primary mineral) contains 

about 5 percent beryllium, but beryl itself is biologically inert. Such 

compounds as beryllium chloride, beryllium fluoride, and beryllium 

sulfate are toxic to plants. Bidwell (1974) stated that beryllium is able 

to replace magnesium as an essential element in some fungi and partly 

in tomatoes. Further, it apparently stimulates the growth of some 

plants (ryegrass and kale) while inhibiting others (bean) (Bidwell, 

1974). We have no reports of beryllium toxicity to plants under field 

conditions.

Under man-induced conditions Because of new demands for the 

general use of beryllium in industry (particularly space and atomic 

energy research) there is concern that the concentration of beryllium 

in agricultural soils may be increasing. Very little is known, apparently, about beryllium cycling or its ability to enter the human food 

chain by being assimilated by crops. Romney and Childress (1965) 

found that beryllium (as beryllium chloride) at levels greater than 2 

ppm in nutrient solutions reduced the growth of alfalfa, lettuce, peas, 

and soybeans. Also, they reported that the yield of beans and wheat 

was reduced when beryllium occupied the equivalent of 4 percent of the 

cation-exchange capacity of soils. (Their experiments included a 

cation-exchange capacity for beryllium as high as 16 percent.) In a 

nutrient solution containing 16 ppm beryllium, plants showing toxicity symptoms of brown-root and stunted foliage had concentrations of 

beryllium in plant tops ranging from 27 ppm (dry weight) in alfalfa to 

75 ppm in peas. These authors concluded that, for the crops they 

studied, beryllium was not readily translocated to other plant parts 

from the roots. One report (Griffitts and others, 1977, p. 9) stated, 

"There is no evidence at present that beryllium is moving from soils
12 ELEMENT CONCENTRATIONS TOXIC TO PLANTS, ANIMALS, AND MAN

into food plants in the United States in amounts that are detrimental 

to plants, animals, or people."

Animals

Under natural conditions We have no reports of beryllium toxicity 

to animals grazing on native vegetation.

Under man-induced dietary conditions The toxicity of beryllium 

when ingested at chronic levels appears to be indirect. MonierWilliams (1949, p. 493) wrote, "Beryllium salts, when fed to rats, 

poultry, etc., produce the so-called beryllium rickets, due to immobilization of phosphorus by formation of insoluble beryllium phosphate." 

Beryllium, like cadmium and lead, has a long biological half-life and 

therefore tends to accumulate in animal tissues, particularly bone. 

When inhaled it generally causes chemical pneumonitis and once 

absorbed by the animal, competes with magnesium for enzymes 

(Dulka and Risby, 1976). These authors reported the LD50 for beryllium 

to mice as 0.5 mg/kg of body weight. The Subcommittee on Nutrient 

and Tbxic Elements in Water (1974) reported from the literature that 

28.5 mg/L beryllium was not very toxic to goldfish, minnows, and 

snails. Apparently, beryllium given to laboratory animals parenterally or by aerosols is strongly carcinogenic (Schroeder, 1974b).

Man

Although considered by Schroeder (1974b) to be, perhaps, the most 

toxic of all "environmental" metals, relatively few cases of beryllium 

poisoning in man have occurred. Ill effects on workers associated with 

beryllium was first noted in this country in 1940 (Schubert, 1958) 

among workers processing beryllium ores. Subsequently, many beryllium poisonings were reported in association with the fluorescent tube 

industry when exposure to phosphor dust was involved. Schubert 

(1958, p. 29) wrote, "By 1949 the list of cases had grown to such 

alarming proportions that the major manufacturers of fluorescent 

tubes decided in consultation with officials of the U.S. Public Health 

Service to discontinue the use of beryllium phosphors." Beryllosis is 

mainly a granulomatous disease of the lungs; however, ulcers and 

granulomatous skin lesions can result from beryllium absorbed directly into cuts and abrasions. Schroeder (1974b) reported that as little 

as 45 jug inspired beryllium has caused chronic beryllosis and that the 

disease has occurred when air containing 0.1 /u-g/m3 was inhaled (no 

time period given). Schubert (1958, p. 33) stated that ". . . the acute 

disease could be attributed to air concentrations of soluble salts in 

excess of 100 micrograms per cubic meter, and that when the air level 

exceeded 1,000 micrograms of beryllium, nearly everyone developed 

acute beryllium poisoning." Schroeder (1974b) reported that the combustion of coal (which can contain from 1-3,000 ppm beryllium) con-
BORON 13

tributes to the total amount already in the air from other industrial 

sources.

BORON

[Essential only for higher plants]

Plants

Under natural conditions The difference between required 

amounts of boron and toxic amounts is very small commonly only a 

few parts per million in soil. Analysis of total-soil boron is not very 

useful in predicting toxicity; the boron may be held in relatively 

insoluble compounds such as tourmaline, or in organic residues or 

marine sediments where it is more readily available. The amount of 

water-extractable boron in soil is a good index of essential or toxic 

levels (Bradford, 1966a). For example, early work by Kelley and Brown 

(1928) in California showed that >2.3 ppm water-soluble boron in the 

soil of citrus and walnut orchards was probably the toxic threshold. 

Sauchelli (1969) reported that extractable boron in the range of 0.5-1.0 

ppm promotes normal growth of orchard trees, whereas values above 

1.0 ppm are high and values above 2.0 ppm indicate possible toxicity. 

Boron tolerance varies widely among plant species; examples of this 

range of tolerance follow: sensitive lemon and other citrus trees, 

peach, navy be'an, and pecan; semitolerant lima bean, tomato, corn, 

wheat, and cotton; tolerant carrot, lettuce, onion, alfalfa, beet, and 

asparagus. Branson (1976) reported that, in general, the limits of boron 

tolerance, as measured in saturation extracts of soil, are 5 ppm for 

semitolerant and 10 ppm for tolerant crops. The following concentrations (ppm, dry matter) of boron in leaf tissue are considered excessive: 

>260, Navel and Valencia oranges (Embleton and others, 1976); >80, 

pears and plums; >85, almonds; >90, apricots; MOO, apples and 

peaches; >250, avocados (Jones and Embleton, 1976); >300, grapes 

(Cook and Wheeler, 1976); and >250, rutabaga (Gupta, 1977).

Under man-induced conditions Because the difference between 

essential and toxic amounts is so small, most cases of toxicity are 

caused by excessive amounts applied in fertilizers. John, Chuah, and 

Van Laerhoven (1977) found that hot-water soluble boron concentrations ranging from 16.4 to 50.1 ppm (resulting from the application of 

50-100 ppm boron) in three different soil types from British Columbia 

were toxic to spinach and corn. Tissue concentrations of boron in these 

experiments ranged from 348 to 409 ppm in spinach (dry matter) and 

from 1,077 to 1,758 ppm in corn. Tbxic amounts may also be introduced 

in irrigation water (Kelley and Brown, 1928). Where the boron content 

of water is 0.15 0.30 mg/L or more and 45 cm/ha (or more) of water is 

used, boron deficiency is unlikely. But if the boron content of the water
14 ELEMENT CONCENTRATIONS TOXIC TO PLANTS, ANIMALS, AND MAN

is greater than 1.1 mg/L, some sensitive crops will begin to show

toxicity symptoms (Bradford, 1966a).

Animals

Under natural dietary conditions Underwood (1971, p. 434) stated, 

"Boron intakes by grazing animals must be very variable, depending 

upon the soil type and on the plant species consumed, because the 

boron concentrations are influenced by the species and the boron 

status of the soil. These intakes would invariably be much higher, per 

unit of body weight, than those of humans consuming mixed diets 

containing a substantial proportion of foods of animal origin." The 

pastures of solonetz and solonchak soils of the Kulundinsk steppe in 

Russia were reported by Plotnikov (1960) to be so high in boron that 

gastrointestinal and pulmonary disorders occured in lambs. Moreover, 

the water supplies were unusually high in boron (0.2-2.2 mg/L), 

which probably contributed to the boron toxicity. 

Man

Underwood (1971, p. 434) stated, "The boron in food, and boron added 

as sodium borate or boric acid, is rapidly and almost completely absorbed and excreted, largely in the urine. Where high intakes occur 

either accidentally or from the treatment of large burns with boric 

acid, similar high absorption and urinary excretion take place, but 

sufficient boron may be temporarily retained in the tissues, especially 

in the brain, to produce serious toxic effects." Bowen (1966) listed 4,000 

mg boron (borate) as toxic in a 750-g/day dry-weight diet, duration not 

given.

BROMINE

[Considered nonessential for plants and animals]

Plants

Under natural conditions The bromine content (principally as 

bromides) in normal soil is so low, ranging from 10 to 40 ppm, that 

bromine toxicity has not been a problem in crop production in the past 

(Martin, 1966a).

Under man-induced conditions Most cases of bromine toxicity to 

plants are related to residual bromine in the soil following fumigation 

with bromine compounds (principally ethylene dibromide and methyl 

bromide). However, the possibility exists of bromine contamination of 

soils by motor vehicle and industrial emissions. In land plants bromine 

normally ranges from trace concentrations to about 260 ppm in the dry 

tissue. It is especially high in melons, carrot tops, celery tops, and 

mushrooms. In contrast to land plants, marine plants contain as much 

as about 2,000 ppm (Martin, 1966a). Plant species differ greatly in 

their tolerance to soil bromine; onion is so sensitive that it has been
CADMIUM 15

used as a test plant for detecting soil bromide (O'Bannon, 1958). Other 

sensitive plants include bean, beet, cabbage, celery, citrus, pea, peanut, 

pepper, potato, spinach, sugar beet, sweet potato, and turnip. The 

bromine content of dry leaf tissue has been used as an indication of 

toxicity; for example, leaf bromine concentrations in citrus seedlings of 

0.17, 0.33, 0.4,1.3, and 1.8 percent were associated with 12, 22, 31, 57, 

and 90 percent reduction in growth, respectively (Martin and others, 

1956). Concentrations of water-soluble soil bromine were reported to 

have the following effects: 38-83 ppm reduced growth of bean and 

cabbage; 26-53 ppm injured carnation plants; 15 ppm reduced growth 

of citrus seedlings, and 600 ppm severely injured the plants; and 

growth of beans was greatly retarded by 300 ppm (summaries given by 

Martin, 1966a).

Animals

Under natural dietary conditions Although the bromine content of 

animal tissues and milk is greatly influenced by the bromine in the 

feeds, we have no reports of bromine toxicity from feed sources.

Under man-induced dietary conditions Bowen (1966) listed as lethal to rats 800 mg Br+ in a 10-g/day dry-weight (80,000 ppm), duration 

not given.

Man

Dietary bromine is retained for only short periods in the tissues and 

is excreted mostly in the urine. Underwood (1971, p. 435) stated, "Human dietary bromine intakes have probably increased in recent years 

in areas where organic bromides are used as fumigants for soils and 

stored grains, and in motor fuels." However, there appear to be no 

toxicity problems associated with this intake. Thomas (1973) gave 

500-5,000 mg/kg body weight of bromides (sodium, potassium, ammonium, and others) and 50-500 mg/kg body weight of bromate salts 

as the probable lethal oral dose for an adult.

CADMIUM

[Considered nonessential for plants and animals]

Plants

Under natural conditions No toxicity has been demonstrated. 

Cadmium is a relatively rare element that is rather uniformly distributed in the most abundant rocks of the Earth's crust, which has an 

average content of 0.15-0.2 ppm (Fleischer and others, 1974). The only 

natural concentrations of commercial importance are those in sulfide 

deposits, especially those containing zinc, lead, and copper; and the 

toxicities of these elements in the deposits are most likely more severe 

than the toxicity of the low concentrations of the cadmium.
16 ELEMENT CONCENTRATIONS TOXIC TO PLANTS, ANIMALS, AND MAN

Under man-induced conditions Brooks (1972) stated that the general toxicity of this element to plants was moderate. It has been noted 

(Allaway, 1968) that, in general, 3 ppm cadmium in the tissue of plants 

depressed growth. For example, Miller, Hassett, and Koeppe (1976) 

reported that growth depression occurred in soybeans when shoots had 

3-5 ppm cadmium. Cadmium was reported to reduce plant growth at 

the following nutrient solution concentrations: 0.2 ppm, beets, beans, 

and turnips; 1 ppm, corn and lettuce; 5 ppm, tomato and barley; and 9 

ppm, cabbage (Page and others, 1972). Traynor and Knezek (1973) 

reported that corn grown on cadmium-enriched soils readily absorbed 

and translocated the element. They also found growth reduction in 

corn at its maximum when 281 ppm cadmium was added to the soil 

resulting in a plant concentration of 131 ppm (ash weight basis). The 

concentrations of cadmium in soils that were required to damage 

plants were higher than even those in soils of contaminated areas 

(Fleischer and others, 1974). 

Animals

Under natural dietary conditions The cadmium content of plants 

under natural conditions is low (Shacklette, 1972), and various animal 

studies have suggested that the absorption of cadmium from the gastrointestinal tract is poor (Fleischer and others, 1974), therefore 

poisoning of animals is unlikely.

Under man-induced dietary conditions Mammals have no effective 

mechanism for the elimination of ingested cadmium; with time it tends 

to accumulate in the liver and kidney. Its relative toxicity to mammals 

has been rated from moderate to high (Allaway, 1968). Cadmium from 

industrial or vehicular pollution can be absorbed by plants, or deposited on plant surfaces, to the extent that the plants are toxic to animals. 

For example, Goodman and Roberts (1971) reported that grass contaminated by industrial pollution contained 9.9 ppm cadmium, 

whereas control samples of the grass contained only 1 ppm; this contaminated grass caused the death of a horse (but the immediate cause 

of death was attributed to plumbism). They found that contaminated 

grass contained as much as 40 ppm cadmium in ash. Cadmium was 

suspected of killing a horse that contained 80 ppm cadmium in its liver 

and 410 ppm in its kidneys (Lewis, 1972). Thirty to sixty ppm cadmium 

in the diet of sheep for 191 days was shown to reduce growth and feed 

intake (Doyle and others, 1972). Forty-five ppm cadmium in the diet of 

rats for 6 months caused slight toxic symptoms (Underwood, 1971). 

Bowen (1966) stated that 0.5 mg/day Cd2+ in a total dry weight diet of 

10 g (500 ppm) is toxic to rats, whereas 16 mg/day (1,600 ppm) is lethal, 

duration not given. A subtoxic level of 5 ppm cadmium in the drinking 

water of rats, given for 180-240 days, produced systolic hypertension. It 

has been used as an anthelminthic drug in swine and poultry at
CHLORINE 17

concentrations ranging from 30 to 1,000 ppm in the diet (Stecher, 1968). 

Cadmium appears to be highly toxic to aquatic organisms at low 

concentrations, as follows: lethal to the fiatwormPolycelis nigra at 2.7 

ppm, to the stickleback fish at 0.2 ppm, to goldfish at 0.02 ppm, and to 

Daphnia magna at 0.003 ppm (Schroeder and Balassa, 1961).

Man

Under normal environmental conditions The normal cadmium 

content of food plants is low, ranging from 0.1 to 1 ppm in dry material 

(Shacklette, 1972); therefore poisoning from this source is unlikely.

Under the effects of environmental pollution by cadmium The first 

likely instance of cadmium poisoning in man due to general environmental contamination is that of itai-itai (ouch-ouch) disease in the 

elderly women who lived in the vicinity of a mine in Japan. It was 

demonstrated that the water, rice, and fish in the endemic area contained high concentrations of cadmium and other metals, probably due 

to contamination of the local river by the effluent from a zinc-leadcadmium smelter (Fleischer and others, 1974). Friberg (1975) reported 

that, in 1972, Swedish school children showed severe-gastrointestinal 

symptoms after the consumption of soft drinks made with water containing 16,000 /ng/L cadmium. Bowen (1966) stated that the normal 

dietary intake of Cd2+ , based on a total dry weight diet of 750 g/day, is 

0.6 (0.8 ppm), whereas 3 mg/day (4 ppm) is toxic, duration not given. 

Inhaled cadmium oxide fumes at a concentration of 1 mg/m3 for 8 hours 

causes pulmonary edema, and 5 mg/m3 for 8 hours is considered lethal 

(Bergqvist and others, 1977). A recent study of the environmental 

impact of cadmium (Fleischer and others, 1974, p. 299) concluded, 

"Based on present knowledge, and there are many gaps, there is no 

solid evidence of a hazard to the general population from cadmium in 

food, air, or water. Contamination of food and water rather than air 

would seem to present more of a potential problem. This might not be 

the case with smoking or excessive occupational exposures."

CHLORINE

[Essential for plants and animals]

Plants

Under natural conditions The chloride ion is itself toxic if too 

greatly concentrated; also, if too concentrated, the common natural 

chlorine compound, sodium chloride, is toxic through its effect on 

osmotic pressure within the plant. Symptoms of excess chloride include burning and firing of leaf tips or margins, bronzing, premature 

yellowing and abscission of leaves and, less frequently, chlorosis 

(Eaton, 1966). Within the concentration ranges of sodium chloride 

tolerated by a species of plant, each increase in the osmotic pressure of
18 ELEMENT CONCENTRATIONS TOXIC TO PLANTS, ANIMALS, AND MAN

the substrate solution causes an increase in the osmotic pressure of the 

plant sap; beyond this range, lethal wilting occurs. Under natural 

conditions, areas inundated by seawater or strongly influenced by sea 

spray may accumulate toxic amounts of sodium chloride in the soil. 

Evaporative salt in closed geographic basins may also reach toxic 

concentrations. On natural undrained soil in Australia, the chloride in 

leaf petioles of grape (percent, dry matter) related to leaf toxicity 

symptoms were as follows: 0.81, no toxicity; 1.35, slight burning; 1.55, 

burning; and 2.50, severe burning (Woodham, 1956). The following 

concentrations (percent, dry matter) of chlorine in leaf tissue are 

considered excessive: >0.7, Navel and Valencia oranges (Embleton 

and others, 1976); >0.5, avocado (Jones and Embleton, 1976); >0.2, 

apricots; >0.3, almonds, apples, peaches, pears, plums, prunes, and 

walnuts; >0.5, olives (Beutel and others, 1976); and >0.5, grapes (Cook 

and Wheeler, 1976).

Under man-induced conditions Chloride toxicity may be produced 

in plants by over fertilizing, such as with potassium chloride. Chloride 

toxicity may also result from irrigation using slightly salty water with 

insufficient flushing of the soil. Plants range widely in their resistance 

to toxicity, from the halophytes such as asparagus to highly sensitive 

species. Experimental studies in which grapefruit trees were watered 

with different levels of salt concentration in the water gave the following results (Pearson and others, 1957): 300 ppm salt, relative weight of 

tops was 100, 0.07 percent (in dry matter) in leaves; 1,300 ppm salt, 

relative weight of tops was 46,1.28 percent in leaves; and 2,300 ppm 

salt, relative weight of tops was 38, 1.35 percent in leaves. The two 

higher concentrations produced defoliation, dieback, chlorosis, bronzing, and burning.

Animals

Under natural dietary conditions Forage plants in general are so 

low in sodium chloride that salt must be provided for herbivorous 

animals; therefore, natural chlorine toxicity in these animals is very 

unlikely.

Under man-induced dietary conditions Our only report is one 

given by Bowen (1966) who listed as lethal to rats >900 mg Cl~ in a 

10-g/day dry-weight diet (90,000 ppm), duration not given. 

Man

We have no reports of human toxicity attributed to excessive 

chlorine in the natural environment, although chlorine gas is highly 

toxic to plants, animals, and man. Sax (1975) gave the following toxicity ranges for chlorine gas: 3.5 ppm detectable odor; 15 ppm 

immediate irritation of the throat; 50 ppm dangerous; 1,000 ppm 

fatal even with short exposure. Thomas (1973) gave 50-500 mg/kg 

body weight as the probable lethal dose of chlorate salts for an adult.
CHROMIUM 19 

CHROMIUM

[Considered nonessential for plants; essential trace element for animals]

Plants

Under natural conditions The growth of only certain species on 

"serpentine soils" has commonly been attributed to the high chromium 

levels in such soils (Brooks, 1972); but excessive nickel, unfavorable 

Mg:Ca ratios, and deficiency of molybdenum may also contribute to 

this condition (Vanselow, 1966a). Soil from "poison spots" in Oregon 

contains as much as 2-3 percent chromic oxide (McMurtrey and 

Robinson, 1938), whereas in Maryland, infertility of the soil was associated with 1,000-3,900 ppm chromic oxide (Vokal and others, 1975). 

The concentrations .(dry weight) of chromium in plants growing in 

serpentine soils and showing toxicity symptoms follow: 18 24 ppm in 

leaves and 375-410 ppm in roots of tobacco; 4-8 ppm in corn leaves; 

and 252 ppm in oat leaves (National Research Council, 1974a). Vokal 

and others (1975) wrote, "The concentration of chromium usually present in the air (traces to 0.02 /ug/m3 as Cr) are too low to have any 

significant effect on the growth or yield of vegetation."

Under man-induced conditions Brooks (1972) reported chromium 

toxicity to plants as severe, whereas Allaway (1968) stated it to be 

moderate. Chromium in the form of chromates is particularly toxic 

(McMurtrey and Robinson, 1938). In soil, 1,370-2,740 ppm chromium 

caused chlorosis in citrus; 10-15 ppm chromium (as K2Cr2O7 ) in the 

nutrient solution was toxic to barley (Mertz, 1974a); 150 ppm in soil 

was toxic to orange seedlings; 16 ppm (chromate) reduced growth in 

tomatoes, oats, kale, and potatoes whereas 10 ppm was toxic to corn 

and 5 ppm was toxic to tobacco (National Research Council, 1974a). In 

corn leaves, 4-8 ppm (dry weight) chromium was toxic (Soane and 

Saunder, 1959). Pratt (1966c, p. 136) stated that because of their toxic 

effects, the use of chromium salts should be avoided in all plantproduction media. Wallace, Alexander, and Chaudhry (1977) reported: 

"Plants grown with 10~5N Cr207 were decreased in yield by about 25%. 

.. while the same level of Cr2 (S04 )2 was essentially without effect. For 

the two salts, the leaf, stem, root concentration for Cr, respectively 

were 2.2 and 1.3, 0.7 and 0.7, and 140 and 104 /ng/g." In aquatic plants, 

hexavalent chromium at 0.03-65 ppm has been shown to inhibit the 

growth of freshwater algae; in seawater, 1-5 ppm reduces photosynthesis in kelp (National Research Council, 1974a).

Animals

Under natural conditions Chromium as a metal is considered 

biologically inert. Underwood (1971, p. 263-264) stated, "Chromium, 

particularly trivalent chromium, has a low order of toxicity. A wide 

margin of safety exists between the amounts ordinarily ingested and
20 ELEMENT CONCENTRATIONS TOXIC TO PLANTS, ANIMALS, AND MAN

those likely to induce deleterious effects." Allaway (1975) notes that 

even though Cr(VI) is more toxic to plants and animals and is more 

likely to be soluble and mobile in soil and waters than is Cr(m), no 

naturally occurring minerals contain Cr(VI> . Further, he stated (p. 37) 

that ". . .minerals contain Cr(lll), especially mixed oxides of Cr(lll) and 

Fe, are generally inert and resistant to weathering."

Under man-induced dietary conditions The hexavalent form of 

chromium may be 100 times more toxic than the trivalent form; however, both are relatively nontoxic to mammals and other vertebrates 

(Schroeder and others, 1962a). Underwood (1971) stated that 50 ppm 

chromium in the diet resulted in growth depression of experimental 

animals. Thirty to forty mg/kg of body weight as zinc chromate is lethal 

to calves within 1 month, and about 20 times that amount is lethal to 

cows. Thirty ppm chromium in the liver and 4 //.g/ml in whole blood is 

diagnostic of chromium toxicity (Harrison and Staples, 1955). Five mg 

chromate in a 10-g/day dry-weight diet (500 ppm) is toxic to rats, 

duration not given (Bowen, 1966). Chromium is potentially carcinogenic (National Research Council, 1974a). 

Man

"Chromium as a metal is biologically inert and does not produce 

toxic or other harmful effects in man or laboratory animals" (National 

Research Council, 1974a, p. 42). People who work with hexavalent 

chromium have, however, developed cutaneous and nasal mucousmembrane ulcers and contact dermatitis. The lung is the only organ 

that appears to accumulate chromium, and this may be related to 

airborne exposure to chromium-containing dust (Mertz, 1967). Bowen 

(1966) reported that in a 750-g dry-weight diet, normal consumption of 

chromate is about 0.05 mg (0.07 ppm), whereas the toxic level is 200 mg 

(270 ppm) and the lethal level is 3,000 mg (4,000 ppm). Allaway (1975) 

concluded that since there have been no reports of toxicity to people or 

animals from the consumption of Cr(lll), chromium in plants represents 

an unlikely potential hazard. Schroeder, Balassa, and Tipton (1962a) 

reported that consumption of water containing 1.0-25 ppm chromium 

by a family over several years produced no apparent ill effects. They 

further stated that chromium is one of the least toxic of trace metals.

COBALT

[Essential trace element for blue-green algae and nodule bacteria; considered nonessential for higher plants, 

although growth and yield increases have been reported; essential trace element for animals]

Plants

Under natural conditions Vanselow (1966b) reported that cobalt 

produces toxicity to plants when the amounts available to the plant 

exceed certain low levels, but that a naturally occurring excess of
COBALT 21

cobalt in soils is improbable and that no instances so far had been 

noted. Plant species range widely in their content of cobalt, yet show no 

toxicity symptoms. Some trees have very high concentrations in their 

leaves; black gum leaves, for example, were reported to contain as 

much as 10,000 ppm in ash and persimmon leaves, 2,000 ppm; most 

other species contain much less (Connor and Shacklette, 1975).

Under experimental conditions A number of authors (for example, 

Vanselow, 1966b) have reported that small amounts of cobalt in solution cultures, sometimes as small as 0.1 ppm, produced adverse or toxic 

effects on many crop plants. The symptoms of cobalt excess include 

depressed growth, chlorosis, necrosis, and even death of the plant. The 

chlorosis is frequently described as resembling that of iron deficiency 

(Vanselow, 1966b). From the literature, Vergnano and Hunter (1952) 

reported the following examples of cobalt toxicity to plants growing in 

nutrient solutions: maize and beans, 2-8 ppm; oats, 3-300 ppm; 

wheat, 6-590 ppm; barley and beans, 1-15 ppm; flax, 0.5-5 ppm; and 

oats and sugar beets, 15-30 ppm. Their own studies of cobalt toxicity to 

oats revealed symptoms ranging from slight chlorosis and occasional 

necrosis (5 ppm in nutrient solution) to stunted and severe necrosis (50 

ppm). Sudan grass containing 19-32 ppm (dry weight) cobalt showed 

toxicity symptoms when grown in soils to which 908 kg of cobalt per 0.4 

ha had been added (Fujimoto and Sherman, 1950). 

Animals

Under natural dietary conditions We have no reports of cobalt 

toxicity attributed to consumption of natural feedstuffs; pasturage 

deficiency in cobalt is of far greater concern than are potentially toxic 

concentrations in plants. Kubota (1967, p. 128) stated,". . . there are no 

known areas of cobalt toxicity in the United States as there are areas of 

selenium toxicity."

Under man-induced dietary conditions Cobalt is relatively nontoxic. Sheep can tolerate large doses of cobalt; 0.35 g/100 kg/day produced no ill effects (Becker and Smith, 1951). Smith (1962) listed the 

following in mg/kg body weight/day: rats, 2.5, nontoxic; dogs, 10, nontoxic; sheep, 3, nontoxic; and cattle, about 1, toxic. Bowen (1966) listed 

0.7 mg Coa+ as toxic to rats in a 10-g/day dry-weight diet (70 ppm), 

duration not given. A concentration of 0.1 mg/m3 of metallic cobalt 

powder inhaled by miniature pigs for 6 hours daily, 5 days/week is 

considered toxic (Hellsten and others, 1976). 

Man

The edible parts of food plants contain only <1-10 ppm (ash base) 

cobalt, therefore toxicity attributed to this source is very unlikely 

(Connor and Shacklette, 1975). As with animals, the toxicity to man of 

nonradioactive isotopes of cobalt is of little importance. Hazards associated with the therapeutic use of this element were given (Hellsten
22 ELEMENT CONCENTRATIONS TOXIC TO PLANTS, ANIMALS, AND MAN

and others, 1976, p. 20) as follows: "Poisoning by ingestion has mainly 

occurred in connection with the medical use of cobalt in the treatment 

of certain anemias. In these therapies the daily intake varied between 

25 30 mg cobalt, which is about 100 times the normal dietary intake." 

At a time when cobalt was used in beer in order to preserve the foam, it 

was suspected of causing the "beer drinkers cardiomyopathy" syndrome. Some evidence (Burch and others, 1973), however, implicates 

selenium in conjunction with cobalt as being responsible.' Bowen (1966) 

listed 500 mg Co2+ as toxic in a 750-g/day dry-weight diet (670 ppm), 

duration not given.

COPPER

[Essential trace element for plants and animals]

Plants

Under natural conditions Soil influenced by a high degree of copper mineralization may be toxic to native or cultivated plants. Fraser 

(1961) reported that large trees were absent and tree seedlings were 

killed, in a syngenetic copper deposit in a swamp in New Brunswick; he 

further reported that muck from this swamp killed cucumber plants to 

which it was applied. There are many reports in the literature of copper 

toxicity to plants on or near copper deposits, and the degree of resistance to copper toxicity by different species has been used as a geobotanical method of mineral exploration. One report by Malaisse and others 

(1978) gave the unusually high value of 1.3 percent copper (dry weight 

base) in the tissue of a copper-mineralization indicator plant Aeolanthus biformifolius (Mint Family) from Zaire. Areas in Norway where 

vegetation had been poisoned (containing as much as 895 ppm copper 

in dry material) by naturally-occurring high copper levels in soils (as 

much as 7,400 ppm) could be detected by examining satellite photographs (B^lviken and others, 1977). The following concentrations 

(ppm, dry matter) of copper in leaf tissue are considered excessive: 

probably >22 Navel and Valencia oranges (Embleton and others, 

1976); and >0.25 avocados (Jones and Embleton, 1976).

Under man-induced conditions Copper sulfate (blue vitriol) has 

been used for more than seventy years as an algicide at an achieved 

concentration of 1 mg/L (1 ppm) for the upper 0.5 m of water (Mackenthun and Ingram, 1967). Concerning the toxicity of copper to vascular 

plants, Bennett (1971, p. 675) wrote, "Copper is highly toxic to roots, 

and toxic concentrations are translocated only negligibly via the 

stems. Thus Cu is a widely used toxicant for destroying roots that have 

encroached into sewer lines and septic tank fields." Most copper toxicites in crop plants have been caused by the use of Bordeaux mixture
COPPER 23

(copper sulfate and lime) as a fungicide. Tbxicity to copper in plants is 

usually manifested by chlorosis (yellowing) of the foliage, caused by 

the interference of excessive copper with iron metabolism in the plant. 

Reuther and Smith (1953) found appreciable chlorosis of citrus seedlings occurring when the total copper of a very sandy soil of pH 5.0 or 

below exceeded 150 ppm. Westgate (1952) reported copper toxicity in 

several crops on old vegetable fields having over 400 ppm total copper 

in the topsoil as a result of many years of Bordeaux mixture spraying of 

celery. Copper is added to the environment by industrial pollution and 

vehicular emissions. (Shacklette and Connor, 1973), but we have no 

reports of copper toxicity attributed to these sources. The National 

Research Council (1977b) reported that toxicity to plants has been 

noted in areas receiving manure from swine and poultry that were 

given diets rich in copper (250 ppm). Copper deficiencies in agricultural soils are much more common than copper excesses; and fertilization with copper, especially on highly organic or very sandy soils, is a 

common practice. 

Animals

Under natural dietary conditions Dick (1956) reported that when 

sheep graze on pastures having normal copper but low molybdenum 

content (less than 0.1 ppm), copper accumulates in their livers. This 

accumulation sometimes results in chronic copper poisoning, followed 

by death. On the other hand, when pasture or forage contains a normal 

copper content but high molybdenum (5 ppm or more), a poisoning 

having many of the clinical symptoms of copper deficiency may occur. 

The average (geometric mean) copper content of U.S. soils was reported as 18 ppm, with a range of <1 to 300 ppm, and most soil samples 

contained <3 ppm molybdenum, with high values ranging from 3 to 7 

ppm (Shacklette and others, 1971).

Under man-induced dietary conditions Hemkes and Hartmans 

(1973) found that sheep feeding on either side, and within 20 m of, 

high-tension copper power lines became ill and died after consuming 

dry forage and soil containing copper in excess of 15 ppm. Sheep appear 

to be particularly sensitive to copper intoxication. Case (1974, p. 278) 

stated "Ingestion of as little as 1.5 g [copper]/sheep/day for 30 days was 

fatal to most sheep of the British breeds, an amount easily obtained 

from hog rations supplemented with copper sulfate. .." Chronic copper 

poisoning of animals may occur as a consequence of excessive consumption of copper-containing salt licks or mixtures, or the unwise use 

of copper-containing drenches. Contamination of feeds with copper 

compounds from horticultural or industrial sources is a further cause. 

In all animals the continued ingestion of copper in excess of require^ 

ments leads to some accumulation in the tissues, especially in the liver 

(Underwood, 1971). These liver accumulations were reported by Case
24 ELEMENT CONCENTRATIONS TOXIC TO PLANTS, ANIMALS, AND MAN

(1974) to range from 247 ppm to >6,000 ppm in sheep dying of copper 

intoxication, with >500 ppm usually indicative of poisoning. Copper 

toxicity in mammals, compared to other animals, is of little significance because they possess barriers to copper absorption. Avian and 

mammalian resistance to copper is 100 to 1,000 times greater than is 

that of more primitive animals (Schroeder, Nason, Tipton, and 

Balassa, 1966). For aquatic organisms copper is the most toxic common 

heavy metal; this toxicity, however, is inversely related to the water 

hardness (principally calcium content). Various copper compounds 

(copper sulfate, copper pentachlorophenate, copper tartrate, and 

others) have been used since the 1920's as molluscicides in the control 

of schistosomiasis (National Research Council, 1977b). Bowen (1966) 

reported that a 20 mg Cu2+ (2,000 ppm) ration in a dry-weight diet of 10 

g/day was lethal to rats, duration not given.

Man

Under normal environmental conditions Underwood (1971, p. 106) 

stated, "Continuous ingestion of copper from food or water supply at 

intakes sufficient to induce chronic copper poisoning in man is extremely unlikely, judging by the amounts required for this purpose in 

other monogastric species." From a normal intake of 2-5 mg/day 

(Bowen, 1966), a net balance of zero copper is normally maintained. 

The National Research Council (1977b) reported that 800 jag/L in the 

drinking water of a 15-month-old infant may have caused acrodynia 

(pink disease).

Under excessive copper intake Excessive buildup of copper in the 

liver and central nervous system caused by a metabolic inability to 

excrete copper is the fundamental cause of Wilson's disease (Scheinberg, 1969). Copper toxicosis in humans (and most higher animals) is 

not, however, a major problem. As stated by Hill (1977, p. 126)"... the 

ingestion of excessive copper salts leads immediately to vomiting and 

the expulsion of the copper. The highly reactive ions of copper result in 

complex formations in nature so that the free ion is seldomly encountered." Bowen (1966) reported that 250-500 mg Cu2+ (330-670 ppm) 

in a dry-weight diet of 750 g/day is toxic to normal individuals, duration not given. Soluble copper salts, notably copper sulfate, are strong 

irritants to the skin and mucous membranes (Stecher, 1968).

FLUORINE

[Considered nonessential for plants; essential trace element for some higher animals, improves teeth and bones]

Plants

Under natural conditions Tbxicity is unusual, but plants growing 

in acid soils have accumulated toxic levels of fluorine (Allaway, 1968). 

The amount of fluoride taken up from the soil by plants is usually
FLUORINE 25

unrelated to total soil fluorine, but is controlled by soil type, calcium 

and phosphorus content of the soil, and soil pH (Brewer, 1966a). Brewer 

(1966a, p. 182) reported, "With few exceptions, the usual fluoride content of most plant foliage growing in areas removed from possible 

sources of fluoride air pollution is in the range of 2 to 20 ppm on a 

dry-weight basis. Notable exceptions include tea leaves, which have 

been found... to contain, on the average, 50 to 90 ppm of fluorine. The 

highest fluoride concentrations reported for vegetation, presumably 

attributable to fluorine absorption from the substrate, include 1,900 

ppm in camellia leaves . . . and in excess of 8,000 ppm in tea 

leaves . . .." Mitchell and Edman (1945, p. 82) reported, "Very few foods 

contain less than 0.1 ppm of fluorine on the fresh basis, and few foods 

uncontaminated with the residues of insecticidal sprays and 

fluoriniferous soils and dusts contain more than 2 ppm." They also 

stated that the maximum chlorine [apparently a misprint of fluorine] 

permitted in vegetables is 2.8 ppm and in apples and pears, 7 ppm. 

Embleton, Jones, and Platt (1976) reported that >100 ppm (dry matter) 

fluorine in the fruiting shoots of Navel and Valencia oranges is probably an excessive amount.

Under man-induced conditions Vegetation in the vicinity of superphosphate and elemental phosphorus plants is often injured by 

fluorine emissions (for example, Georgetown Canyon, Idaho, in U.S. 

Department of the Interior and U.S. Department of Agriculture, 1977), 

and plants growing on soil that has been heavily fertilized with phosphate fertilizers may also receive toxic amounts of fluorine from the 

soil. However, most toxicity problems have been associated with industrially polluted air as the major source of fluorine, and this source is 

indicated by abnormally high fluorine content in the tops of plants and 

with a corresponding low content in the roots. Depending on species 

and growth conditions, 30 300 ppm fluorine (dry weight) generally 

reduces growth (National Research Council, 1971). Injury symptoms 

are leaf-margin necrosis, interveinal chlorosis, or both. As a result of 

fluoride emissions from a factory in Czechoslovakia, Marier (1968) 

reported that tree leaves within a 5-km distance were necrosed, had a 

decreased chlorophyll content, and contained 7-72 times more 

fluorine than that normally found. Vegetables and fruit were disfigured in shape and color, and contained 5-21 times the fluoride of 

control samples. 

Animals

Under natural dietary conditions Animals obtain their fluorine 

from the plants that they eat and the water that they drink (Brewer, 

1966a). The fluorine levels of common uncontaminated feed materials 

are too low to constitute a fluorine hazard to livestock, but endemic 

fluorosis has been reported from areas where the drinking water con-
26 ELEMENT CONCENTRATIONS TOXIC TO PLANTS, ANIMALS, AND MAN

tains unusually high fluorine content (Underwood, 1971). The following classification of fluorine concentrations in water relative to the 

health of lambs was given (Case, 1974): 2 ppm, slightly toxic; 5 ppm, 

definitely toxic; and 10 ppm, likely to cause serious damage. Further, 

the recommendation was made that rations for lambs should not contain more than 100 ppm fluorine (dry matter). Lethal fluorosis of sheep 

and other livestock, caused by consuming contaminated vegetation 

and water, occurred following a volcanic eruption in Iceland 

(Thorarinsson, 1970). Some plants (particularly members of the 

Leguminosae) have the capability of synthesizing organo-fluoride 

compounds (specifically fluoroacetate and fluorocitrate) from inorganic sources. Although not particularly toxic to plants, these compounds are very toxic to grazing animals and have caused numerous 

ungulate deaths in Africa and Australia (Lovelace and others, 1968). 

Under man-induced dietary conditions Herbage and water 

supplies of animals that have been contaminated by dust from the 

mining of rock phosphate deposits have caused chronic fluorosis. 

Whereas surface waters usually contain less then 1 ppm fluorine, 

water from deep wells in endemic fluorosis areas contains 3 5 ppm 

fluorine and often 10-15 ppm (Underwood, 1971). Bowen (1966) reported that 0.1 mg F~ in a 10 g/day dry weight diet (10 ppm) is toxic to 

rats, whereas 30 mg (3,000 ppm) is lethal, duration not given. The 

concentrations of fluorine in dietary dry matter, above which normal 

performance may be affected, follow: beef or dairy heifers, 40 ppm; 

horses, 60 ppm; finishing cattle, 100 ppm; broiler chickens, 300 ppm; 

breeding hens, 400 ppm; and turkeys, 400 ppm (National Research 

Council, Committee on Animal Nutrition,.Subcommittee on Fluorosis, 

1974). The following conclusion regarding fluorine toxicosis in bovines 

is given by Church and others (1971, p. 511):"... long-term ingestion of 

fluorine at a rate much above 30 ppm will result in symptoms of 

fluorosis after a period of years. Ingestion of appreciably larger 

amounts (>100 ppm) can be tolerated for time periods of several 

months without undue hazard." These authors further stated that 

fluorine concentrations above 5,500 7,000 ppm (ash base) in bone are 

considered an indication of poisoning. Case (1974) reported that sheep 

fed 10 mg sodium fluoride/kg of body weight developed acute fluorine 

toxicosis; the likely lethal dosage was given as 15 mg/kg. 

Man

Under natural environmental conditions Food is the major source 

of fluorine to individuals not exposed to industrial contamination or to 

naturally or artificially fluoridated drinking water. Very few foods 

contain more than 1 2 ppm fluorine, and most of them contain less 

than 0.5 ppm (dry matter). The consumption of tea can be an important 

determinant of total dietary fluorine intake, as fluorine concentration
IODINE 27

of 100 ppm in tea leaves are common, two-thirds of which passes into 

the infusion, so that one cup of tea can add 0.1 0.2 mg fluorine to the 

diet. Endemic fluorosis from natural waters from deep wells having 

20-50 ppm fluorine has been noted as resulting in mottled teeth and 

bone deformities (Underwood, 1971). Mitchell and Edman (1945, p. 87) 

reported that, in humans, chronic fluorosis is generally caused by 

ingestion or inhalation of fluorine-containing gases and dust. Bowen 

(1966) listed 0.5 mg F~ in a 750-g/day dry-weight diet (0.7 ppm) as the 

normal dietary intake. Consumption of 20 mg (27 ppm) was considered 

toxic and 2,000 mg (2,700) was lethal, duration not given.

Fluoridated drinking water Community water supplies commonly 

are treated with sodium fluoride or fluorosilicate to maintain fluoride 

levels ranging from 0.8 to 1.2 ppm, in order to reduce the incidence of 

dental caries; at concentrations much above these levels, some tooth 

mottling may occur (Underwood, 1971).

IODINE

[Considered nonessential for plants; essential trace element for animals]

Plants

Under natural conditions Although iodine is highly toxic to plants, 

it usually is present in very small amounts in an available form in soils 

and, therefore, seldom presents a toxicity problem (Martin, 1966b). 

The iodine content of land plants varies with the species and the 

amount in the soil. Shacklette and Cuthbert (1967) reported the following average iodine concentrations (ppm, dry matter) for groups of land 

plants: fleshy fungi, 6.2; ferns, 5.7; coniferous trees, 3.9; monocotyledons, 5.9; dicotyledonous trees, 2.7; dicotyledonous vegetables (edible 

parts), 6.9. Iodine in marine brown algae ranged from 55 to 8,800 ppm.

Under man-induced conditions Large applications of kelp (marine 

brown algae) to soil as fertilizer may cause iodine toxicity to sensitive 

plants (Martin, 1966b). Adding 2.5 ppm potassium iodide to soil has 

injured crop plants. In nutrient solutions and sand cultures, iodine is 

toxic to plants at concentrations greater than about 0.5-1 ppm (Martin; 1966b). 

Animals

Under natural dietary conditions We have no reports of iodine 

toxicity in animals fed normal rations. The iodine levels in vegetation 

in some areas are inadequate for animal requirements, and iodine 

supplements must be used in the feed.

Under man-induced dietary conditions In experimental studies, 

significant species differences in tolerance to high intakes of iodide 

were found; however, in all species studied, the tolerance was high in 

comparison with normal dietary iodine intakes, indicating an ex-
28 ELEMENT CONCENTRATIONS TOXIC TO PLANTS, ANIMALS, AND MAN

tremely wide margin of safety for this element. Hens fed 312 5,000 

ppm potassium iodide in their ration ceased egg production. High 

levels also increased embryonic mortality in rats and rabbits (Underwood, 1971).

Man

Under natural environmental conditions Prolonged intake of large 

amounts of iodine by normal individuals markedly reduces thyroidal 

iodine uptake the antithyroidal or goitrogenic effect. In an area in 

Japan, the consumption of large quantities of iodine in the diet was 

reported as the cause of endemic goiter (Underwood, 1971). However, 

areas that are deficient in iodine are far more common than areas that 

have excesses, and iodine supplements to foods are widely used.

Iodine tolerances Bowen (1966) listed 0.2 mg I~ in a 750-g/day 

dry-weight diet (0.3 ppm) as normal, whereas 10,000 mg (13,300 ppm) 

was toxic, duration not given. Thomas (1973) gave 5-50 mg/kg body 

weight as the probable lethal dose of iodine for an adult.

LEAD

[Nonessential for plants and animals]

Plants

Under natural conditions An area in Montana was reported 

(Mudge and others, 1968) where weathering of Devonian carbonate 

has produced a thin soil enriched in lead, containing >5,000 ppm lead 

in the A-, B-, and C-horizons. The pine trees of the area of known lead 

mineralization were dwarfed and misshaped, and their needles were 

yellow-green. Analyses of these trees were not given. The occurrence of 

naturally lead-poisoned soil in Norway was described (Lag and others, 

1969) in which the vegetation was exceptionally sparse in an area 

about 100 m2 that was believed to have been influenced by solutions 

from the weathering of galena-bearing quartzite. The richest soil samples contained 11 percent lead, and the maximum concentration in 

plants was 0.9 percent in dry material. Apparently normal vegetation 

in this area contained around 0.1 percent, and sickly vegetation contained about 0.3 percent in dry matter. The differences in tolerance of 

lead among the species at or near the site were indicated by the absence 

of common species in the lead-rich area. Lead, zinc, and other heavy 

metals often occur together in mineralized outcrops; therefore, it is 

difficult to associate observed toxicity symptoms in plants at these 

sites with lead alone. Plants at these sites may absorb large amounts of 

lead without exhibiting toxicity symptoms; concentrations in stems of 

certain shrubs may be as high as 350 ppm lead in ash of the samples 

(Shacklette, 1960) without producing visible toxicity.
LEAD 29

Under man-induced conditions Elevated levels of lead in plants 

affected by automotive and industrial contamination have been extensively reported. We have no reports that conclusively demonstrate lead 

toxicity to the plant from such contamination. Frank toxicity of lead to 

plants has been shown, however, by laboratory and field experiments. 

Prat (1927) studied uptake of lead from lead chloride solutions; he 

found that broadbean plants absorbed all the lead in less than 3 days, 

but grew very little as a result. Hooper (1937) found that French beans 

growing in solution cultures were damaged by 30 ppm of lead as the 

sulfate alone or in combination with nutrient salts. Plants sprayed 

with lead sulfate solutions were not injured unless sufficient lead 

residue was left to block the stomates. Wilkins (1957), using lead 

nitrate as the nitrogen source, grew sheep fescue in solution cultures 

and reported that root growth was measurably retarded with 10 ppm of 

lead, markedly reduced by 30 ppm, and stopped at 100 ppm. Miller and 

Koeppe (1970) showed that 60/u,molesof lead nitrate added to a nutrient 

solution retarded growth of young corn plants when phosphate was 

deficient. (In young leaves the concentration of lead was 115 ppm in dry 

weight.) At 600/miolesand greater, marked reduction in growth of corn 

was noted with or without sufficient phosphate. (Concentration of lead 

in young leaves was 306 ppm, dry weight.) The use of lead arsenate as 

an insecticide in orchards for long periods has caused high lead concentrations in these soils. Regarding the toxicity of these soils, most of the 

observed damage to subsequent plant growth can be attributed to the 

resulting arsenic concentrations. Connor, Shacklette, and Erdman 

(1971) found 2 percent lead in ash of a red cedar tree that had been 

contaminated by dust from passing ore-carrying trucks; washing the 

samples with different solvents did not appreciably reduce the lead 

content. This tree showed no toxicity symptoms. Most of the lead in 

soils is sparingly soluble and largely unavailable to plants. Brewer 

(1966b) reviewed the reports of soluble lead in many different soils and 

found most soils to contain less than 1 ppm. Lead levels in epiphytic 

plants may be very high, although these plants have no root contact 

with the soil. Spanish moss believed to have been contaminated by 

industrial or vehicular pollution was reported to contain as much as 5 

percent lead in ash (Shacklette and Connor, 1973). We have found some 

tree-growing pendant lichens (Usnea and Alectoria spp.) that contain 

1.5 percent lead in ash, even though collected from areas having no 

obvious source of airborne pollution. None of these epiphytes exhibited 

evidence of toxicity.

Animals

Under natural dietary conditions McMurtrey and Robinson (1938, 

p. 821) wrote, "Normally the quantities [of lead] in edible plants or 

parts thereof are so small as to have no effect on the health of the
30 ELEMENT CONCENTRATIONS TOXIC TO PLANTS, ANIMALS, AND MAN

animal eating the plant." Shacklette (1962b) estimated that a large 

browsing animal eating native tree and shrub foliage in Alaska might 

ingest from 1 to 4 g of lead annually, depending on the region of the 

State. The report on natural lead accumulation in Norwegian soils and 

plants (Lag and others, 1969, p. 151) stated, "Since lead is toxic to many 

animal organisms, even in small amounts, such concentrations as 

found in this case may have an injurious effect on fauna." Examples of 

this possible toxicity, however, were not given.

Under man-induced dietary conditions Lead from industrial operations and vehicular traffic may be absorbed by, or accumulated on, 

forage plants to the extent that the plants are toxic to grazing animals. 

Lead poisoning in cattle and horses that grazed near smelters has been 

reported in Germany by Hupka (1955), in the United States by Dorn 

and others (1972), in Ireland by Egan and O'Cuill (1970), and in 

Canada by Schmitt and others (1971). The latter authors reported that 

excessive amounts of lead in ingested forage was the primary cause of a 

chronic debilitating disease of six young horses and less acute, but 

similar, disorders in 25 older horses. Cattle were less seriously affected. The lead values in the pasture grasses were as follows (ppm, dry 

weight basis): spring, 1-46; midsummer, 4-310; fall, 4-435; and 

overwintered grass, 25-2,800. Animals in the Staten Island Zoo, ranging from reptiles to primates, suffered acute lead poisoning attributed 

largely to intake of lead from atmospheric fallout (Bazell, 1971). 

Schroeder, Balassa, Gibson, and Valanju (1961, p. 417) stated, "It[lead] 

is not as toxic orally for mammals as cadmium and mercury, but is more 

so than copper, manganese, silver, vanadium, zinc, chromium, molybdenum, cobalt, nickel and probably arsenic." They also reported that 

0.01-1.0 ppm lead (chloride) immobilized Daphnia magna and that 

0.1-50 ppm was lethal to various fishes. For comparison, they noted 

that this was the range of toxicity to these organisms for zinc and 

nickel. Migratory waterfowl have been reported to have been poisoned 

by ingesting lead shot that were lodged in bottom sediments (Lisk, 

1972). Many other reports could be cited of poisoning of animals by lead 

that was introduced into the environment by human activity. 

Man

Under natural environmental conditions Lead poisoning from natural sources is very unlikely. Brewer (1966b, p. 214) commented, "The 

extremely low lead content of edible parts of the majority of crops is 

reassuring, in light of the potential toxicity of lead to animals, including man." Poisoning of man has occurred when drinking water containing 0.18 to more than 1.0 ppm Pb2+ (0.4-2.5 mg daily, in addition to 

lead in food) has been consumed over an unspecified period of time 

(Schroeder and others, 1961). Water should not exceed 0.05 ppm lead 

(World Health Organization, 1963). "Normal" rural air contains about
LITHIUM 31

0.05 /w,g lead per cubic meter (Patterson, 1965). However, it should be 

pointed out that very few humans today live in a natural, unpolluted 

environment.

Lead intakes and toxicities The average daily intake of lead from 

food and beverages in the United States is now estimated at about 0.30 

mg, with only about 10 percent of this being absorbed from the intestinal tract. In addition, some lead is inhaled and absorbed through the 

respiratory tract; the relative importance of this respiratory exposure 

is a matter about which there is some dispute (Goldsmith and Hexter, 

1967). These authors concluded that the absorption of lead from the two 

sources may be of similar magnitude. In another study (Rabinowitz 

and others, 1973), in which a healthy man was fed a diet normal in lead 

content and labeled with 204Pb it was concluded that about two-thirds 

of his assimilated lead was dietary in origin and the remainder was 

inhaled. Studies have generally shown that less than 10 percent of 

ingested lead is absorbed, whereas 25-50 percent of inhaled lead is 

absorbed (Goldsmith and Hexter, 1967). The possible physiological 

significance of environmental lead was discussed at length by Warren 

(1974), who listed the sources of lead insult as air, dust, leaded paint, 

cigarette tobacco, beer and wine, drinking water, food, fertilizers (particularly, sewage sludge), leaded gasoline, and miscellaneous, which 

included smelters, vegetables grown over refuse dumps, glazed pottery, 

plastics, solders, and fillers in alkaline piping. Bowen (1966) reported 

that the normal consumption of Pb2+ in a 750-g/day dry-weight diet 

was 0.3-0.4 mg (0.4-0.5 ppm) and that a consumption of 10,000 mg 

(13,300 ppm) on the same basis may be considered lethal, duration not 

given. Schroeder, Balassa, Gibson, and Valanju (1961b) speculated that 

poisoning in man would be eventually achieved if 1 or 2 percent of the 

total body content of lead (80 mg) were ingested daily (0.8-1.6 mg). 

Patterson (1965) noted that a concentration of Pb2+ in 0.5 0.8 ppm in 

the blood is the threshold for acute lead poisoning. Friberg (1975) 

reported that 53 percent of 1 to 9-year old children living near a lead 

smelter in El Paso, lex., were found to have blood lead values above 40 

/xg/100 ml (0.4 ppm).

LITHIUM

[Considered nonessential for higher plants and animals, but an essential trace element for some micro-organisms]

Plants

Under natural conditions Naturally occurring instances of lithium 

toxicity to plants are not known, except in the case of citrus (Bradford, 

1966b), which are very sensitive to small amounts of lithium. (Embleton and others, 1976, reported that >35 ppm, dry weight, lithium in 

leaf tissue of Navel and Valencia oranges is probably an excessive
32 ELEMENT CONCENTRATIONS TOXIC TO PLANTS, ANIMALS, AND MAN

amount.) However, a report on lithium in the environment (Mertz, 

1974b, p. 40) stated, "Crops grown in closed basins in California, 

Nevada, and Arizona are exposed to toxic levels of lithium." Lithium 

excesses occur most commonly in soils derived directly from igneous 

rocks rich in ferromagnesian minerals, and in soils derived from 

sedimentary deposits rich in clays or micas (Bradford, 1966b). The 

lithium concentration in 912 samples of soils from throughout the 

conterminous United States was reported (Shacklette and others, 

1971) as follows: range, 5-136 ppm; arithmetic mean, 24.7. Bradford 

(1966b, p. 221) stated, "There is no evidence available to indicate that 

total lithium in soils is in any way related to plant availability. . . . 

Plant content of this element is at present the best guide to the lithium 

status of the soil."

Under man-induced conditions Many crops are susceptible to injury when lithium is applied to the soil in the form of soluble salts 

(McMurtrey and Robinson, 1938), and many plants are tolerant of high 

lithium levels (Mertz, 1974b). Lithium was toxic to citrus when concentrated (as Li2SO4) in soil to 2 5 ppm, and when concentrated in leaves 

to 140-220 ppm in dry weight (Aldrich and others, 1951). Lithium 

toxicity has also been observed in avocado, celery, corn, olive, and 

wheat. In contrast, cotton seems to be very resistant to lithium toxicity, 

even to as much as 2,270 kg of lithium nitrate per hectare. Lithium 

content in citrus leaves ranging from 4-40 ppm in dry weight has 

caused moderate to severe toxic effects (Sauchelli, 1969). Beans grown 

in culture solutions were sensitive to 0.5xlO~3 M lithium, which resulted in 10 ppm lithium in leaves, 48 ppm in stems, and 24 ppm in 

roots. Higher concentrations of lithium produced marked reductions in 

plant yield accompanied by increased lithium concentrations in leaf, 

stem, and root tissues (Wallace, Romney, Cha, and Chaudhry, 1977). 

Lithium ions are toxic to various lactic acid bacteria (Voors, 1969). 

Animals

We have no reports of lithium toxicity in animals. 

Man

Voors (1969, p. 1339) stated, "From the available data on lithium 

levels of commonly used foods and drinks it can be concluded that, in 

general, the daily lithium intake through drinking water exceeds the 

intake through foods. It has to be conceded, however, that there is 

incomplete knowledge concerning the presence of accumulator plants 

in human food." Our own data on lithium in fruits and vegetables from 

areas of commercial production in the United States show striking 

regional differences in concentrations of this element. Among fieldcollected samples of these food plants, the lithium content of those from 

Michigan, New York, New Jersey, and Florida was below the detection 

limit (<4 ppm in ash), whereas samples from Texas and States west-
MANGANESE 33

ward commonly contained measurable, often high (as much as 28 ppm 

in California oranges), concentrations. For example, the concentration 

in snap bean samples from the Eastern States was <4 ppm, while in 

those from California it ranged from 5 to 27 ppm in ash. Tbxic 

symptoms that have been reported at the pharmacological-dose level 

in humans include development of goiter and congenital malformations (Mertz, 1974b). Massive doses of lithium were reported to reduce 

aggressive behavior in humans and other vertebrates (Levy, 1968). 

Bowen (1966) gave 200 mg/day Li+ in a 750-g dry-weight diet (270 

ppm), duration not given, as the toxic dose in humans.

MANGANESE

[Essential trace element for plants and animals]

Plants

Under natural conditions Berger and Gerloff (1947) reported that 

acid soils (pH 5.0) mobilized manganese and that soil solutions containing >2.0 ppm soluble manganese were toxic to potatoes in Wisconsin. An acid soil (pH 4.8) with an ammonium acetate-extractable 

manganese concentration of 7.8 ppm was toxic to cotton in Virginia 

(Foy and others, 1969). Morris (1949) found that the exchangeable 

manganese content of 25 naturally acid soils varied from 1.2 - 638 ppm. 

Lespedeza and sweet clover grown on these acid soils made poor 

growth, contained high concentrations of soluble manganese, and 

showed typical symptoms of manganese toxicity. In general, plants 

having more than 400-500 ppm manganese (dry weight basis) in their 

tissues showed toxicity symptoms. The following concentrations (ppm, 

dry matter) of manganese in leaf tissue are considered excessive: 

>1,000, Navel and Valencia oranges (Embleton and others, 1976); 

>1,000, avocados (Jones and Embleton, 1976); 200, soybean, >500, flax 

(Moraghan, 1977); and 160, soybean (Ohki, 1977).

Under man-induced conditions Reuther, Smith, and Specht (1949) 

found that 600 800 pounds of manganese had accumulated in the top 

foot (approximately equivalent to 300-400 ppm) of acid sandy soils in 

Florida after 15 years of continuous fertilization of orange trees with 

manganese compounds. These amounts were toxic to some plants. 

Amounts found in comparable virgin soils were 34-46 kg total manganese per hectare. Plant species range greatly in their tolerance of 

excess manganese; Fergus (1954) found that kidney beans, a good 

indicator plant for excess manganese, showed toxicity symptoms when 

grown on a soil having a pH of less than 5.0 because of the easily 

reducible manganese in the soil. Vlamis and Williams (1967) reported 

that the following concentrations (ppm, dry weight) showed symptoms
34 ELEMENT CONCENTRATIONS TOXIC TO PLANTS, ANIMALS, AND MAN

of manganese toxicity in old leaves of plants grown in solution culture: 

1,200, barley; 7,000, rice; 1,400, rye; and 800, ryegrass. Schroeder, 

Balassa, and Tipton (1966) reported the following toxic concentrations 

(ppm) of the divalent manganous ion in water supplied to cultures: 

yeast, 550; legumes, 1 10; orange and mandarin seedlings, 5; tomatoes, 5-10; soybeans, 10-25; flax, 25-100; and oats, 150-500.

Animals

Under natural dietary conditions Cotzias (1962) reported from the 

literature that spontaneous lactation tetany has been recorded in cows 

grazing on pastures high in manganese. Further, consumption by 

animals of large amounts of certain tree foliage, which contains more 

manganese than do most herbaceous plants (Shacklette and Severson, 

1975), potentially could be toxic. Herbage of mixed-species composition 

in pastures in Spain was reported to reach the toxicity limit (15 ppm, 

dry weight basis) for cattle in only 1 of 19 pastures studied (Gonzales 

and others, 1959).

Under man-induced dietary conditions The Mn+2 form has a low 

order of toxicity to living organisms, especially to vertebrate animals 

(Schroeder, Balassa, and Tipton, 1966). The hexavalent form is highly 

toxic but does not occur in nature. The above report listed the following 

as toxic concentrations (ppm) of Mn2+ in diets: Daphnia magna, 50; 

flatworms, 700; freshwater fish, 2,420-3,450; birds, 4,800; chicks, 

4,800; rats, >2,000; rabbits, 1,250-6,000; pigs, 500-2,000; and lambs, 

5,000.

Man

Underwood (1971, p. 202) reported, "Chronic manganese poisoning 

occurs in miners working with manganese ores. The manganese enters 

the lungs as oxide dust from the air and also enters the body via the 

gastrointestinal tract. The disease is characterized by a severe psychiatric disorder (locura manganica) resembling schizophrenia, followed 

by a permanently crippling neurological (extrapyramidal) disorder 

clinically similar to Parkinson's disease." Cotzias (1962) reported that 

a particle size of manganic oxide <5/u, was responsible for the disorder. 

The National Research Council (1973) reported that manganism in 

miners, voltaic-cell factory workers, iron and steel industry workers, 

and others has been reported from Spain, Sinai, Germany, Chile, 

Morocco, Cuba, Italy, and Japan, to name a few. From the literature, 

these authors also reported a case of acute manganese intoxication of a 

family that ingested well water contaminated by old buried dry cells. 

Bowen (1966) reported that the normal consumption of Mn2+ in a 

750-g/day dry-weight diet was 3-10 mg (4-12 ppm), duration not 

given.
MERCURY 35 

MERCURY

[Considered nonessential for plants and animals]

Plants

Under natural conditions Mercury in living tissues is believed to 

be largely organic and primarily methyl mercury. The conversion of 

inorganic mercury to methyl mercury or dimethyl mercury is accomplished by anaerobic bacteria in the bottom muds of streams. 

Dimethyl mercury, stable in alkaline solutions, dissociates to ionic 

methyl mercury at low pH values such as may exist in the anaerobic 

bottom muds of streams and lakes. Methyl mercury is soluble in water 

and is available for incorporation into the tissues of aquatic organisms; 

thus, it can enter the food chain of higher animals and man. Or the 

methyl mercury may enter the higher organisms by direct assimilation from the surrounding medium (Greeson, 1970). Mercury compounds inhibit the growth of bacteria and have long been used as 

antiseptics and disinfectants. In contrast, most higher (vascular) 

plants are remarkably resistant to mercury poisoning, although they 

may accumulate high concentrations of mercury in their tissues. 

Shacklette (1970) reported as much as 3,500 parts per billion (ppb) in 

dry material of labrador tea that grew where its roots were above 

cinnabar mineral deposits, but the plant showed no toxicity symptoms. 

The geometric mean mercury concentration in 912 samples of soil from 

throughout the conterminous United States was reported as 71 ppb 

(Shacklette and others, 1971). Shacklette (1970) stated that the few 

available reports of mercury analysis of plants suggest that this.metal 

is not concentrated to a great extent, if at all, in the tissues of most 

plants that grow in normal soils. Mosses are tolerant of high mercury 

levels in their substrate (Shacklette, 1965b).

Under man-induced conditions Fungicides containing mercury 

compounds have been widely used on agricultural and horticultural 

crops. These compounds, if sprayed on plants, may be absorbed by the 

plants and translocated from one part of the plant to another. Novick 

(1969) stated that mercury compounds from sprays applied to apple 

leaves may be translocated to the fruits, and sprays applied to potato 

leaves may be moved to the tubers. In addition, the sprays may produce 

surflcial deposits on the leaves that are not easily removed. The mercury compounds, as applied, have no toxic effects on the plants themselves. Shacklette and Connor (1973) reported 0.5 ppm mercury (dry 

weight basis) in Spanish moss plants that presumably resulted from 

airborne industrial pollution, but toxic effects on the plants were not 

noted. Some greenhouse flowers, notably roses, are sensitive to volatilized elemental mercury, in that very low concentrations in the air 

cause toxic symptoms (Shacklette, 1970).
36 ELEMENT CONCENTRATIONS TOXIC TO PLANTS, ANIMALS, AND MAN

Animals

Under natural dietary conditions We have no reports of toxicity 

resulting from animals grazing on normal vegetation; it is likely that 

the small amounts present in the plants are well within the elimination rates of animals. Wershaw (1970, p. 31) stated, "Natural surface 

waters contain tolerably small concentrations of mercury except in 

areas draining mercury deposits."

Under man-induced dietary conditions The concentration of mercury, that was derived from the soil and that is present in crop plants 

probably is never toxic. However, the mercury compounds applied as 

fungicides to plant leaves, seeds, and grains may reach levels that are 

toxic to animals. Bowen (1966) reported that the consumption of 8 

mg/day Hg2+ in a total-dry-weight diet of 10 g (800 ppm) was lethal to 

rats, duration not given. 

Man

Greeson (1970, p. 33) stated, "Aquatic organisms, as well as man, 

will concentrate mercury within their bodies. . ... The result ... is a 

buildup with time to the extent that the accumulated mercury can 

become toxic and, eventually, lethal." In Japan about 50 persons, out of 

more than 100 affected, died of the "Minamata disease," caused by the 

consumption offish and shellfish obtained from a bay that had received 

large amounts of methyl mercury compounds in the waste effluents 

from a plastics factory (Kurland and others, 1960). Mercury poisoning 

was reported among citizens of Iraq who consumed bread made from 

seed wheat that had been treated with methyl mercury (Bakir and 

others, 1973). They stated that the wheat contained 8 ppm mercury, 

and acute concentrations (resulting in many patient deaths) were 

measured at 0.5-0.8 mg of mercury per kilogram of body weight. The 

biological half-life of methyl mercury in man is about 70-80 days. It is 

readily absorbed by the gastrointestinal tract. Ldfroth (1972, p. 66) 

stated, ". .. clinical methylmercury poisoning in adult people can 

occur at a mercury level of about 400 ng/g in the red blood cells ... 

corresponding to a regular daily intake of 0.3 mg mercury as methylmercury, i.e. 0.004 mg/kg body weight." Bowen (1966) reported that the 

normal daily consumption of Hg2+ was from 0.005-0.02 mg when 

based on a 750-g dry weight diet (0.007-0.03 ppm). Consumption of 

150-300 mg on the same basis (200-400 ppm) was considered lethal, 

duration not given. The U.S. Public Health Service (1962) proposed a 

tentative upper limit of 5.0 ppb mercury in drinking water.

MOLYBDENUM

[Essential trace element for plants and animals]

Plants

Under natural conditions There are no recorded instances of a field
MOLYBDENUM 37

occurrence of molybdenum toxicity to plants (Johnson, 1966), although 

high levels may be accumulated in the plants. Dye and O'Harra (1959) 

reported that, among forage plants, legumes usually collect more 

molybdenum than do grasses; they cited a high value of 372 ppm 

molybdenum (dry weight basis) in a sample of black medic from a 

Carson Valley, Nev. ranch. Warren and Delavault (1965) stated that 

many trees and lesser plants growing over commercial, or potentially 

commercial, molybdenum deposits may be expected to carry upwards 

of 500 ppm molybdenum in their ashes and that relatively few should 

be found with less than 250 ppm. Deficiency levels for plants are 

usually indicated by less than 0.10 ppm in their tissues (Johnson, 

1966), whereas Embleton, Jones, and Platt (1976) reported that >100 

ppm (dry matter) molybdenum in the fruiting shoots of Navel and 

Valencia oranges is probably an excessive amount.

Under man-induced conditions Tbxicity in the plant is observed 

only under extreme experimental conditions; in solution-culture experiments using 1,000-2,000 ppm molybdenum, tomato plants developed an intense golden yellow color in their leaves, and seedlings of 

cauliflower turned an intense purple (Johnson, 1966). Wallace, Romney, Alexander, and Kinnear (1977) wrote the following: "A level of 10~3 

M H2Mo04 was toxic to bush beans grown in solution culture. Leaves, 

stems, and roots, respectively, contained 710,1054, and 5920 /xg Mo/g 

dry weight." 

Animals

Under natural dietary conditions "Molybdenum toxicity, variously 

referred to as molybdenosis, teart disease, and peat scours, has been 

reported from many parts of the world .... In most instances toxic 

amounts of molybdenum in forage consumed by ruminants have resulted from naturally occurring excess molybdenum in the soil or 

irrigation water" (Johnson, 1966, p. 287). This toxicity in ruminants is 

a complex matter, involving not only excess molybdenum but also low 

copper levels and high sulfate-sulfur concentrations in the forage. 

Molybdenosis occurs when the copper in forage is normal (8-11 ppm in 

dry matter) and the molybdenum is above normal (more than 5-6 ppm 

for cattle or 10-12 ppm for sheep) (Dye and O'Harra, 1959). Molybdenosis in grazing animals has been observed in the San Joaquin 

Valley of California (Barshad, 1948) and in Nevada and Oregon 

(Kubota and others, 1961,1967). The amount of molybdenum absorbed 

by plants is not strongly correlated with total molybdenum in the soil, 

because soil pH and other soil properties greatly affect availability to 

plants, molybdenum being more available at high pH values. The area 

in Kern County, Calif., reported by Barshad (1948) to produce molybdenosis in cattle, had alkaline soils with total molybdenum concentrations of 1.5-5.0 ppm; these soils supported pasture plants, a large 

proportion having 20 or more ppm molybdenum (dry weight).
38 ELEMENT .CONCENTRATIONS TOXIC TO PLANTS, ANIMALS, AND MAN

Under man-induced dietary conditions Applying molybdenum fertilizers, or liming to release previously unavailable molybdenum, may 

result in the forage containing amounts of the element that are toxic to 

animals. Mining activities may expose deposits having concentrations 

of molybdenum and other elements that can be considered anomalous 

in the natural geochemical environment of plants and animals. An 

area in Missouri was studied (Ebens and others, 1973) where clay 

mining operations had contaminated adjacent areas to the extent that 

beef cattle grazing these areas exhibited symptoms of metabolic imbalance thought to be chronic molybdenosis due principally to 

copper-molybdenum imbalance. G. A. Christianson and G. A. Jacobson 

(written commun., 1974) reported molybdenosis in beef cattle in North 

Dakota in the vicinity of a lignite ashing plant. Apparently emissions 

from the plant raised the molybdenum level in the forage, creating a 

molybdenum-induced copper deficiency in the cattle. Molybdenum 

concentrations in fecal material from contaminated fields ranged from 

16 to 26 ppm (dry weight). Bowen (1966) reported that 5 mg molybdate 

in a 10-g/day dry-weight diet (500 ppm) was toxic and 50 mg (5,000 

ppm) was lethal to rats, duration not given. Owing to poor absorption, 

horses and pigs have low susceptibility to molybdenosis (Underwood, 

1971). 

Man

At normal environmental concentrations of molybdenum, toxicity 

is of little concern. Underwood (1971, p. 135) stated, "Molybdenum is 

apparently of so little practical significance in human nutrition, either 

in health or disease, that few people have been stimulated to undertake studies with this element." The only incidence of molybdenosis in 

humans of which we are aware was reported by Agarwal (1975). He 

found that peasants in India who consumed sorghum that was grown 

in alkaline soils high in molybdenum and fluorine as a staple, developed a crippling syndrome of knock-knees (genu valgum). No instances of the disease were reported prior to the construction of a large 

dam that raised the water table in the surrounding district and caused 

an increase in alkalinity and concurrently the uptake of molybdenum 

by the sorghum. No specific concentrations of molybdenum in sorghum, soils, or humans were given.

NICKEL

[Suspected as being essential for some plants and animals]

Plants

Under natural conditions Mitchell (1945) stated that the normal 

nickel content of plant material, dry weight basis, ranges from 0.10-5 

ppm, depending on the species, the part of the plant, maturity, time of 

sampling, and other factors. Extremely high nickel concentrations of
NICKEL 39

1-2 percent (dry weight) in the leaves and 25.74 percent in the latex of 

Sebertia acuminata from New Caledonia have been reported by Jaffre 

and others (1976). The plant appears to be restricted in its growth to 

areas of ultrabasic substrates in which nickel concentrations are relatively high (0.85 percent in soil). No toxicity symptoms were expressed 

in response to these extreme tissue concentrations. Excessive nickel in 

serpentine soils may be a factor contributing to the restricted growth of 

plants on these soils, as reported by many investigators; but excessive 

chromium, unfavorable magnesium-calcium ratios, and deficiency of 

molybdenum may also limit plant growth (Vanselow, 1966a). The 

amount of nickel absorbed by plants on serpentine soils ranges widely 

among species; Shacklette (1966) reported the following concentrations (ppm in ash) from a site in Alaska: aspen, 10; white birch, 50; and 

low juniper, 150. The soil at this site contained 50-75 ppm nickel, and 

the basaltic greenstone on which the soil developed contained 100 ppm 

nickel. Malyuga (1964) described apetalous forms of anemone growing 

over nickel deposits, attributed to toxicity of the nickel.

Under man-induced conditions Tbxicity of nickel to many plants, 

even at relatively low concentrations, has been noted; 40 ppm (dry 

weight) in tomato plants was toxic, and 150 ppm stopped growth 

(Sauchelli, 1969). Soane and Saunder (1959) reported 12-246 ppm (dry 

weight) in leaves of corn and 14-34 ppm in leaves of tobacco both 

kinds of plants developed toxicity symptoms. The following concentration ranges for nickel in nutrient solutions are reported from the 

literature by Vergnano and Hunter (1952) as being toxic: 2-40 ppm, 

beans and maize; 2-60 ppm, buckwheat; 3-300 ppm, oats; 2-15 ppm, 

barley and beans; and 15-30 ppm, oats and sugar beets. These authors 

also reported from their own studies that nickel toxicity was observed 

in oats that had nutrient solutions ranging from 1 to 1.5 ppm (slight 

leaf mottling) to 10 30 ppm (chlorosis and necrosis). Soybean plants 

were killed in a soil of pH 6 when 1,000 ppm nickel was added to the 

soil. Higher pH decreased the toxicity of nickel (Wallace, Romney, Cha, 

Soufi, and Chaudhry, 1977). 

Animals

Under natural dietary conditions Mitchell (1945) recorded levels of 

0.5-4 ppm (dry weight) nickel in pasture herbage; Allaway (1968) 

reported that toxicity to animals was moderate to low. In view of these 

relationships, toxicity to grazing animals seems unlikely.

Under man-induced dietary conditions Compared to many other 

trace metals, the concentration of nickel in foods is high. A mechanism 

in mammals, however appears to limit its intestinal absorption. The 

toxicity of nickel to mammals is low (ranking with the essential trace 

elements) except in astringent doses. Nickel salts irritate the mucosal 

lining of the gut more than they cause inherent poisoning (Schroeder,
40 ELEMENT CONCENTRATIONS TOXIC TO PLANTS, ANIMALS, AND MAN

Balassa, and Tipton, 1962b). Underwood (1971) reported that 700 ppm 

nickel in the diet of chicks depressed growth, 1,600 ppm depressed 

growth of young mice, and 1,000 ppm had no apparent toxic effect on 

rats or monkeys. The National Research Council (1975) reported the 

following from the literature: 1 3 g/kg body weight of nickel metal, 

non toxic to dogs; 250, 500, and 1,000 ppm each of nickel carbonate, 

nickel soaps, and nickel catalyst (Raney nickel) in the diet of young 

rats for 8 weeks, non toxic; 5 ppm nickel acetate in the drinking water 

of mice over their lifetime, non toxic; 5 mg/kg nickel metal orally 

administered to guinea pigs, lethal; and 500 mg/kg nickel fluoborate 

orally administered to rats, lethal. Bowen (1966) gave as toxic to rats a 

ration of 50 mg Ni2+ in a 10-g/day dry-weight diet (5,000 ppm), duration 

not given. He listed the element as potentially carcinogenic. 

Man

The toxicity of nickel to humans is low. Workers in nickel refineries 

have developed "nickel dermatitis" and respiratory-tract neoplasia; a 

direct link between the elemental form and these pathologies, however, has not been made (Schroeder, Balassa, and Tipton, 1962b). 

Nickel carbonyl, used in nickel refining, nickel plating, and the petroleum industry, is the only organic nickel compound that has been 

recognized as a cause of human systemic toxicity (National Research 

Council, 1975). The toxicity of this compound was summarized (Blomberg and others, 1977, p. 22) as follows: "Nickel carbonyl poisoning is 

considered mild if the urinary nickel concentration is less than 100 

ptg/L, moderately severe if the concentration is 100-500 /otg/L and severe if the concentration is more than 500 /Ag/L." Nickel carbonyl, if 

inhaled, is extremely toxic and can be lethal.

SELENIUM

[Considered nonessential for most plants; essential trace element for most animals] 

Plants

Under natural conditions "There are no recorded instances of naturally occurring selenium causing damage to plants in the field" (National Research Council, 1976, p. 70). The occurrence and ecological 

relationships of selenium-indicating plants have been documented by 

many investigators. Two groups of native species may be recognized: 

the primary indicator plants are those found growing only on 

seleniferous soils and which absorb large amounts of selenium; the 

second group is composed of those species that are also capable of 

absorbing selenium in concentrations toxic to animals if growing on 

seleniferous soils but which may also grow elsewhere. Excess soil 

selenium may prevent plants not in these two groups from growing on 

seleniferous soils by causing toxicity symptoms to develop. These
SELENIUM 41

symptoms are never seen in crop plants grown on naturally seleniferous soils, but under experimental conditions the symptoms in grasses 

ordinarily are snow-white chlorosis of the leaves and pink root tissue; 

symptoms in other plants vary, but commonly include stunting, yellow 

chlorosis, and pink leaf veins (Ganje, 1966). Lakin (1972) stated that 

certain species of Astragalus utilize selenium in an amino acid peculiar to these species and that-they absorb many times as much selenium 

as do other plants growing in the same soil. These plants convert 

selenium into forms absorbed by non seleniferous species through 

foliage decomposition and oxidation to inorganic salts or soluble organic compounds (Ganje, 1966). The plants, both fresh and dried, often 

have a strong garlicky odor. Byers and Lakin (1939) analyzed about 

300 samples of shales, soils, and plants collected in seleniferous areas 

of Canada and found the selenium of shales to vary from 0.3 to 3.0 ppm; 

of soils, from 0.1 to 6 ppm; and of vegetation, from 3 to 4,190 ppm in dry 

matter. The organic compounds of selenium in soil are derived from 

partially decayed seleniferous vegetation. Inorganic selenium exists 

as the element; as ion selenide; as a substitute in sulfide minerals, 

particularly pyrites; as selenite, particularly basic ferric selenite; and 

as selenate, particularly calcium selenate. Basic ferric selenite seems 

to be the most common form in soils, while very little is present in the 

elemental form. Selenate and organic selenium are the forms most 

available to plants (Ganje, 1966).

Under man-induced conditions Soils producing seleniferous vegetation have been found only in arid or semiarid regions, at least in the 

United States, where the mean annual rainfall is less than 20 inches. 

For crop plants, only the soil content of water-soluble selenium is 

important, because elemental selenium and selenite are of only slight 

availability to these plants, as was demonstrated by Hurd-Karrer 

(1934). Corn grown in culture solutions containing 5 ppm of selenite or 

organic selenium accumulated 200 and 1,000 ppm selenium, respectively. At the 10-ppm level, corn accumulated 300 ppm from the selenite form and more than 1,500 ppm from the organic selenium form 

(Ganje, 1966). Resistance to selenium toxicity among plant species 

ranges so widely that a general toxicity level cannot be reliably estimated. 

Animals

Under natural dietary conditions There are numerous accounts in 

the literature of grazing animals being poisoned after consuming certain types of vegetation. Some of the very early descriptions of the 

disease symptoms (such as sloughing hooves) leave little doubt that 

many of these cases were the result of selenium intoxication (Trelease 

and Beath, 1949). These authors presented an interesting history of 

selenium poisoning, the documentation of which goes back to 1857 (in
42 ELEMENT CONCENTRATIONS TOXIC TO PLANTS, ANIMALS, AND MAN

an area of western South Dakota) and perhaps to 1295 (in an area of 

western China as described by Marco Polo). Lakin (1972, p. 49-50) 

reported, "Acute poisoning of cattle and sheep occurs when herds or 

bands are being driven from one pasturage to another. Animals, under 

these conditions, eat forage indiscriminately and many may die overnight. Both seleniferous Astragalus species and alkaloids are probably 

involved.. . . Subacute poisoning, known locally as blind staggers, loco 

disease, or pushing disease, has been reported in western United 

States and in South Africa. This is probably another instance of the 

confusion between selenium toxicity and naturally toxic vegetation. 

The actual cause of these diseases is in debate. Chronic poisoning is 

caused by daily ingestion of cereals and grasses containing 5 to 20 ppm 

selenium. . . . Subchronic poisoning has been reported by Brown and 

de Wet (1962) in South Africa. They suggest'. . . the moderate selenium 

content of the diets of these animals has weakened them and made 

them more susceptible to disease.' " Byers (1935) suggested 4 ppm (dry 

weight) of selenium in plants as a tolerance limit for animals that 

consume them and considered 5 ppm to be potentially dangerous. 

Forage with selenium concentrations of 10-30 ppm (dry weight) was 

considered capable of producing toxicity symptoms in cattle (Church 

and others, 1971). Water containing 0.5 ppm selenium may also be 

dangerous (Ganje, 1966).

Under man-induced dietary conditions Because of the dual role of 

selenium as a micronutrient and a toxin to animals, the selenium 

concentrations in feeds can be critical factors in the health of the 

animals. Underwood (1971, p. 346) stated, "A dietary intake of 0.1 ppm 

[in dry feeds] provides a satisfactory margin of safety against any 

dietary variables or environmental stresses likely to be encountered 

by grazing sheep and cattle." Many factors determine the level of 

selenium in feeds that are toxic to animals, but amounts of 5 ppm (dry 

weight) or more may generally be considered toxic. Underwood (1971, 

p. 356) stated, "Signs of chronic poisoning are common in rats and dogs 

given diets containing 5-10 ppm selenium, and, at 20 ppm, there is 

complete refusal of food and death in a short time. Young pigs fed 

seleniferous diets containing 10-15 ppm selenium develop signs of 

selenosis within 2 to 3 weeks. Diets containing lower levels than these 

would induce similar effects if fed for a longer period. The minimum 

toxic levels for grazing stock are more difficult to determine. They 

probably lie close to 5 ppm selenium. Edible herbage in seleniferous 

areas commonly contain 5-20 ppm selenium." Church and others 

(1971) summarized numerous studies and reported that acute selenium 

toxicosis can be produced in cattle and sheep by feeding them plants 

that supply about 2 mg of selenium per kg of body weight. He also 

stated that selenium was lethal to cattle, under feedlot conditions, at a
SELENIUM 43

rate of about 1.1 mg/kg of live weight (dosed 3 times weekly). Overt 

expressions of poisoning were observed when selenium in the blood 

exceeded 3 ppm. In work with sheep he reported that a dose of sodium 

selenate equivalent to about 1.8 mg/kg of live weight was lethal and 

that consumption of plant material containing 400-800 ppm selenium 

may be fatal when fed in quantities of 8 16 g/kg of body weight. 

Sauchelli (1969) reported that wheat can grow in soil containing 1 ppm 

selenium. If grain containing 8-10 ppm selenium was fed to rats, it 

retarded growth and killed them after a few weeks. Selenium may be 

introduced into the environment through the burning of coal, in phosphate fertilizers, and in selenium-containing insecticides, but the latter source has very little application to toxicity problems at present 

because the use of these insecticides on food plants is prohibited, except 

in special circumstances. 

Man

Under dietary conditions in seleniferous regions Lakin (1972, p. 51) 

wrote, "Soils producing crop plants that are toxic because of selenium 

are confined to small areas but occur throughout the world. Such soils 

are confined to semiarid regions or areas of impeded drainage. They 

contribute no significant hazard to human health and only locally to 

animal health." The selenium content of certain foods may reach levels 

that could affect human health. For example, the selenium content of 

tuna was reported (Kifer and others, 1969) to average 4.63 ppm (dry 

weight) and to range from 3.4 to 6.2. A daily intake of 1 mg selenium in 

food is probably not harmful to an adult person. Allaway (1975) reported that a concentration of selenium of 3-4 ppm in human and 

animal diets is considered safe. Robinson (1936) found that seleniferous wheat may be blended with sufficient selenium-free grain to drop 

the selenium concentration to the tolerance level. Hadjimarkos (1970) 

reported that the incidence of dental caries appears to be greater in 

areas naturally high in selenium. This is particularly true among 

children who consume small amounts of dietary selenium in addition 

to the naturally high amounts in the local water. Selenium concentrations of 0.08 ppm in the urine identified those individuals with increased incidence of dental caries. The situation regarding selenium 

poisoning in man was summarized by Lakin (1972, p. 50) as follows: 

"Fortunately, the human diet is rarely restricted solely to the products 

of a highly seleniferous area. Thus, selenium poisoning through the 

food-plant cycle is rare in the world human population and tends to be 

restricted to combinations of highly seleniferous areas whose populations depend largely on local agricultural produce." Chronic selenium 

poisoning in humans was reported to occur in Mexico by Byers (1937) 

and in Columbia by Ancizar-Sordo (1947) and Leonidas and Hernan 

(1970).
44 ELEMENT CONCENTRATIONS TOXIC TO PLANTS, ANIMALS, AND MAN

Under the effects of environmental pollution by selenium Sauchelli 

(1969) reported that the maximum amount of selenium that man can 

consume in the whole diet without ill effects is believed to be 3 ppm. 

Bowen (1966) listed as toxic 5 mg Se(IV) (selenite) in a 750-g/day dryweight diet (7 ppm), duration not given. Pollution-related selenium 

intoxication is most commonly associated with industrial exposure 

(Cooper, 1967), because selenium compounds are absorbed through the 

lungs in dust or fumes and through the skin. Whether ingested or 

inhaled, Cooper (1967, p. 186) stated, "... there is marked variations 

between and within animal species in their response to selenium at 

what may be considered toxic levels."

SILVER

[Considered nonessential for organisms]

Plants

Under natural conditions We have no reports of silver toxicity in 

plants growing under natural conditions. The concentration of silver 

in plants is usually less than 0.5 ppm in ash; higher values, however, 

have been found in a wide variety of plant groups including mosses (as 

much as 7 ppm, Shacklette, 1965a); club moss (5 ppm); ferns (bracken, 3 

ppm); coniferous trees (highest value reported was 200 ppm in dwarf 

juniper); deciduous trees (bur oak, 15 ppm); and vegetables (tomato 

fruits, 7 ppm, Connor and Shacklette, 1975). These levels of silver 

produced no observed toxicity in the plants. Warren and Delavault 

(1950) reported finding 0.1-1.4 ppm silver in ash of trees and herbs 

that grew in areas containing no known silver mineralization. The 

silver concentration in "normal" soils seldom exceeds 0.5 ppm, but a 

concentration of 5 ppm has been reported (Shacklette and others, 1971); 

concentrations may be much higher at mineralized sites.

Under man-induced conditions Brooks (1972) reported that the 

toxicity of silver to plants was severe, but he did not give the conditions 

under which this toxicity occurred. Clark (1899) found that silver in a 

concentration of 0.0098 /u,g/ml was fatal to corn and that 0.0049 /xg/ml 

was fatal to lupines. Wallace, Alexander, and Chaudhry (1977) wrote 

the following concerning silver toxicity to bush beans: "Silver was very 

lethal at 10~4 M AgNO3 ; at 10~5 M yields were greatly decreased, but 

plants were grown without symptoms. Leaf, stem, and root concentrations of Ag for this treatment, respectively, were 5.8,5.1, and 1,760 /w-g/g 

dry weight." Silver readily forms insoluble compounds, which reduces 

the risk of environmental contamination; but insoluble compounds or 

metallic silver can form minute amounts of ionic silver, either through 

chemical reactions or electrolysis, that can be toxic to microorganisms 

(Goetz and others, 1940). Its toxicity to a variety of microbes has been
SILVER 45

utilized in the preservation of medicines and in water purification 

(Smith and Carson, 1977). Romans (1968) reported that water containing 15 g/L silver sand killed the bacterium Escherichia coli in 2-24 

hours, depending on numbers of bacteria. Concern with the effects of 

silver iodide fallout from cloud seeding for increasing precipitation 

centers around the sensitivity of soil microorganisms to the silver ion. 

In a report of experiments on these organisms, Sokol and Klein (1975, 

p. 211) concluded, "These results suggest that high concentrations of 

seeding agent potentially can alter the soil microbial environment by 

inhibiting organic matter decomposition, but that the silver levels 

which accumulate in seeded target areas should have no overt effects 

on the soil environment." 

Animals

Under natural environmental conditions We have no report of 

silver toxicity in animals under these conditions. Silver apparently is 

not bioconcentrated, and silver in natural deposits is largely in an 

un-ionized state, therefore is unlikely to cause animal toxicity.

Under man-induced conditions Cooper and Jolly (1970, p. 89) 

stated, in regard to silver, "... it is relatively harmless to higher 

animals, including man." Bowen (1966) gave the silver content of 

mammalian tissue as ranging from 0.01 ppm (in dry matter) in bones to 

0.04 ppm in certain soft tissues. Younger and Crookshank (1978) reported that silver iodide (Agl) used in weather modification may be 

deposited on forages in the seeded target area and enter the food chain 

of livestock. In their experiments with sheep, 15 ewes were given oral 

doses of Agl at 0.1, 1.0, or 10 mg per kg per day without developing 

clinical signs of toxicity. Silver was absorbed from the gastrointestinal 

tract and deposited in soft and hard tissues of the ewes; the maximum 

concentration found was 17 ppm in the liver of a ewe that received the 

highest dose rate. In administering the Agl doses, the gelatin capsules 

were inadvertently broken in the mouths of two ewes; these ewes died 

from acute hemorrhagic pharyngitis within 72 hours after the accidental breakage. These investigators concluded that Agl from cloudseeding operations is not likely to induce overt toxic effects on livestock.

Silver in minute amounts in water is very toxic to fish, probably by 

interference with gas exchange by the gills. Doudoroff and Katz (1953) 

found that solutions containing 0.0001 /xg/ml were harmful to freshwater fish. Schmahl and Steinhoff (1960) reported that colloidal silver 

produced tumors in experimental animals. 

Man

Smith and Carson (1977, p. 355) stated, "No systemic pathology has 

been directly attributable to silver among workers occupationally 

exposed to it." Cooper and Jolly (1970, p. 90) reported, "Silver, even in
46 ELEMENT CONCENTRATIONS TOXIC TO PLANTS, ANIMALS, AND MAN

highly soluble form, is only moderately harmful to mammals. Because 

of caustic action on the intestinal tract, 10 g of AgNO3 is usually fatal to 

man, but 3 g can be taken safely." Continued intake of silver salts 

causes an irremedial discoloration of the skin and mucous membranes 

(argyria) from the deposition of organo-silver compounds that are 

reduced to dark-colored forms by sunlight. There are no other ill effects 

from this silver deposition (Sax, 1975). Because of the extremely low 

silver concentrations in food, dietary intake of silver by man probably 

is of no consequence.

SULFUR

[Essential for plants and animals]

Elemental sulfur is of little concern as a toxic substance. In this form 

it has long been used as a pesticide, particularly for the control of 

certain plant diseases. Compounds of sulfur, in contrast, may constitute important environmental pollutants that have adverse or frankly 

toxic effects on plant and animal tissues. Practically all sulfur toxicity 

problems of environmental concern in plants, animals, and man are 

caused by the mining of ores and fuels and the processing and use of 

these materials. 

Plants

Under natural conditions Areas barren of vegetation may exist at 

locations where natural deposits of sulfur-rich materials occur at or 

near the surface. "Oxidation of sulfur in soils can occur either as 

non-biological (auto-oxidation) or as biological oxidation, the latter 

being more important" (Blair, 1971, p. 117). The resulting S03~2 and 

S04~2 in the presence of water can form H2SO4 (sulfuric acid). The 

localized "acid spots" that are formed bear little or no vegetation more 

because of low soil pH than of toxicity to the sulfite or sulfate ions. 

Although sulfur dioxide (SO2) is formed naturally by oxidation of 

hydrogen sulfide that occurs in bogs and swamps, we have no reports of 

damage to plants from this source.

Under man-induced conditions Sulfur dioxide is increasing in importance as a plant toxicant. By far the largest amount of airborne 

sulfur compounds (principally SO2) in areas affected by industrial 

operations is of man-made origin, although in certain areas sulfur 

from natural sources is significant. Grey and Jensen (1972, p. 1099) 

noted, "On a yearly basis, the major source of atmospheric sulfur 

compounds in and near Salt Lake City, Utah, is industrial. Isotopic 

studies suggest that the next most important source is bacteriogenic 

sulfur released by anaerobes from muds. On a seasonal basis, the 

bacteriogenic source of sulfur compounds may rival the industrial 

source in importance." Background levels of sulfur dioxide in air pro-
SULFUR 47

bably range from 0.28 to 2.8 /xg/m3 (1-10 ppb), whereas phytotoxic 

effects begin to appear between 27 and 224 /ug/m3 (10-80 ppb) mean 

annual local concentration (Nash, 1973). Lichens, bryophytes, and 

fungi are the most sensitive plants to sulfur dioxide insult and generally are damaged at concentrations of less than 100 /xg/m3 (<35 ppb) 

(Saunders and Wood, 1973). Species of coniferous trees probably are the 

most sensitive of the higher plants. Nash (1973) reported the following 

toxicity thresholds from the literature: Douglas-fir seedlings, 812 

/ag/m3 (290 ppb) after 44 hours; and eastern white pine, 280 Atg/m3 after 

8 hours. He also reported that the most sensitive non-coniferous higher 

plant species generally exhibit chronic toxicity symptoms at concentrations of 280-840 /ig/m3 (300-500 ppb).

The symptoms of acute injury to plants were summarized by Daines 

(1969, p. 1) as follows: "Acute injury, resulting from the rapid absorption of a toxic dose of SO2 , manifests itself as marginal or intercostal 

necrotic areas which at first have a dull dark green water-soaked 

appearance and on drying and bleaching become an ivory color in most 

plant species, but in some browns and reds predominate. The necrotic 

areas extend through the leaf and are visible on both surfaces. The 

areas immediately bordering the veins are seldom injured. These areas 

are characterized by few stomata and very limited intercellular spaces. 

The younger fully expanded leaves are most susceptible to SO2 , followed by the older leaves, while the enlarging leaves are the last to 

show acute injury."

Acid rain, produced when sulfur dioxide is oxidized to sulfuric acid, 

is a potentially serious toxicant to plants. Carrier (1977, p. 8-1) summarized as follows, "Acid rain, largely the result of sulfur dioxide 

pollution, may damage plants at distances of up to 1000 km from the 

pollution source. Indirect evidence suggests that it has caused a reduction in forest productivity in certain areas, and it has been shown to 

cause plant abnormalities and to have detrimental effects on plant 

nutrition. Acid rain also can destroy the protective waxy layers of 

foliage, cause enhancement of disease, and decrease plant productivity. 

Because the uptake of heavy metals is increased by lower than normal 

pH values, a synergistic effect can reasonably be expected where fallout of heavy metals and acid rain appear simultaneously." 

Animals

Under normal dietary conditions Sulfur toxicity in animals caused 

by feed or water that is normally consumed is unlikely because of the 

low sulfur content of these materials. Postgate (1968, p. 267) wrote, 

"Though certain animals, notably ruminants, can tolerate appreciable 

free sulphide in their intestines, H2S is normally toxic to aerobic plant 

and animal tissues." He stated further (p. 278), "The rumina of sheep 

contain sulphate-reducing bacteria and the sulphide they form has
48 ELEMENT CONCENTRATIONS TOXIC TO PLANTS, ANIMALS, AND MAN

been shown, by isotope experiments, to contribute to the sulphur 

nutrition of sheep. Sulphate-reducing bacteria are found in the guts of 

insects where they may have a similar function."

The toxicity of sulfur to grazing animals is indirect. Copper deficiency diseases have been reported in lambs (Underwood, 1971) following the consumption of herbage naturally high in sulfate or from 

grazing in mining areas rich in sulfur minerals. These imbalances 

result from a synergistic metabolic relationship between copper, 

molybdenum, and sulfate. Underwood (1971, p. 133) wrote,"... chronic 

copper poisoning can occur in sheep with moderate copper intake and 

very low levels of molybdenum and sulfate, and, conversely, the depletion of the animal's copper reserves, to the extent of clinical signs of 

copper deficiency, can arise on normal copper and high-molybdenum 

and -sulfur intakes."

Under man-induced environmental conditions The effects on aquatic organisms of mine drainage waters that are highly acidic because of 

the oxidation of pyrite (FeS2) are well known and have been extensively reported. Again, the toxic effects are largely related to pH, not to 

the sulfur content, of the water. Tbxic effects on animals of sulfur 

dioxide presumably are similar to those on humans that are discussed 

below, although we have no reports of these effects on domestic or other 

animals. Acid rain has been reported to have caused the death of fish 

by lowering the pH of water in lakes that naturally have a low buffering capacity. Attempts have been made to correct this toxicity by 

adding lime to the water.

Man

Under the effects of atmospheric pollution Saunders and Wood 

(1973) stated that sulfur dioxide concentrations of 500-3,000 /ug/m3 

(0.18-1.07 ppm) have a detectable odor and that concentrations 

greater than 8,500 /u,g/m3 (3.04 ppm) are very pungent and irritating. 

Lillington (1974, p. 316) reported, "Sulfur dioxide primarily affects the 

upper respiratory tract and larger bronchi. Ciliary action and mucous 

flow are inhibited at concentrations of 10 to 15 ppm. Increased airway 

resistance (due to reflex broncho-constriction) occurs regularly with 

exposures of 4 to 6 ppm breathed by mouth for ten minutes, and some 

unusually sensitive individuals respond to concentrations of 1 ppm. 

... Asthmatic and bronchitic subjects are clearly more sensitive in 

inhaled SO2 . . . . Sulfur dioxide in the atmosphere can be oxidized to 

sulfur trioxide which forms sulfuric acid when dissolved in water. 

Sulfuric acid is considerably more toxic than SO2 , but the magnitude of 

this conversion in smog is not well established."
THALLIUM 49 

THALLIUM

[Considered nonessential for organisms]

Plants

Under natural conditions Very few data are available on the normal concentrations of thallium in vegetation growing in the United 

States. The following parts per million in ash were reported 

(Shacklette and others, 1978) for trees and shrubs in the Rocky Mountain region: subalpine fir needles 2 100, stems 2 70; limber pine 

needles 2-5, stems 3-5; lodgepole pine needles 2-5, stems 3-7; 

Engelmann spruce needles 2-10, stems 15; myrtle blueberry stems 

and leaves 2-7; phyllodoce stems, 2; and ponderosa pine stems 15. 

Carson and Smith (1977) gave unpublished data from the U.S. Geological Survey on thallium concentrations in U.S. plants; 2 7 ppm in ash 

was considered anomalous and 10 ppm, highly anomalous. Most 

values, if detected (in about 1 percent of the samples), ranged from 0.4 

to 0.5 ppm in ash. Berg (1925) reported 0.1 mg thallium in 100 g (1 ppm) 

of spinach and rye samples. Thallium in some European food and feed 

plants, given by Geilmann and others (1960) as parts per million in dry 

weight, follow: head lettuce, 0.021; red cabbage, 0.040; green cabbage, 

0.125; leek, 0.075; endive, 0.080; clover, 0.008-0.010; and meadow hay, 

0.020-0.025. Reports of thallium in ash of native plants in the Soviet 

Union (Dvornikov and others, 1976) gave a range of about 0.01 to 1.0 

g/ton (0.01 to 1.0 ppm). The average for soils that they analyzed was 

0.023 g/ton (0.023 ppm). The plant concentration factor, based on 14 

species of plants and 38 soil samples, was calculated to be 1.74. Tbxic 

levels of thallium were reported by Zyka (1972) in native vegetation of 

a region in Yugoslavia that was remarkable for high levels of thallium 

in the substrate. He found thallium in ash of herbaceous plants to 

range from 10 ppm in Eryngium to 17,000 ppm in bedstraw. Tbadflax 

contents ranged from 3,000 to 3,800 ppm. He also noted zonation of 

species related to soil concentrations of thallium, which indicated the 

degree of toxicity of the element to certain plant species.

Under man-induced conditions McMurtrey and Robinson (1938, p. 

827) stated, "When artificially applied it [thallium] is probably taken 

up by the plant, and as little as 35 ppm in sandy soils has practically 

prevented the growth of plants." A bait for poisoning predators consisting of 7 g ground meat and 0.5 g thallium that was placed on stakes a 

few centimeters above the ground in Hawaii produced bare patches on 

the ground 3-6 dm long and about one-third as wide; no plants grew in 

these patches for at least two years (Brooks, 1932). Carson and Smith 

(1977) noted, "Many crop plants are injured by concentrations of about 

7 ppm in the soil. Gramineae and seeds are more resistant. Tbbacco 

plants are especially sensitive, showing toxic effects at 1 ppm in the
50 ELEMENT CONCENTRATIONS TOXIC TO PLANTS, ANIMALS, AND MAN

soil, or 4 ppm in water." Twelve-day-old crop plants in loam soil are 

completely inhibited by 1,100 ppm in irrigation water (Horn and 

others, 1936). Concentrations of 0.04 ppm in water induced chlorosis in 

tobacco seedlings (Carson and Smith, 1977). Wheat in sandy loam soil 

was injured with a concentration of 1.4 ppm in soil and killed at 28 ppm; 

toxic effects on buckwheat, alfalfa, and perennial ryegrass at near the 

same thallium concentrations were similar (McCool, 1933). Thallium 

levels of 2 -3 ppm in freshwater reduces the photosynthetic activity of 

algae (Overnell, 1975), and at 7 ppm, definite toxicity occurs (DiGaudio, 1975, as cited in Carson and Smith, 1977, p. 315). 

Animals

Under natural dietary conditions Zyka (1972, p. 94) reported, regarding the high thallium region of Yugoslavia cited above, "The high 

thallium contents in the plants explain their toxic effects on cattle." 

Marsh (1958) and MacPherson and Hemingway (1969) reported natural poisoning by thallium of sheep in Israel. We have no other reports of 

thallium poisoning resulting from the consumption of vegetation by 

animals. Case (1974) stated that there was no effective antidote for 

thallium poisoning in sheep.

Under man-induced dietary conditions Carson and Smith (1977, p 

315) reported, " 'Non-effect levels' for mammals have not been established experimentally, but levels of near 3 ppb thallium in an animal's 

diet are likely to produce toxic effects detrimental to the individual's 

survival." The lethal dose for dogs was found to range from 35 to 253 

mg/kg body weight; thallium in the blood of poisoned animals ranged 

from 5.8 to 3,470 ppm; and the range in other tissues was from 0.0 to 

1,540, the latter concentration occurring in the spleen. Bowen (1966) 

reported that 7.5 mg Tl+ in a 10-g/day dry-weight diet (750 ppm) was 

lethal to rats: Fatal doses of thallium for guinea pigs was found to be 

20-80 mg/kg (Weinig and Walz, 1971). Meat from all marine seafood 

from Minamata Bay in Japan (where polluted water caused a serious 

disease in humans who ate seafood) averaged 0.08 ± 0.02 ppm thallium (Hamaguchi and others, 1960). Where algae containing as much 

as 0.85 ppm thallium serve as the principal food of aquatic animals, 

bioconcentration and direct toxicity to the consumer may occur (Carson and Smith, 1977).

Man

Thallium compounds are highly toxic to humans. McMurtrey and 

Robinson (1938, p. 827) wrote, "Thallium compounds have been used as 

depilatories with disastrous effects." Thomas (1973) gave 5-50 mg/kg 

body weight as the probable lethal dose of thallium salts for an adult, 

whereas Bowen (1966) listed 600 mg/day in a 750-g dry-weight diet 

(800 ppm) as lethal. Zitko and Carson (1975) concluded that there is no 

danger of thallium accumulating in aquatic mollusks to levels that are
TIN 51

toxic to humans. The concentration factor (stomach contents/tissue) 

for elk and deer was found to range from 0.04 to 0.14 in muscle and from 

14 to 22.7 in bone (Carson and Smith, 1977), and they concluded that 

there seems to be little danger of human toxicity caused by eating meat 

of these animals. In regard to thallium toxicity from eating plants, 

Carson and Smith (1977, p. 164) wrote, "The highest value seen for U.S. 

soils is 5 ppm. If plants grown on such soils served as an entire human 

diet and had a concentration factor of 10, then this 'worst case imaginable' would provide a daily dietary intake of 80 mg or [about] 1 mg/kg." 

There has been much concern about the use of thallium poisons to 

control predatory animals resulting in the poisoning of other animals 

and birds. Shaw (1933) found that the minimal lethal dose of thallium 

on coated grain was 15 mg/kg body weight for mallard ducks and wild 

white geese, and for starved quail, 12 mg/kg. Tissues of these birds still 

retained 33 to 71 percent of the original dosage after 13 days. He 

concluded that secondary thallium poisoning in humans from eating a 

game bird was improbable. Carson and Smith (1977, p. 218), however, 

in commenting on Shaw's data, stated, "Continual eating of such birds 

might have been slightly more hazardous.... A man eating from 0.25 

to 0.5 Ib of such fowl per day would ingest about 2 to 4 mg thallium 

daily. This value is certainly much lower than the recommended single 

therapeutic epilant dose for an adult human of 300 mg but about 1,000 

times more than the estimated normal dietary intake of thallium."

TIN

[Considered nonessential for plants and most animals, but recently found essential for rats]

Plants

Under natural conditions Measurable amounts of tin are only 

rarely found in native plant species and, when found, are usually in 

concentrations of 20-30 ppm in ash (Connor and Shacklette, 1975). 

Harbaugh (1950) reported 17 ppm tin in ash of oak twigs, and Millman 

(1957) found 0.36 ppm (dry weight basis) in twigs of birch. Wallihan 

(1966, p. 476) stated, "Unlike lead, tin is generally a biologically 

innocuous element, as shown by its use for storing and conducting 

distilled water and in tin-coated food containers. Plants absorb it only 

to a very slight extent. . . ." We have no reports of tin toxicity to plants 

under natural conditions that are substantiated by data, although 

Brooks (1972, p. 225) stated, "Tbxicity to plants, severe."

Under man-induced conditions Prince (1957a, 1957b) reported 2.94 

ppm (dry weight) tin in corn grains, Duke (1970) reported 0.10 ppm tin 

in dry material of avocado, and tin was reported in ash of one sample 

each of carrot root (20 ppm), corn grains (30 ppm), and beet root (20 

ppm) (Connor and Shacklette, 1975). We have no other reports of tin in 

food plants. Forty ppm Sn2+ (stannous ion) solution in sand cultures
52 ELEMENT CONCENTRATIONS TOXIC TO PLANTS, ANIMALS, AND MAN

has been reported as not affecting the growth of sugar beets (Schroeder, 

Balassa, and Tipton, 1964). Wallihan (1966, p. 476) wrote, "There 

appears to be no substantial evidence that tin is essential or beneficial 

to plants in any way, and it has not been shown to be detrimental under 

field conditions." 

Animals

Under natural dietary conditions We have no reports of animal 

toxicity attributed to naturally occurring tin in the environment.

Under man-induced dietary conditions Schroeder, Balassa, and 

Tipton (1964) reported from the literature that relatively large doses of 

tin in the diet of laboratory animals are needed to produce toxicity. For 

cats and rats, 30-50 mg/kg body weight, and for dogs, 850-1,000 

mg/kg, were toxic. They noted that a diet of 1 g every 6-10 days caused 

death in rabbits after 1 to 2 months. Further, 1,000 ppm tin in a tank of 

goldfish was fatal after 1.5 hours; at a concentration of 626 ppm, after 

4.5 hours. 

Man

Bowen (1966) reported 2,000 mg tin as toxic in a dry weight diet of 

750 g/day (2,700 ppm), duration not given. Schroeder, Balassa, and 

Tipton (1964) reported from the literature that severe gastrointestinal 

symptoms in man have resulted from consumption of fruit punch (pH 

3) that contained 2 g/L tin. Tin-plated containers for canned foods can 

be a source of large amounts of tin, particularly for foods that are 

acidic. However, the double-lacquered metal cans currently in use 

greatly reduce the tin in canned foods.

URANIUM1

[Considered nonessential for organisms] 

Plants

Under natural conditions Carnotite and minerals of the uranitepitchblende series are the two kinds of uranium minerals likely to 

occur most abundantly in significant outcrops or near-surface deposits. 

Minerals of the pitchblende series seem to have no physiological effects 

on native plant species. Extensive examination by one author 

(Shacklette) of natural outcrops of this material and of tailings resulting from milling at Great Bear Lake, N.W.T., Canada, revealed no 

apparent effect on plant occupancy of these sites, or of decreased vigor 

of growth other than that which could be attributed to deficiencies of 

the major nutritive elements in the substrate. Tailings settling basins 

were rapidly colonized by species having highly efficient seed dispersal 

(especially, plants of the Compositae Family); the progress of plant 

succession on these tailings, however, was not determined by succes1This discussion examines only the chemical toxicity of uranium, not the effects of 

associated radiation, on organisms.
URANIUM 53

sive visits to the site. The prospecting methods for sedimentary 

uranium deposits in Western United States was studied extensively by 

Cannon (1957, 1959, 1960a, 1960b, and 1964) and by Cannon and 

Kleinhampl (1956), on the basis of both the analysis of plant tissue for 

uranium concentration and the presence of indicator plants that accumulate selenium (an element commonly associated with uraniferous deposits in western United States). Cannon (1959, p. 235) stated, 

"Trees rooted in ore commonly contain one to two parts per million in 

the ash compared to an average of 0.5 ppm in trees rooted in barren 

ground." The natural concentration of uranium minerals (principally 

carnotite) at these sites was not reported to have toxic effects on the 

native vegetation that was present. Connor and Shacklette (1975) 

reported uranium concentrations in 48 samples of soil from Wyoming 

and Montana to range from 1.7 to 7.0 ppm.

Under man-induced conditions Brooks (1972) stated that the toxicity to plants was moderate; however, the evidence for this statement 

was not presented. Cultivated soils from 11 areas of commercial production of fruits and vegetables in the United States, although containing as much as 4 ppm uranium, caused no obvious damage to the 

produce growing thereon (Shacklette, unpub. data, 1978). Doubtless 

some uranium compounds of industrial origin are chemically toxic to 

plants under experimental conditions, but we have no evidence that 

uraniferous ores or mine tailings are chemically toxic. 

Animals

Under natural dietary conditions We have no reports of uranium 

toxicity caused by animals grazing on plant material from natural 

uraniferous locations, and we believe that toxicity from this kind of 

diet is unlikely. The uranium levels in vegetation are low (Brooks, 

1972, gave the concentration in plant ash as 0.6 ppm); the areas of 

uraniferous deposits are usually small; and animals generally are not 

confined to grazing on these areas.

Under man-induced conditions Wills (1949, p. 237) quoted from the 

literature that"... uranium is the most poisonous of all metals when 

injected intravenously or subcutaneously."He stated further, "When 

uranium compounds are given by mouth, the water-soluble salts are 

the most toxic forms of the metal, but such water-insoluble compounds 

as uranium oxide and sodium uranate are appreciably toxic because 

they are fairly soluble in dilute hydrochloric acid. When uranium 

compounds are applied to other surfaces of the body, the water-soluble 

salts appear to be the most toxic. The salts containing anions of strong 

acids tend to be corrosive." The primary effect of injection of uranyl 

salts is kidney failure; this starts a train of secondary effects leading to 

deterioration of other organs and blood, terminating in muscular 

apathy, progressive emaciation, excretory disfunction, coma, and de-
54 ELEMENT CONCENTRATIONS TOXIC TO PLANTS, ANIMALS, AND MAN

ath. These salts can also produce similar symptoms if inhaled as a dust 

concentration of 1.0 mg/m3 of air (Wills, 1949). Uranium compounds in 

the air may be ingested by the animal swallowing mucus from the 

bronchial passages, licking its body, or eating feed contaminated with 

the compounds. Maynard and Hodge (1949) conducted extensive experimental studies of laboratory animals that were fed uranium compounds and provided the following classification (p. 310):

Non toxic (little effect was observed when the diet contained 20

percent) UO2 , U3O8 , UF4 . 

Tbxic (growth diminished when the diet contained 1 percent or

less) UO3 , UO2Ac2 , UO4 , UC14 , UO2F2 , UO2 (NO3)2 - 6H2O. 

They reported further that feeding the toxic compounds at levels of 20 

percent of the diet frequently killed all the animals in a few days, and 

that for the more toxic compounds 2 percent killed most of the animals 

within a week. In general, non lethal doses of these compounds caused 

reduction in growth. The naturally occurring uranium compounds 

included in the above experiments can be summarized as follows: 

Non toxic The oxidation series from UO2 (uraninite) to U3O8 ,

sometimes referred to as pitchblende. The other compounds

listed do not occur as natural minerals. 

Tbxic ^ The UO3 radical occurs in the minerals becquerelite,

masuyite, schoepite, and ianthinite. The other compounds listed

do not occur in nature.

We have no reports of studies of ingested dosages of carnotite, K2 (UO2)2 

(VO4)2 1 -3 H2O, a common uranium ore, but the oxidation state of the 

uranium suggests that it may be non-toxic. Although the experiments 

reported above identified some of the uranium compounds as relatively 

non-toxic to rats, rabbits, and dogs, ingestion of these compounds by 

other species of animals (particularly, the ruminants) having high 

concentrations of hydrochloric acid in their gastric secretions (pH as 

low as 2) may present a toxicity hazard. These compounds could possibly be ingested with the soil on vegetation, or as water-suspended 

particles by animals grazing over uraniferous deposits or spoil, although we have no references to this condition having actually occurred. 

Man

With the reference material we have at hand, it is best only to 

suggest toxic effects on man of naturally occurring uranium minerals 

as extrapolated from research data on animals. In this respect, the 

comments by Hodge (1949, p. 7-8) seem appropriate, "The not too 

satisfactory, but widely accepted, basis for expressing the toxicity is the 

collection of as much information about as many species as seems 

practical. Man would be expected to form a part of the series if all 

species were arranged from the most susceptible to the most resistant.
VANADIUM . 55

There are no rules of order about the susceptibility of a given species. 

. . . Nevertheless, these generalities can be offered:

1. Somewhere in the line-up of susceptibility, man must stand.

2. It has generally been the case that a given compound is highly 

toxic to many species, moderately toxic to many species or 

relatively non-toxic to many species.

Thus, by obtaining the relative toxicity of one of the uranium conv 

pounds in several species, the order of magnitude of the toxicity in man 

may be postulated. ... In general, no better procedure has been 

suggested than obtaining the limits of toxic effect as related to dosage 

on a number of species and judging that the effects on man would be 

produced by doses of the same order of magnitude."

VANADIUM

[Considered nonessential for higher plants and most higher animals, although reported to be beneficial for some; 

essential trace element for some algae and other microorganisms, and for chicks and rats]

Plants

Under natural conditions Pratt (1966b) stated that he had found no 

reports indicating either deficiency or toxicity of vanadium to plants 

under field conditions. Some food plants may accumulate high levels of 

vanadium without exhibiting toxicity symptoms, as is shown by the 

following data (maximum parts per million found in ash): snap bean, 

700; cabbage, 50; tomato fruits, 30; and asparagus, 20 (Connor and 

Shacklette, 1975).

Under man-induced conditions Literature reports indicate that 

vanadium is toxic to germinating seeds, but even more toxic at later 

stages of growth. Chiu (1953) reported that 500 ppm of vanadium oxide 

in culture solutions produced toxicity in rice seedlings and that 1,000 

ppm killed all the seedlings. Cannon (1963) conducted plot experiments in a desert environment by adding sodium vanadate to the soil. 

After a few weeks' time, 840 ppm of vanadium was found in the 

soil-water solution, and no planted species was able to grow in the plots 

during the first season. By the second year after a winter of leaching, 

four species were grown and harvested from the plots which contained 

140 560 ppm vanadium in the soil solution. The toxicity symptoms 

exhibited by these plants were extreme dwarfing and chlorosis. Pratt 

(1966b) suggested that vanadium toxicity may be indicated by two or 

more ppm vanadium (dry weight basis) in the tops of pea or soybean 

plants. He concluded that concentrations of 0.5 ppm or greater in 

nutrient solutions are toxic to plants, and that additions of the element 

to soils have produced toxicity for a variety of crop plants. As soluble 

vanadium, the following solution concentrations were reported as 

slightly toxic by Schroeder, Balassa, and Tipton (1963): 10-20 ppm for
56 ELEMENT CONCENTRATIONS TOXIC TO PLANTS, ANIMALS, AND MAN

soybeans, 26 ppm for beets, 40 ppm for barley, 20 ppm for wheat, and 22

ppm for oats.

Animals

Under normal dietary conditions We have no reports of toxicity 

attributed to vanadium in feedstuffs.

Under man-induced dietary conditions Vanadium is a relatively non 

toxic metal to animals. Schroeder, Balassa, and Tipton (1963) reported 

that 160 ppm in the diet of rats over an unspecified period of time was 

lethal owing to gastrointestinal irritation. Similar values were given 

by Bowen (1966), who listed 0.5 mg V(V) (vanadate) as toxic to rats in 

10-g/day dry-weight diet (50 ppm) and 1.5 mg (150 ppm) as lethal, 

duration not given. The LD50 for mice given vanadium trioxide orally is 

reported from the literature as 130 mg/kg (National Research Council, 

1974b), and for vanadium pentoxide and trichloride, as 23 mg/kg. 

Underwood (1971) gave the following concentrations and manifestations: >20 25 ppm vanadium in the diet resulted in growth depression in chicks; and 25 ppm was toxic to rats, whereas 50 ppm caused 

diarrhea and mortality. He listed the following relative toxicities for 

five elements to rats when fed 25-ppm diets: arsenic < molybdenum < 

tellurium < vanadium < selenium. 

Man

Vanadium is not a particularly toxic metal to man. Not only is 

vanadium poorly absorbed by the gastrointestinal tract, but it results 

in minimal irritation to the lungs when inhaled. Curran and Burch 

(1967, p. 98) stated, "A specific toxicity from naturally occurring vanadium salts or those contacted in industry would seem to be minimal." 

There are in the literature, however, reports of workers who were 

exposed to vanadium oxide dust or aerosols for several days developing 

vanadium toxicosis (National Research Council, 1974b). Vanadium 

irritates the mucousal membranes and, therefore, symptoms of vanadium poisoning include eye, nose, and throat irritations; cough; 

wheezing; productive sputum; and "green tongue." Schroeder, Balassa, 

and Tipton (1963) fed patients 4.5 mg/day as the oxytartarovanadate 

for 16 months with no apparent toxicity. Underwood (1971) reported 

that experiments with ammonium vanadyl tartrate given orally to six 

subjects for 6-10 weeks produced no toxic effects other than some 

cramps and diarrhea at the larger dose levels.

ZINC

[Essential for plants and animals]

Plants

Under natural conditions Zinc concentrations of 0.43 10.16 percent in New York peat soils were reported by Staker and Cummings
ZINC 57

(1941) to be severely toxic to vegetable crops such as spinach, lettuce, 

and carrots. The effects of the several metals that commonly are 

associated with zinc in areas of natural enrichment cannot be distinguished with certainty by visual inspection; therefore, visible toxicity 

effects are often attributed to the zinc. A translation of a statement by 

Ernst (1974, p. 3) follows: "In nature soils rich in heavy metals are 

found over ore bodies that crop out at the surface or extend in the 

near-surface zone to within 30 m of the surface. . .. Because of the 

diversity of bedrock types, the distribution of the quality and quantity 

of heavy metals in the naturally metal-rich soil is quite variable. . . . 

At a concentration of at least 0.1 percent, all heavy metals have a 

strongly selective effect on vegetation. As a rule, zinc-rich soils (0.1 -10 

percent zinc) are distinguished also by having a high content of lead 

(0.1-3.2 percent), but not of cadmium." The following concentrations 

(ppm, dry weight) of zinc in leaf tissue are considered excessive: >300, 

Navel and Valencia oranges (Embleton and others, 1976); >300, avocado (Jones and Embleton, 1976); and 200, soybean (Ohki, 1977). 

Many reports in the literature of zinc toxicity to vegetation in natural 

environments are based on circumstantial evidence, in that the exact 

cause of the symptoms was not determined.

Under man-induced conditions Contamination of vegetation with 

zinc, as well as with other heavy metals, is common in the vicinity of 

metal-working industries. For example, Ernst (1974) reported the concentrations in soil (mg/kg, dry soil) with distance from the sources as 

follows: zinc smelter, at 250 m, 4,500; at 400 m, 1,300; and at 4,000 m, 

210; brass foundry, at 250 m, 4,520; at 400 m, 350; at 4,000 m, 173, and 

at 10,000 m, 91. These zinc values contrast with the geometric mean 

zinc concentration in U.S. soils of 44 ppm (Shacklette and others, 1971). 

Fields and orchards fertilized over a long period of time have been 

reported to have accumulated toxic levels of zinc when the soil has been 

acid. Keisling and others (1977) reported (from studies of peanuts in 

acid fields) tentative toxicity critical values of 12 mg/kg zinc for soil 

(acid extractable) and 220 mg/kg for plant tissue. Thorne, Laws, and 

Wallace (1942) found that total zinc differentiated zinc-deficient soils 

from those not deficient in zinc as well as did Hibbard's extraction 

procedure, but researchers prefer to judge deficiencies and toxicities on 

the basis of soluble zinc in soils. The zinc content of plant leaves as 

indicative of nutritional sufficiency and toxic excesses was summarized by Chapman (1966) as follows: deficiency levels are characterized by less than 20-25 ppm in dry matter; ample but not excessive 

levels are 25-150 ppm; and amounts greater than 400 ppm may 

indicate zinc excess. However, there is a wide range in content of zinc 

among plant species; likewise, tolerance to high levels of soil zinc 

ranges widely. For example, Robinson, Lakin, and Reichen (1947)
58 ELEMENT CONCENTRATIONS TOXIC TO PLANTS, ANIMALS, AND MAN

reported that a good indication of zinc-mineral outcrops is the presence 

of luxuriantly growing ragweed when other vegetation is stunted. At 

the location which they studied, total zinc in the soil was 12.5 percent. 

Animals

Under normal dietary conditions We have no reports of zinc toxicity to animals resulting from the consumption of ordinary feedstuffs. 

Underwood (1971, p. 242-243) stated, "Zinc is relatively nontoxic to 

birds and mammals and a wide margin of safety exists between normal 

intakes and those likely to produce deleterious effects. Rats, pigs, 

poultry, sheep, and cattle exhibit considerable tolerance to high intakes of zinc, the extent of the tolerance depending upon the composition of the basal diet, particularly its content of minerals known to 

affect zinc absorption and utilization, such as copper, iron, and cadmium."

Under man-induced dietary conditions Zinc compounds are relatively non toxic to organisms, particularly to mammals. Schroeder and 

others (1967) reported that a diet for laboratory animals containing 

0.25 percent (2,500 ppm) zinc salts is apparently non toxic. The following summary was obtained from Underwood (1971): rats dietary intake of 2,500 ppm zinc, no discernible effects; 5,000 ppm, severe growth 

depression and severe anemia; and 10,000 ppm, heavy mortality; 

weanling pigs dietary intake of 1,000 ppm zinc, no ill effects; higher 

levels, growth depression; and 4,000-8,000 ppm, high mortality; 

lambs dietary levels of 1,000-1,500 ppm zinc, depressed feed consumption, reduced gains, and increased mineral consumption; 

steers dietary levels of zinc of 500 ppm or less, no detrimental effects; 

900 ppm, reduced gains and lower feed efficiency; and 1,700 ppm, in 

addition, a depraved appetite with excessive salt and mineral consumption and wood chewing. Bowen (1966) listed 50 mg Zn2+ in a 

10-g/day dry-weight diet (5,000 ppm) as toxic to rats and 150 mg (15,000 

ppm) as lethal, duration not given. A daily dose of 30 40 mg/kg 

produced severe chronic poisoning in young calves within 1 month 

(Clarke and Clarke, 1967, p. 68-69). The lethal dose for mature cattle 

is about 20 times this amount. 

Man

Unlike the aberrant syndromes for most of the essential trace elements, no primary disorder of zinc metabolism has been described for 

humans. Moderate zinc toxicity was reported by Van Keen (1966) in 

individuals who breathed zinc oxide for as much as 12 minutes at a 

calculated zinc concentration in air of 600 mg/m3 . Underwood (1971) 

noted that a wide margin of safety existed between normal zinc intakes 

and those likely to produce deleterious effects. Acute zinc poisoning is 

commonly reported, however, when acidic foods stored in galvanized 

iron containers have been ingested. Schroeder and others (1967) specu-
OTHER ELEMENTS THAT POSSIBLY PRESENT A TOXICITY HAZARD 59

lated that cadmium intoxication may also be associated with these 

cases. Thomas (1973) listed 50-500 mg/kg body weight of zinc salts 

(chloride, sulfate, acetate, and others) as probably lethal to adults. 

Bergqvist and others (1977) reported that 6 g of zinc chloride and 45 g of 

zinc sulfate taken orally are considered lethal doses; however, 1 g or 

more of most zinc salts results in vomiting and therefore expulsion of 

the intoxicant.

OTHER ELEMENTS THAT POSSIBLY 

PRESENT A TOXICITY HAZARD

The toxicity to organisms of some elements at levels that might be 

expected to occur in natural or polluted environments has been indicated by reports in the literature, but the data are too meager for 

adequately appraising the possible hazard. Brief notes on these elements follow.

BARIUM

[Considered nonessential for organisms]

We have only one report (Chaudhry and others, 1977) that gives 

toxicity levels of barium in plants. These authors stated, "Barium is 

ubiquitous in soils and all plants contain a small quantitity of it 

usually in levels of around 4 to 50 /ug/g dry weight of plants. It is a 

constituent of geothermal brines and, hence, there is a possibility that 

it may become spilled into the environment in case of accidental 

release. . . . Barium levels of about 2% in bush bean leaves and 1% in 

barley leaves decreased yields considerably. The levels were obtained 

after application of 2,000 /ug Ba per g of soil as Ba(NO3)2 with equivalent nitrate added in controls." Brooks (1972) stated that barium toxicity to plants was moderate.

We have no reports of barium toxicity to animals or man.

GERMANIUM

[Considered nonessential for organisms]

Hermann (1970, p. 32-L-l) reported, "The Ge content of plants never 

exceeds 10 ppm Ge in ash. Experimental investigation on the Ge 

content of plants (Kudelasek, 1960) gave the results that at 10 ppm the 

toxic properties of Ge cause death of plants. The following plants were 

used in the experiments: Equisetum arvense, Equisetum hiemale, Picea 

excelsa, Secale cereale." Bidwell (1974, p. 246) reported, "Germanium 

inhibits silicon metabolism and may be toxic to organisms which 

require or use silicon, such as diatoms, rice, and tobacco." Shacklette
60 ELEMENT CONCENTRATIONS TOXIC TO PLANTS, ANIMALS, AND MAN

and Connor (1973) reported 15 ppm in ash of 1 sample of Spanish moss, 

the only 1 of 123 samples having detectable concentrations of germanium. This sample probably was affected by urban and industrial 

pollution. Dry material of alpine fir needles was found to contain 5 ppm 

germanium (Gary C. Curtin, written commun., 1976). Mr. P F. M. Paul 

(written commun., 1953), in discussing the germanium research of Dr. 

Hans Brauchli, stated that Dr. Brauchli had found 5 percent germanium in ash of lettuce, the highest value in any plant material he 

had examined, but that more frequently values of 2 percent to hundredths of a percent were found. On the bases of our experience, these 

concentrations seem much too high, and we question the accuracy of 

his analyses. Brooks (1972) gave 5 ppm as the concentration of germanium in plant ash and said the toxicity to plants was slight. Some 

organic compounds of germanium are toxic to animals (Sax, 1975), but 

poisoning from naturally occurring compounds seems unlikely.

MAGNESIUM

[Major essential element for plants and animals]

True magnesium toxicity to plants is apparently unknown. Kelley 

(1948) cited an example of a soil near Napa, Calif, in which more than 

90 percent of the cation exchange capacity was saturated with magnesium and stated that this soil was almost completely unproductive. 

In this case, the inhibition of vegetation was due to deprivation of other 

elements induced by excess magnesium, not to the magnesium itself. 

Sievers (1924) reported that magnesium oxide dust from a magnesite 

processing plant in the State of Washington was deposited on the 

surface of adjacent soil in quantities great enough to be toxic to plants. 

In sand culture experiments, Carolus (1935) showed that magnesium 

toxicity in potatoes resulted when magnesium was extremely high and 

potassium was extremely low.

We have no reports of magnesium toxicity in animals. High levels of 

available soil potassium reduce magnesium uptake by plants, especially in low magnesium soils, and this condition may produce pastures 

(especially grasses) that are extremely low in magnesium (<0.2 percent, dry weight basis). Animals grazing on this grass may develop a 

nutritional disease called ,hypomagnesaemia or grass tetany 

(Mortvedt and Cunningham, 1971). Whereas the inhalation of fumes of 

freshly sublimed magnesium oxide may cause "metal fume fever" in 

man there is no evidence that magnesium itself produces true systemic 

poisoning (Sax, 1975).
OTHER ELEMENTS THAT POSSIBLY PRESENT A TOXICITY HAZARD 61

RUBIDIUM

[Considered nonessential for organisms]

Steinbach (1962) stated that rubidium appears not to be an essential 

component of living matter, but rather a toxic agent that may partly 

substitute for potassium. He reported rubidium in non-woody plants to 

range from 11.3 to 36.7 ppm (dry weight basis). Smales and Salmon 

(1955) found rubidium concentration in seven species of marine algae 

to range from 0.61 to 2.4 ppm of wet plants. Connor and Shacklette 

(1975) reported rubidium concentration in ash of hickory and oak 

stems to range from 18-40 ppm. Although Sax (1975) reported 

rubidium chromate, rubidium chromium sulfate, and rubidium dichromate as recognized carcinogens and rubidium hydroxide as highly 

caustic and toxic, the kinds and concentrations of rubidium compounds 

in plants and other natural materials most likely are not hazardous. 

We have no reports that poisoning of animals or man has occurred from 

natural occurrences of rubidium.

TELLURIUM

[Considered nonessential for organisms]

The following information was obtained mainly from the excellent 

review of the literature on tellurium toxicity by Cerwenka and Cooper 

(1961). Apparently, elemental tellurium (like so many of the metals) is 

biologically inert whereas salts of tellurium yielding telluride and 

tellurate ions are somewhat toxic. These authors reported no serious 

cases of industrial tellurium intoxication but warned against exposure 

to tellurium vapors or tellurium oxide. Ingested tellurium salts are 

reduced to elemental tellurium in the gut by bacteria. Much of the 

absorbed tellurium is converted to dimethyl tellurdie, which is volatile 

and readily lost via exhaled air. This compound has a distinctive 

garliclike odor which, along with other symptoms such as nausea, 

giddiness, and metallic taste, can indicate tellurium poisoning in humans. These authors reported that as little as 0.5 /Ltg of tellurium 

dioxide given orally produced "garlic breath" for 30 hours and 15 mg for 

237 days. Rats fed 750 ppm tellurium showed no change in growth 

rates, whereas rats fed 1,500 ppm showed some reduction in growth 

rate but no pathological or anatomical abnormalities.

TITANIUM

[Considered nonessential for organisms]

We have only one report (Wallace, Alexander, and Chaudhry, 1977) 

that gives quantitative data on titanium toxicity to plants. Titanium 

was reported to be somewhat more mobile than vanadium and to cause
62 ELEMENT CONCENTRATIONS TOXIC TO PLANTS, ANIMALS, AND MAN

considerable yield decrease in bush bean at 10~4 Af; leaf, stem, and root 

titanium concentrations, respectively, were 202, 48, and 2,420 //,g/g 

(dry weight). Symptoms were chlorosis, necrotic spots on leaves, and 

stunting. 

We have no reports of titanium toxicity to animals and man.

TUNGSTEN

[Considered nonessential for organisms]

Krauskopf (1970, p. 74-L-l) stated, "Like other heavy metals, 

tungsten in more than traces is poisonous to most organisms. An 

important biogeochemical role for the element is therefore hardly 

likely, but minor concentrations in organic processes is certainly possible and is strongly suggested by the fragmentary data on carbonaceous 

metamorphic rocks." The toxicity of tungsten to plants was said by 

Brooks (1972) to be moderate, and the concentration in plant ash, 0.5 

ppm. Dekate (1967) observed that plants growing in a mineralized zone 

contained 2-18 times the concentration of tungsten that was considered to be the background value (2.7 ppm). Hmgsten in the ash of 

trees was reported as follows: Douglas-fir stems, 50 ppm; dwarf juniper 

leaves, 50 ppm, stems, 100 ppm; and alpine fir stems, 5-50 ppm (Gary 

C. Curtin, written commun., 1976). Connor and Shacklette (1975) 

reported tungsten concentrations in ash of single samples of the following trees: sassafras leaves, 50 ppm; and sweet gum stems, 30 ppm, 

leaves, 70 ppm. They found 1,000 ppm tungsten in one of 492 samples of 

soil from western United States.

We have only one reference giving quantitative data on the effects of 

feeding tungsten to animals. Sax (1975, p. 1221) stated, "Tungsten 

compounds are considered somewhat more toxic than those of molybdenum. However, industrially, this element does not constitute an 

important health hazard. Exposure is related chiefly to the dust arising from the crushing and milling of the two chief ores of tungsten, 

namely, scheelite and wolframite. There is very little published with 

reference to its toxicity. The feeding of 2, 5, and 10 percent of diet as 

tungsten metal over a period of 70 days has been shown to be without 

marked effect upon the growth of rats, as measured in terms of gain in 

weight. . . . Recent studies have failed to indicate any serious toxic 

effect following the inhalation or ingestion of various tungsten compounds, although heavy exposure to the dust or the ingestion of large 

amounts of the soluble compounds produces a certain rate of mortality 

in experimental animals." Judged from this report, tungsten probably 

does not constitute an important environmental hazard to animals and 

man.
RARE EARTH ELEMENTS (LANTHANIDES) 63

ZIRCONIUM

[Considered nonessential for organisms]

Zirconium is a common constituent in ash of some kinds of plants 

and is found less frequently in others. A part of the reported concentrations in plant samples may be due to soil contamination, as indicated 

by the fact that soil values nearly always are greater than plant 

values. Parts of some plants that are protected from surface contamination by soil, however, have been found to contain measurable concentrations of zirconium. For example, Connor and Shacklette (1975) 

reported pea and lima bean seeds that had been removed from the pods 

to contain 20-70 ppm zirconium in ash. They also reported stems of 

trees and shrubs that contained 20-500 ppm zirconium in ash, part of 

which may have been the result of contamination by soil.

Sax (1975, p. 1257) stated, "Zirconium is not an important industrial 

poison. Deaths in rabbits have been caused by intravenous injection of 

150 mg/kg of body weight. Most zirconium compounds in common use 

are insoluble and considered inert. Pulmonary granuloma in zirconium workers has been reported and sodium zirconium lactate has 

been held responsible for skin granulomas. Avoid inhalation of Zr 

containing aerosols which can cause lung granulomas."

Zirconium selenate was listed by Sax (1975) as a recognized carcinogen, and sodium zirconium lactate, in inhalation experiments with 

rabbits, produced bronchiolar abcesses, lobar pneumonia, and peribronchial granulomas.

Because of the very low solubility of naturally occurring zirconium 

compounds and the low concentrations of zirconium in plants, this 

element seems unlikely to constitute an environmental hazard under 

most conditions.

RARE EARTH ELEMENTS (LANTHANIDES)

[Considered nonessential for organisms]

Certain of the rare earth elements have been found toxic to experimental animals if ingested, or to cause illness in humans on inhaling 

dust containing the element or its compounds. Because of their infrequent occurrence in high concentrations in natural materials, they 

are not expected to be of great environmental concern, and the greatest 

hazard probably is occupational exposure or reactions from pharmaceutical applications. However, experimental studies on the effects 

of these elements on organisms seem to be few and to have largely 

excluded plants and humans; therefore, an adequate appraisal of potential hazards cannot be made. We have no reports of chemical toxicity, either naturally occurring or experimentally produced, in plants.
64 ELEMENT CONCENTRATIONS TOXIC TO PLANTS, ANIMALS, AND MAN

Brief summaries of known toxicities of these elements, based largely 

on the reports of Sax (1975), follow. Radiation effects are omitted.

CERIUM

The insoluble salts of cerium are said to be non toxic, even in large 

doses. Doses of 0.05-0.5 g are used to prevent vomiting in pregnancy. 

The toxicity of cerium compounds may be taken to be that of elemental 

cerium, except when the anion has a toxicity of its own. Cerium 

tartrate has a direct injurious action on the hearts of small animals. 

The effects on the nervous system of humans through inhalation may 

preclude the use of welding rods or compounds that contain the rare 

earth elements. Salts of cerium increase the blood coagulation rate.

Cerium in rocks and soils commonly ranges from <150 to 300 ppm; it 

is seldom reported above 150 ppm in plant ash, but extreme values of 

300 ppm in tomatoes and 700 ppm in hickory trees were found by 

Connor and Shacklette (1975). Duke (1970) reported the following 

concentrations in dry material of food plants: breadfruit, 0.1 ppm; taro, 

0.5 ppm; and cassava, 0.05 ppm.

, LANTHANUM

This element is reported to delay blood clotting, leading to hemorrhages, and has caused liver injury in experimental animals. Inhalation and ingestion cause readily reversible symptoms which disappear 

after the end of exposure. Compounds of lanthanum cause somewhat 

more severe, but not lethal, reactions.

Concentrations in rocks and soils are frequently less than 30 ppm 

but, when determinable, generally range from about 30 to 200 ppm. 

The lanthanum content of trees and shrubs generally range from <30 

to 300 ppm in ash, except for hickory trees which have concentrations 

of as much as 2,000 ppm (Connor and Shacklette, 1975).

DYSPROSIUM, GADOLINIUM, HOLMIUM, NEODYMIUM, PRASEODYMIUM, 

SAMARIUM, TERBIUM, AND THULIUM

As lanthanides, these elements are suspected of having at least a 

moderate degree of toxicity to animals and humans, but experimental 

evidence is very limited. Some are known to depress blood coagulation, 

leading to hemorrhage, and the others are suspected of causing this 

effect. We have no reports of natural exposures or experimental treatments causing toxicity in plants.
*" REFERENCES CITED 65

These elements are seldom detected in soils and plants by routine 

analytical methods; and, when detected, concentrations are generally

* low.

'. W,

ERBIUM, EUROPIUM, AND LUTETIUM

*

, We have no reports of toxicity in plants, animals, or man attributable to these elements.

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APPENDIX

[Common plant names with corresponding scientific names]

Common names, as used in the text, are listed alphabetically. Generally, only common 

names were given in the publications consulted in preparing this report. For most of 

these names there is no doubt as to their proper corresponding scientific names; for 

others, only the genus name is given here. If several cultivars of a species are listed, 

they are so identified. The common names used are those generally applied in the 

United States.

Alfalfa, Medicago saliva L. 

Almond, Prunus amygdalus Stokes 

Alpine fir, Abies lasiocarpa Nutt. 

Anemone, Pulsatilla patens Mill. 

Apple, Pyrus malus L. 

Apricot, Prunus armeniaca L. 

Asparagus, Asparagus officinalis L. 

Aspen, Populus tremuloides Michx. 

Avocado, Per sea gratissima Gaertn. f.

Barley, Hordeum vulgare L.

Bean, Phaseolus vulgaris L.

Bedstraw, Galium sp.

Beet, Beta vulgaris L.

Birch, Betula sp.

Black gum, Nyssa sp.

Black medic, Medicago lupulina L.

Bracken, Pteridium aquilinum (L). Kuhn

Breadfruit, Artocarpus altilis (Parkinson) Fosberg

Broadbean, Vicia faba L.

Buckwheat, Fagopyrum sagittatum Gilib.

Bur oak, Quercus macrocarpa Michx.

Bush bean, Phaseolus vulgaris L.
APPENDIX 79

Cabbage, Brassica oleracea var. capitata L.

Camellia, Camellia japonica L.

Carnation, Dianthus caryophyllos L.

Carrot, Daucus carota var. saliva DC.

Cassava, Manihot esculenta Crantz

Cauliflower, Brassica oleracea var. botrytis L.

Celery, Apium graveolens var. du/ce DC.

Clover, Trifolium pratense L.

Club moss, Lycopodium obscurum var. dendroideum (Michx.) D.C. Eat.

Corn, Zea mays L.

Cotton, Gossypium sp.

Cucumber, Cucumis sativus L.

Douglas-fir, Pseudotsuga menziesii (Mirb.) Franco 

Dwarf juniper, Juniperus communis subsp. nana Syme

Eastern white pine, Pinus strobus L.

Endive, Cichorium endivia L.

Engelmann spruce, Picea engelmannii Parry

Eryngium, Eryngium sp.

Flax, Linum usitatissimum L.

Fig, Ficus carica L.

French bean, Phaseolus vulgaris L. cultivar

Grape, Vi^is vinifera L. 

Grapefruit, Citrus paradisi Sw.

Hickory, Carya sp.

Kale, Brassica oleracea var. acephala DC. 

Kidney bean, Phaseolus vulgaris L. cultivar

Labrador tea, Ledum decumbens (Ait.) Lodds

Lactic acid bacteria, Lactobacillus sp. , i

Leek, Allium porrum L.

Lemon, Citrus limonia Osbeck

Lespedeza, Lespedeza sp.

Lettuce, Lactuca sativa L.

Lima bean, Phaseolus limensis Macf.

Limber pine, Pinus flexilis James

Lodgepole pine, Pinus contorta var. latifolia Engelm.

Low juniper, Juniperus communis subsp. nana (Willd.) Syme

Lupine, Lupinus sp.

Mandarin, Citrus nobilis var. deliciosa Swingle 

Myrtle blueberry, Vaccinium myrtillus L.

Navy bean, Phaseolus vulgaris L. cultivar .

Oak, Quercus sp. 

Oats, Avena sativa L. 

Olive, Olea europea L.
80 ELEMENT CONCENTRATIONS TOXIC TO PLANTS, ANIMALS, AND MAN

Onion, Allium cepa L. 

Orange, Citrus sinensis Osbeck

Pea, Pisum sativum L.

Peach, Prunus persica L.

Peanut, Arachis hypogaea L.

Pear, Pyrus communis L.

Pecan, Carya illinoensis Koch

Pepper, Capsicum frutescens var. grossum Bailey

Perennial ryegrass, Lolium perenne L.

Persimmon, Diospyros virginiana L.

Phyllodoce, Phyllodoce empetriformis (Smith) D. Don

Plum, Prunus sp.

Ponderosa pine, Pinus ponderosa Laws.

Potato, Solarium tuberosum L.

Prince's plume, Stanleya pinnata (Pursh) Britt.

Prune, Prunus sp.

Radish, Raphanus sativus L. 

Ragweed, Ambrosia artemisiifolia L. 

Red cedar, Juniperus virginiana L. 

Redtop, Agrostis alba L. 

Rice, Oryza sativa L. 

Rose, Rosa sp.

Rutabaga, Brassica napobrassica Mill. 

Rye, Secale cereale L.

Sassafras, Sassafras albidum (Nutt.) Nees 

Sheep fescue, Festuca ouina L. 

Snap bean, Phaseolus vulgaris L. cultivar 

Sorghum, Sorghum vulgare Pers. 

Soybean, Glycine max Merr. 

Spanish moss, Tlllandsia usneoides L. 

Spinach, Spinacia oleracea L. 

Subalpine fir, Afeies lasiocarpa Nutt. 

Sudan grass, Sorghum halepense (L.) Pers. 

Sugar beet, Beta vulgaris L. cultivar 

Sweetclover, Melilotus sp. 

Sweet gum, Liquidambar styraciflua L. 

Sweetleaf, Symplocos tinctoria (L.) UHer. 

Sweet potato, Ipomea batatas L.

Taro, Colocasia esculenta Schott.

Tea, TViea sinensis L.

Timothy, Phleum pratense L.

Tbbacco, Nicotiana tabacum L.

Tomato, Lycopersicum esculentum Mill.

Toadflax, Linaria triphylla Jacq.

Turnip, Brassica napus L.

Walnut, Juglans regia L.

Wheat, Triticum aestivum L.

White birch, Betula papyrifera Marsh.

Yeast, Saccharomyces sp.

»U.S. GOVERNMENT PRINTING OFFICE: 1979-677-026/57