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CONTENTS
Letter of transmittal
Membership of the Advisory Conrnittee
Report
Introduction
Charge
Background
Sections
1. Chemistry and Arsenic Cycle - D.V, Frost
2. Arsenic Trioxide and Lead Arsenate in Soil - P.J. Zinke
3. Turf Management Aspects - A.E. Hiltbold
^. Effects on Fish and Wildlife - E.H. Dustman
5. Toxicology - D.J. Birmingham
Discussion
Recommendations
Appendices 1 and 2
Persons Conferring with Committee
Persons Responding to Letters from Committee
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Consultant - Nutrition Biochemistry
48 HIGH STREET
BRATTLEBORO, VERMONT O63O1 " * *•*' J
Mr. William D. Ruckelshaus
Administrator '
Environmental Protection Agency
Washington, D.C. 20^60
Dear Mr. Ruckelshaust
As chairman of the PAX Company Arsenic Advisory Committee, I am
privileged to submit our report. We trust this will help you to assess
the safety in use of the PAX product and o.f related arsenicals. Although,
as one might expect, there is not unanimity as regards attitudes towards
the safety of PAX, the Committee seems unanimous in urging further research.
Your Committee was impressed with the aid accorded us by Clayton
Bushong and Charles Lewis. The arsenical literature is vast. We could
not cover it in the time allotted, but great efforts were made to enable
us to do so.
In about 4-0 years study of the arsenical prob]«m, I have become
convinced that overreactions to arsenophobia, plus the inability to relate
the basic importance of A_£ to life,has led to many unscientific regulations.
It has negated the safe uses of arsenicals in medicine. Anti-arsenic
regulations vary greatly between countries. But all reflect the basic
mistrust of this versatile and useful element. As noted elsewhere, we tend
to misjudge the toxic trace elements. One can only hope that, to correct
such misjudgments, your agency will recognize the futility of laws and
regulations which run counter to biology itself. If this is accomplished,
and followed by purposeful research to clarify the beneficial roles of
trace elements, agriculture, medicine and the environment will surely
benefit. Further repression of safe uses of the toxic trace elements will
be tolerated for a time, but is inconsistant with Nature and must lead to
eventual failure. The pattern seems clear in the confusion shown by
governments regarding the safe uses of selenium and mercury in agriculture.
Ihese are semantic problems, best understood in light of Korzibsky's
Science and Sanity, and Wendell Johnson's People in Quandaries. Both point
out that the only way man can solve controversial problems is to depend
on objective interpretation via the scientific method, i.e. repeatable
experiments. Sufficient has been done with PAX to warrant that, except
for avoidable accidents, the product can be used safely. The crux of the
problem appears in the letter to the Committee by Drs. Kearney and Woolson.
Respectfully
Douglas V. Frost, Chairman
PAX Company Arsenic Advisory Committee
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MEMBERS CF THE PAX COMPANY ARSENIC ADVISORY COMMITTEE
Douglas V. Frost, Ph.D. Chairman Consultant, Nutrition Biochemistry
1? Rosa Road
Schenectady, N.Y. 12308
Donald J. Birmingham, M.D.
Eugene H Dustman, Ph.D.
Professor, Department of Dermatology,
Wayne State University School of Medicine
1^00 Chrysler Freeway,
Detroit, Mich 4820?
Patuxent Wildlife Research Center
U.S. Department of.the Interior
Laurel, Maryland 20810
(Retired)
Arthur E. Hiltbold, Jr. Ph.D. Professor, Department of Agronomy and Soils'
Auburn Universicy
Auburn, Alabama 36830
Paul J.Zinke, Ph.D.
Associate Professor, Forestry and Soil Science
School of Forestry and Conservation
University of California.
Berkeley, California 9^720
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REPORT OF THE PAX COMPANY ARSENIC ADVISORY COMMITTEE
The Committee is charged to investigate and to weigh risks versus
benefits of the PAX Company Three-Year Crabgrass Control product con-
taining 23.11 % arsenic trioxide, 8.25 1° lead arsenate and b % nitrogen
as ammonium sulfate. Under Interpretation 25 of the Federal Insecticide,
Fungicide, and Rodenticide Act, products for use in and about the home
shall contain no more than 1.5 $ arsenic trioxide or 2 $ sodium arsenite.
On the basis of evidence presented by Done and Peart (1), the United States
District Court for the District of Utah (Central Division), held that
PAX Three-Year Crabgrass Control had not been Aown hazardous to humans
and that Interpretation 25 was inappropriate. Despite the reassuring
evidence by Done and Peart that the PAX Company Crabgrass Control product
did not present a hazard to humans, reports appeared by William B. Buck (2),
veterinary toxicologist at Iowa State University, clearly establishing
that grass clippings from PAX-treated lawns might be lethal to animals.
Misunderstandings stemmed from 1) the efficacy of P^X depends on action
at the soil surface to inhibit germination of crabgrass and growth of
the annual blue grass, Poa annua. It is not absorbed to any extent by
grass, but may be picked up, particularly by rotary mowers, along with
grass clippings. 2) as now stated on the PAX labeling, (but not always
so stated in the past), PAX-treated grass clippings should not be fed
to animals.
Whereas PAX is used in Utah and other western states for turf
improvement on golf courses, somewhat similarily to calcium arsenate and
lead arsenate, the primary sale is for use on home lawns. Variations of
PAX, all based on combinations of arsenic trioxide and lead arsenate,
have been marketed for about 20 years for home use. This use is covered
under a U.S. Patent (3)» Beginning in 1970, variouc states enacted
laws requiring the licensing of qualified applicators for the use of
toxic pesticides. Because arsenicals are widely known for their toxicity,
their use on home lawns was banned in effect in many states by such
licensing requirements.
The i?ederal Environmental Pesticide Control Act of 1972 (Public
Law °2-5l6) -iay in time require that each state establish regulations for
certi''-.it\i application of hazardous pesticides. Under this law, each state
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would regulate the sale and use of pesticides within state boundaries.
Such action would eliminate the right of individuals to use many materials
used safely, with few exceptions, for decades.
The safe uses of arsenicals have challenged science and man's ingen-
uity throughout recorded history. Although virtually taboo now for use
in medicine, inorganic arsenicals were among the first medications and
certain organic arsenicals were medicine's first "magic bullets" (cure
for veneral disease). Inorganic arsenicals were man's first economic
poisons and first pesticides. The uses of inorganic and organic arsenic
in agriculture are too varied and complex to discuss here (^,5|6). ,
Suffice it to say that science still has much to learn of the benefits
to be derived from this amazing but controversial element. Clearly,
inorganic arsenicals, such as PAX, exert beneficial effects on turf.
The advantages of such effects can, however, only be realized by consid-
eration of the fact that misuses of the product can represent definite
hazards to animals. Such hazards are avoidable if the product of PAX-
treated grass clipping is not fed.
The ability to employ compounds of toxic traf? elements such as
arsenic to man's advantage is one of the great challenges of our times.
Available sources of phosphate, the limiting ingredient of fertilizers, are
being rapidly depleted. How arsenicals influence phosphorylations in
plants and animals is a major scientific question. Evidence seems clear
that the benefits from arsenical use in obtaining good turf depend in
part on the avoidance of added phosphate. Whether and to what extent
arsenic may substitute for phosphate in plants, particularly in turf
grasses,deserves consideration as an economic measure in phosphate conser-
vation. The extended (three year) turf improvement effects claimed for
PAX, verified by unsolicited testimonials (Appendix 1), also warrant
economic consideration in the assessment of risks vs. benefits. The
value of arsenicals to stimulate nitrogen fixation, thus sparing nitrogen
fertilization of turf is a further economic consideration (40,^-Oa).
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SECTION I
CHEMISTRY AND ARSENIC CYCLE
Section 1. Chemistry and Arsenic Cycle - D.V. Frost
Milestones in the chemistry of arsenic have been prominent in the
history of both chemistry and biology. Greater emphasis has been placed
on adverse effects and suppositions of such adverse effects than on the
good faces oF arsenic. To place the situation in perspective, it seems
appropriate to outline many of the milestones in A_s history. Clearly,
~~~ i
there has been and still remains much subjectivity in how man veiws
matters relating to "arsenic",
Milestones
2000 BC Arsenicum, arsenik (As 0_). The sublimate from copper and iron ores.
used by professional poisoners. Laws finally passed against
such uses.
BC Hippocrates used arsenic sulfide salves to treat ulcers.
1250 AD Elemental Ajs prepared by Albertus Magnus.
Middle
Ages
1775
Scheele volatized arsine, AsH~; a way to separate As from most other
elements.
1786 Bowler's solution, 1 % As?0_, as potassium arsenite. Still said in
1912 to be the best medicinal in the pharmacopoeia.
1820 Arsenic cancer myth begins in writings or J.A. Paris
1836 Marsh test for As, via Scheele 's arsine.
1839 Gmelin wrote of volatile arsines produced by molds.
1842 Cacodyl, (CH«)pAs-As(CH_)_, first organic arsenical. Coincided with
Vohler's synthesis of urea.
1868 First pesticide-copper acetoarsenite-controlled Colorado potato
beetle. Shades of the Irish potato famine, 20 years before.
1887 Hutchinson's idea: Fowler's solution — > hyperkeratosis — ^skin cancer.
The idea grew by reiteration into medical tradition. Industrial
exposure to As?0- fails to cause cancer ^
1900-3 Royal Commission on Arsenical Poisoning established world's first
tolerance, unofficial, and without scientific basis, but ending up
with force in courts of law.
1910 Chemotherapy began with Ehrlich's magic bullet, arsphenamine .
1938 Moxon found arsenicals can counteract selenium toxicity.
19^2-3 Kennaway-Hueper polemic in Lancet re Hueper's allegations against As
based on J.A. Paris' writings"^l820-2.
19^-6 Organic arsenical feed additives control diseases in poultry and
: swine, stimulate growth and improve feed efficiency.
1956 Arsenic acid emerges as a desiccant for cotton? cacodylates and
mothanearsonates as desiccants, defoliants, herbicides.
1958 Arsenical feed additives impugned under Delaney clause.
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1959 France bans organic arsenicals, antimonials, and estrogens from use
in poultry feeds. EEC countries follow suit. England legalizes an
Arsenic in Foods Regulation, its first official tolerance.
1962 France bars impo"-4". of poultry from countries where arsenicals are
permitted; exempts poultry livers used in French pate.
1963-7 Food and Drug Administration clears four organic arsenical feed addi-
tives of carcinogen stigma. Arsenic acid permitted as desiccant for
cotton .
I
1968 AAAS-DOD polemic on defoliants and herbicides in Viet Nam.
1969 Safety of PAX upheld in Utah District Court. Fallen water incident.
Accidental poisoning of horses fed PAX-treated grass clippings in
Iowa. Dr. Buck confirmed possibility at Iowa State. t
1970 Mew York classed arsenicals as residual pesticides requiring licensed
use. Cacodylic acid use in Viet ^am stopped by executive order.
1971 Licensed uses of tricalcium and lead arsenates on golf courses
achieved acceptance in most states.
1992-3 Retrospective study of orchardists exposed to lead arsenatie in 1930s
and '49s revealed no adverse health effects, possibly improved health.
Arsenic trioxide
The form in which arsenic first became available was as the sublimate
(or distillate) from metallic ores. "White arsenic" or simply arsenic
as it was known for centuries, is the oxide of the element. It is only
sparingly soluble in water and is non-ionic. In granular form, it is
only aboxit one tenth as toxic as when dissolved in alkali to form a
water-soluble salt, such as sodium arsenite. Failure to understand the
chemistry and biochemistry of As_0_ appears in the definition of Fowler's
solution as a 1 4-. solution of arsenic trioxide. Vfaen arsenic trioxide
is dissolved in water, it forms arsenious acid. When the solution is
evaporated, all water is lost, forming again the anhydide As?0_. It
becomes available biologically only if dissolved to yield arsenous acid.
The rate at which As?0_ dissolves in the tract of animals varies with
particle size and between species. This is developed in the report by
Done and Peart (1). Interpretation 25 assigned greater toxicity to
arsenic trioxide than it did to sodium arsenite. This is in retrospect
an obvious error. But the tendency to view arsenic trioxide as compar-
able to soHium arsenite is so firmly grained in the literature that
only conscious effort and reeducation can set the record straight.
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Many inorganic arsenicals in soils are far less soluble than arsenic
trioxide. ^So0o is probably not a common constituent of soil, being
converted to even less soluble forms by chemical reaction. Evidence
suggests that arsenic may enter into active global cycling and that
As?0_ in dust may be an important part of this cycle, Ferguson and
Gavis (7), in an excellent review of the arsenic cycle in natural waters,
stated that "There is no evidence that man is likely to change world-
wide distribution of arsenic appreciably.,,We must conclude that present
knowledge of the pathways of the arsenic cycle is inadequate to allow
good management...". That concentrations of arsenic represent a public
health hazard appears valid only for the ...nique situation in which
very large amounts of As,,C_ are permitted to escape from smelters.
Harkins and Swain (8,9).detailed one such occurrence early in the century;
Birmingham (10) and others (lOa) more recently. The fact that water
supplies can become contaminated with toxic levels of arsenic, again
around smelters, was described by Borgono and Greiber (11).
Occurrence of high levels of arsenic in natural waters was reported
by Grimmett et el.(12). This study of the possiole relation of arsenic
in soils and waters in a geothermal area of New Zealand deserves special
consideration and calls for more research. The study showed that remark-
ably high levels of bound form's of arsenic, such as arsenic sulfide in
muds, were non-toxic to cattle. On the other hand, the experimental
feeding of sodium arsenite to a heifer at a relatively low level of
arsenic proved to be lethal. Working in the same area, Lancaster et al.(13)
reported that 288 ppm of arsenic in lake weed proved entirely non-toxic
when fed at 20 # of the daily ration for sheep. The biochemical data
suggests that the arsenic in the lake weed was in bound form and was
less toxic than more available forms of arsenic might have been. As is
true for many other species, there is little agreement on the toxicity
comparisons for arsenite in sheep. For instance, Clarke and Clarke (HO
reported that as little as 2.6 mg A_s as sodium arsenite per kg of body
weight proved lethal to sheep On the other hand, Bucy et al. (15)
reported no toxic effects for 56 days to lambs fed 9.1 mg A£ Per kg per
day as potassium arsenite. If nothing else, such comparisons serve to
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show how variable the toxicity of even the most toxic forms of arsenic
may prove to be among investigators. The Lancaster study raises further
questions about those combined forms of arsenic which occur in the
arsenic cycle.
The key role of microorganisms to release undue concentrations of
arsenic from soils is part of the arsenic cycle depicted by Frost (6).
In view of advancing knowledge, the As cycle can how be shown as follows:
ARSENIC ECODIAGRAM - D.V. Frost
ARSENIC '
IN DUST
ARSENIC
IN DUST
ATTACHMENT
O- As TO DUST
AIRBORNE ARSENIC
RAIN
FCSSIL FUEL
BURNING
\
SMELTING
V
\ \
PYRITES
VOLGA NOS-
METHYLARSINES
t
MICROBIAL ACTIOM
t
ORGANIC MATTER -<.
I\' SOILS
FERTILIZER
PHOSPHATE ROCK
OCEANS, STREAMS, LAKES
\
UPTAKE BY PLANTS, ANIMALS
- EXCRETION
DECOMPOSITION
FOSSIL riJttMATIONS
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Because the arsenate is readily precipitated by metal hydroxides, only
about 0.003-0.02 ppm of A_s is found in most natural waters. Nevertheless,
aquatic plants transmit A£ at relatively high levels to fish and sea foods
as part of the food chain. Land animals contain lower levels of A_s on
average, again as part of the food chain.
Goldschmidt (16) in his classical review of the geochemistry of
arsenic noted that forest humus contains up to 300 ppm of arsenic. He
hypothesized that over eons of time, this led to the high concentrations
of AJS in fossil fuels. Coal, metal ores, and phosphorites all contain
appreciable .levels of As, strongly suggesting that As_ is associated with
biology and with elements essential to life. The burning of fossil fuels
releases large amounts of A_s to the atmosphere. Whether this is more or
less than the amounts released by biological mechanisms is not known.
Although quantitative estimations are difficult, it has been estimated
il
that about 29 x 10 tons of arsenic were released via the burning of coal
from 1900 to 1971. The estimated 50,000 metric tons of arsenic produced
commercially each year calculates to be about 10 times the release of As
from the burning of coal. Sulfite ores, predominately arsenopyrite (FeAsS),
and the various non-ferrous ores from which connercial arsenic is obtained,
impart appreciable levels of As?0_ to the atmosphere through smelting.
Hnless the arsenic is artificially removed, phosphate fertilizers
impart appreciable levels of arsenic to soils. Superphosphates made with
sulfuric acid also containing A£ as impurities, may contain up to 0.14 %
A_s (25). The benefit possible from a relatively high level of As in soils
is not well documented.
According to Williams and Whetstone (17), soils from various parts of
the United States and Mexico contained from .3 to 40 ppm As. Olson et al.
(18) reported 7-18.4 ppm of arsenic in South Dakota soils with plants
containing from 1.2 to 4.3 ppm of As. In only a few cases did the soils
studied have more than 3 ppm As. Except under very artificial conditions,
such as the poisoning of soils by lead arsenate spray, or the occurrence
of high levels of bound ^s_ in geothermal areas (12), high concentrations
of A_s do not appear to be a problem in soils. Arsenophilic molds, fungi,
and bacteria are stimulated by unusual concentrations of arsenic in most
o? its forms aid are known to release methylated arsines to the atmosphere
from soils of high A_s content (16),
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The role played by As?CL as an aerosol particle in the arsenic cycle
appears from many considerations to be significant. A remarkably high
level of AJ; in city dusts, averaging above 5 ppm, was reported by various
authors (19,20,21). In a careful review of the air pollution aspects of
arsenic and its compounds, prepared in 19&9 ^or th® National Air Pollution
Control Association, Sullivan and others (22) provided the most complete
i
treatise so far available on levels of A_s in city vs. urban air. Other
than the well-defined arsenical pollution problems which have occurred in
and around smelters, no evidence of adverse effects from arsenical air
pollution were reported. Although skin abnormalities in humans were re-
ported, particularly among arsenical workers (10,10a), no adverse systemic
illnesses in humans have been clearly related to exposure to arsenicals.
For purposes of this review, attention may be called to the very recent
disclosure by ¥. C. Nelson et al. (23). This retrospective epidemiologic
study of orchard workers exposed to lead arsenate spray around Wenatchee
In the 1930s and »40s indicated that those exposed had, if anything, a
somewhat better health record than was true for people of similar age not
so expose^.
In a report of various trace elements in the atmospheric environment,
Peirson et al. (2^) note that the air concentration of As is far less in
rural than in industrial areas This study again points the need for
aerosol identification of the form or way in which As_ is transported through
i
the atmosphere. The level of arsenic was reported to be far less than that
of the macroelements, Na, Al, Cl, and Ca. The A_s level was reported well
below levels of Fe, Zn, Pb, Cu, Mn, Ni, V, and Br, - about comparable to
the level of Cr, but more than that of Se, Co, or Hg. The rate at Which
various trace elements return to earth in rain or as dust was also consid-
ered It appears from this study that most elements are cyclical in nature.
The critical question remains as to what levels are beneficial and what
levels harmful for each element.
An excellent study by Tremearne arc Jacob (25) on the arsenic in
natural phosphates and phosphate fertilizers, revealed a range of 0.^ to 188
ppm ^s in mineral phosphates, ',/hether this association results from bio-
concentration of As; with phosphorus is still not clear. The following con-
clusion was drawn: "When all the ^actors affecting the action of arsenic
on plants and on soil organisms under practical conditions of farming are
taken into consideration, -.^ seems very unlikely that the quantities of
arsenic contributed to the soil in phosphate fertilizers are sufficient
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to produce toxic effects even with very large annual applications of the
fertilizer over extended periods of time.". Despite this (JSDA Technical
Bulletin of 19^1, the British government succumbed to arsenophobia in the
late 1950s to the point of requiring that superphosphates made in England
be so treated as to contain relatively little arsenic. As noted elsewhere
(26,27), this action resulted in the inadvertant removal of selenium as
well as As. This led in turn to an epidemic of selenium deficiency in many
species of livestock in New Zealand.
In the United States, the chronic fear of arsenic led to governmental
action in the early '60s to reduce the arsenic limit in food phosphates from
10 to 3 ppm.(6). Subsequent studies showed (28,28a) that representative
foods in the U.S. contain quite low levels of arsenic, generally well
below existing tolerances. Indeed, one may wonder if the level of arsenic
in human foods has not been reduced too much. The fact that certain arsonic
acids have been shown to improve the well being, feed efficiency,, and
reproductive performance of turkeys, chickens, and pigs, raises the question
whether arsenicals may have an as yet unrecognized nutritional value for
humans, as well as for animals. Morrison (29) established experimentally
that the arsenic content from kitter in poultry houses did not appreciably
increase the arsenic content of soils or crops when used as a fertilizer.
Various other reports have indicated that A_£ is not cumulative in the
human food chain. This can be explained by 1) the fact that A_s is only
sparingly absorbed by plants, 2) the apparent fact that As in plants is
not readily available to animals, and 3) that microorganisms to a very
large degree prevent the accumulation of Ass in soils, making for a contin-
uing cycle of arsenic via water, land, and the atmosphere.
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10
Meed for Hj.sj.oric Perspective for Safe Arsenical Uses
Laws, regulations, and medical taboos have repeatedly gotten ahead of
science regarding the safa uses of arsenicals. Confusion between the toxicity
of A_s and Se first led to an association between "arsenic" and "cancer",
later to placing sole blame for the British Beer Poisoning Epidemic of 1900
on A_s (6). This in turn led to the tolerance setting for all types of
arsenical residues, even for traces of arsenic in food phosphates (26).
There are many indications that arsenicals play a positive role in the nutri-
tion of plants and animals. Thus, the tendency to avoid as much arsenic as
possible may in time prove harmful to health.
For the purpose of this review, it seems rignificant to note that the
diverse roles of A_s in biology involve its oligodyramic potential to act as
a catalyst in trace amounts but as a toxin at higher levels. These effects
of lead arsenate and other arsenicals were well described in the early 1900s,
For instance, Haywood and McConnell of the U.S. Dept. of Agriculture (37)
noted early in this century "in very minute quantities, arsenic appears to
exert a stimulating effect or act as a tonic (on foliage) as it does on
animals. It is probably this action which, by accelerating the functional
activity of the leaf and producing more rapid assimilation, causes the
excessive reddening and hastens the maturity of thefruit. On the other
hand, if too large an amount is absorbed, it has a toxic effect, resulting
in retarded assimilation, which in turn will .cause the fruit to shrivel
and drop before it has matured." This refers to the use of lead arsenate
in apples. The use of lead arsenate to accelerate the maturation and sweet-
ening of citrus fruits must also reflect stimulation of plant metabolism
by traces of arsenic (38). This effect, although still not well understood,
was first reported before 1900 and is of value in the economy and timing of
citrus production. Stewart and Smith (39) reported visible stimulation of
plant growth, particularly root growth, for peas, radishes, beets, potatoes,
and beans, with traces of arsenates. They concluded "...that the accumu-
lation of arsenic in soil, as the result of spraying of orchards if not
continued to excess, may be beneficial rather than injurious".
Extensive studies by Greaves (^0) on the relation of arsenic to nitrogen
fixation by soils indicated that the nitrification was greatest when the
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11
water soluble arsenic content of the soils was about 10 parts per million.
Greaves noted that sodium arsenite became toxic to plants at a concentration
of 40 ppm but that lead arsenate was not toxic and continued to stimulate
nitrogen fixation by soil Azotobacter even at 400 ppm. The optimal .level
of 10 ppm As conforms to that of Iroolson et al. (36) regarding the effect
of As level on growth of corn. Greaves, who worked at the Utah Experiment
Station, also noted the ability of arsenate ions to increase the bioavail-
ability of phosphate ions to plants, a most significant observation in
light of the phosphate resource limitation facing agriculture.
The remarkable versatility of arsenic is thus glimpsed in evidence that
it has something to do with both phosphoryi::tion and with nitrogen metabolism-
As early as 1897, Stoklasa (41) had reported that, although arsenic acid
could not replace phosphoric acid in the living cell, it did appear to
substitute in part by stimulating plant growth. In 1901, Stutzer (42)
raised the question whether the arsenic naturally present in superphosphates,
i.e. up to 0 1 $ could be harmful. He concluded after experimentation that
it would be harmless to soils, plants, or consumers of foods grown on such
soils. The irrational fear of "arsenic" led more 'Chan 50 years later to
removal of A_£ from superphosphates made in England, This led in turn to a
tragic loss of livestock in New Zealand from selenium deficiency. Dr. John
Barnes of the British Medical Research Council wrote me in private communi-
cation that this need not have occurred (26), It is precisely this'type
of overreaction to the safe uses of arsenicals that one may hope to avoid here.
Such can be accomplished best by further research and by public recognition
and appreciation of the benefits to be derived from safe uses of the toxic
trace elements.
A level of about 14 ppm of arsenic was reported in the National Bureau
of Standards Standard Reference Material, orchard leaves. This was a com-
posite sample from various fruit trees in which leaves from arsenical-sprayed
trees were excluded. Again, trying to learn from history, one finds in early
work by Jadiri and Astruc (42), the statement "The chlorophyll-bearing parts
of plants always give a higher arsenic content than any other portion."
If A_s indeed stimulates photophosphorylation (31)• this association with
chlorophyll-bearing parts of plants and the stimulatory effects of As for
turf grasses becomes more understandable.
The "catalytic fertilizer" effect at about 10-75 ppm of available
A£ in soils, along with its toricity to plants at higher levels, was thus
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12
known to agronomists at least 60 years ago. Prolonged soil sterilization
with sodium arsenite and high levels of arsenic trioxide came about in the
1930s (32). Discovery that desirable grasses were improved by arsenic
trioxide and lead arsenate at levels which suppressed weeds, undesirable
grasses, grubs and worms, and that this effect extended for several years,
again came about through careful and painstaking research (3i33). More
I
recently, Liebig (44-) provided criteria to diagnose the arsenic status of
soils for control of arsenic toxicity. His extensive tables showed that
little arsenic gets into the edible parts of plant products, with roots
and leaves showirg the highest levels. He stated "Apparently, the effect
of arsenic toxicity is such that plant growth is limited before large amounts
of arsenic are absorbed and translocated to tht top."
In reviewing air pollutants which affect aniraOs, recent studies by
Lillie (45) found no reported adverse effects from arsenic inhalation. He
noted that the phosphate levels were reduced below normal in tissues of
arsenate-poisoned rabbits. This fits the hypothesis that excesses of arsenate
ions interfere with phosphorylation, thus causing general metabolic toxicity.
It is consistent with evidence that low levels of arsenate catalyze
phosphorylation (6).
In & plea for reality in evaluation of environmental health problems,
Stokinger (46) listed seven guidelines, He exemplified the need to avoid
unnecessarily severe standards by relating the situation in Fallen, Nevada.
F'allon city water has exceeded the PHS-WHO limit for 40 years, with no evidence
of toxicity to the people who use the water. This is a striking demonstration
of the unreality prevalent among those not aware of the entire situation.
That the setting of unrealistic standards must make in time for failure of
our society was argued by Stokinger.
In my view, ability to be scientifically right about elements must
in time determine our capacity for survival among them. The need to balance
risks versus hazards in this controversial situation and to arrive at a wise
decision should go hand in hand with the encouragement of arsenical research.
S'ull advantage may thus in time be realized for the diverse roles apparent
for arsenicals in agriculture, turf improvement being only one of many.
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References
1. Done, A.M. and A.J. Peart. 1971. Acute toxicities of arsenical herbi-
cides. Clinical Toxicol. 4(3):343-355.
2. Buck, W.B. 1969. Pesticides and economic poisons in the food chain.
Proc. 73rd Ann. Meeting of U.S. Animal Health Ass. p221-226.
2a. Buck, W B. 1972. Hazardous arsenical residues associated with the use of
a lawn crabgrass control preparation. Veterinary Toxicol. In press.
(Special report prepared for use by the PAX Review Committee, llpp.)
3. Stewart, J.C. 1962. Method of and composition for eliminating crabgrass
infestations U.S. Patent 3,057,709.
4, Vallee, B.L., D.D. Ulmer and W.E.C. Wacker. I960. Arsenic toxicology and
biochemistry Arch. Ind. Health 21:13^-151.
5. Underwood, E. 1971. Trace Elements in Human and Animal Nutrition.
Academic Press, New York.
6. Frost, D.V. 1967. Arsenicals in biology-retrospect and prospect. Federa-
tion Proc. 23(1):194-208.
7. Ferguson, J.F. and J. Gavis. 1972. A review of the arsenic cycle in
natural waters. Water Res. 6:1259-12?4.
8. Harkins, W.D. and R.E. Swain. 1907. The determination of arsenic and
other solids in smelter smoke. J. Amer. Chem. Soc. 29:977-999.
9. Harkins, W.D. and R.E. Swain, 1908. The chronic poisoning of herbivorous
animals J. Amer. Chem. Soc. 30:928-946.
10. Birmingham, D.J. and M.M. Key. 1965. An outbreak of arsenical dermatitis
in a mining community. Arch. Derm. 91:457-464.
lOa.Oyanguren, H. and E. Perez 1966. Poisoning of industrial origin in a
conrnunity. Arch. Environ. Health 13:185-189.
11. Borgono, J.M and R Greiber. 1972. Epidemological study of arsenicism
in the city of Antofogasta. Conf. Trace Substances in Environmental
Heall1?::^ 13-14, Univ. Missouri, Columbia. '
12. Grimmett, P.E.R., I.G. Mclntosh, L.W.N. Fitch, E.M. Wall, and G.B. Jones.
1939. Occurrence of arsenic in soils and waters in the Waiotapu Valley
and its relation to stock health. N.Z. J. Sci. Tech. 21(3A):137A-l60A.
13. Cancaster, R.J., M.R. Coup and J.W. Hughes. 1971. Toxicology of arsenic
present in lakeweed. N.Z. Veterinary J. 19:141-145.
14 Clarke, E.G.C. and M.L. Clarke. 196?. Garner's Veterinary Toxicology.
3rd Ed. Balliere, Tindell and Cassell, London".
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15. Bucy, L.L., fl.S. Garrigus, R,M. Forbes, H.W. Norton and W.W. Moore.
1955. Toxicity of some arsenicals fed to growing-fattening lambe. J.
Animal Sci.14:435-445.
16. Goldschmidt, V.M l°''t. Geochemistry. Oxford-Clarendon Press. Oxford,
England.
17. Williams, K.T. and P.R. Whetstone. 1940. Arsenic distribution in soils
and its presence in certain plants. U.S.D.A. Tech. Bull. 732.
18. Olson, O.E , L.L Sisson and A L Moxon. 1940. Absorption of selenium and
arsenic by plants from soils under natural conditions. Soil Sci. 50:115-18.
19. Satterlee, H S 1958. Sources of error in microdetermination of arsenic.
A.M.A. Arch. Ind. Health 17:218-229.
20. Liebscher, K. and H, Smith. 1968. Essential and non-essential trace
elements Arch Environ. He<h 17:881-890.
21. Goujden, F, , EL. Kenneway and M. E. Urquhart. 1952. Arsenic in suspended
matter of town air. Brit. J. Cancer 6:1-7.
22. Sullivan, R.J. et al. 1969, Air pollution aspects of arsenic and its
compounds. National Air Pollution Control Administration-Consumer Protec-
tion and Environmental Health Service, H.E.W., Contract No. PH-22-68-25.
23. Nelson, W.C., M.H. Lykins, J. Mackey, V.A. Hewhill, J.F. Finklea and D.I.i
Hammer. 1973. Mortality among orchard workers exposed to lead arsenate
spray; a cohort study. J. Chron. Dis. 26:105-118.
24. Peirson, D.H. . P.A. Cawse, L. Salmon and R.S. Cambray. 1973. Trace
elements in the atmospheric environment. Nature 241:252-256.
25. Tremearne, T H. and K.D. Jacob. 1941 Arsenic in natural phosphates
and phosphate fertilizers, U.S.D.A. Tech. Bull. 781 U.S. Gov't. Prtg.
Office, Washington,
26. Frost, D.V. 1970. Tolerances for arsenic and seleniumj a psychodynamic
problem. World Rev. Pest Control. 9:6-28.
27, Frost, D V 1972 The two faces of selenium; Can selenophobia be cured?
CRC Crit. Rev. in Toxicol. 1:467-514.
28. Duggan, R.E. and J. R. Weatherwax. 1967. Dietary intake of pesticide
chemicals. Science 157:1006.
28a. Martin, H. and R.E. Duggan. 1968. Pesticide residues in total diet
samples. Pesticide Monitoring J. 1:11.
29. Morrison, J.L. 1969. Distribution of arsenic from poultry litter in broiler
chickens, soil, and crops. Agri. arid I'ood Chem. 17:1288-1290.
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30. Chan, T,, B R. Thomas and C.I. Wadkins. 1969. The formation and isolation
of an arsenylated component of rat liver mitochondria. J. Biol Chem. 244i
2883-2890.
31. Dilley, R.A. 1970. The effect of various energy-conversion states of
chloroplasts on proton and electron transport. Arch. Biochem. & Biophys.
137:270-283.
32. Crafts, A.S. and R.S. Rosenfels. 1939- Toxicity stusies with arsenic in
eighty California soils. Hilgardia 12:177-199.
33. McNulty, I.R. and E..A. Rhodes. 1955, The use of arsenicals for the control
of crabgrass. Utah Acad. Proc. 32:125-130.
34« House, E.B; et al. 1967. Assessment of ecological effects of extensive
or repeated use of herbicides. Clearinghouse for Federal Scientific and
Technical Information, Springfield, V?. 22151. Final Report AD824314.
35« McLean, H.C,, A.L. Weber, and J.S- Joffe. 1944. Arsenic content of vegeta-
bles grown in soils treated with lead arsenate. J. Economic Entom. 37s315-16.
36. Woolson, E.A., J.H. Axley, P.C. Kearney. 1973. The chemistry and phyto-
toxicity of arsenic in soils. II Effects of time and phosphorus. Soil
Sci. Soc. Amer. (Mar.-April).
37 • Haywood, J.K. and C.C. McConnell. 1908. Lead arsenate. U.S.D.A. Bull. 131.
U.S. Gov't. Prtg. Office, Washington.
38. Reitz, H.J. 1949. Arsenic sprays on grapefruit in relation to the new
citrus code. Proc. Fla. State Hort. Soc 49-55.
38a. Reese, R.L. 1970. Arsenate sprays on temple oranges? rates, timimg and
residues. Proc. Fla. State Hort. Soc. 15-20.
39. Stewart, J. and E.S. Smith. 1922. Some relations of arsenic to plant
growth. Soil Sci. 14S111-126.
40. Greaves, J.E. 1916. The stimulation influence of arsenic upon the
nitrogen-fixing organisms of the soil. J. Apr. Res. 6(11):389-416.
40a. Greaves, J.E, 1917. The influence of arsenic on the bacterial activities
of a soil.Sci. Mo. 5(3):204-209.
41. Stoklasa, J. 1897. Concerning the substitution of arsenic acid for phos-
phoric acid in nutrition of plants. Ann. Agron. 23:471-477.
42. Stutzer, A. 1901. Is the arsenic in superphosphates harmful? Deut. Landw.
Presse 28(9):61
43. Jadin, F. and A. Astruc. 1912. The presence of arsenic in the plant king-
dom. J. Phar et Chim. 6:529-535.
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44. Liebig, G ?. 1966 Arsenic, in Diagnostic Criteria for Plants and Soils.
H.D. . Charipan, Ed - Div. Agr. Sci., Univ. Calif., Riverside. 13-22.
45. Lillie, R.J 1970. Air pollutants affecting the performance of domestic
animals. U.S.D.A. Agric. Handbook. U.S. Gov't. Prtg. Office, Washington.
46. Stokinger, H.E. 1971. Sanity in research and evaluation of environmental
health. Science 1745662-665.
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SECTION II
ARSENIC TRIOXIDE & LEAD ARSENATE IN SOIL
\ ,
ARSENIC TRIOXIDE AND LEAD ARSENATE IN SOIL
with
Recommendations Regarding PAX ^00 3yr. Crabgrass Control
Dr. Paul J. Zinke
Introduction
The ultimate decision regarding the relative safety of adding to
soil a combination of lead arsenate and arsenic trioxide as used in
the PAX 3 year Crabgrass Control depends upon several factors. Among
these are: 1. The concentration of the material in the soil, 2. the
relative solubility of the various arsenical compounds which it will
form in the soil, 3. the possibility of the later formation of even
more toxic compounds in the soil, and k. the possible physical concen-
tration which may occur by various processes of soil movement.
These factors will be discussed in this report and a recommendation
made regarding the apparent hazards and possible methods of safe use of
the product will be made.
PAX frOO As A Soil Additive
The main concern with the use of this material lies in its content
of arsenic. An important aspect to be considered in evaluating the
relative safety of the product is the amount of arsenic and its possible
concentration as added to the soil. The material as added is 25% Arsenious
Oxide (As^) and 8.25% arsenate of lead (Pb (AsO^) ). Assuming 82. k
As in the arsenious oxide, and 16. 6& as in the lead arsenate the total
arsenic content in the PAX 400 is estimated to be 22%.
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When given the specified application rate of the material to the
soil as kO ]bs. per 2000 5qu_.e feet the rate of application on a
square meter basis is 99-7 grams of PAX kOQ containing 21.kS grams of
elemental arsenic. This is approximately 191-26 pounds of elemental
arsenic per acre.
It is of interest to determine the concentration which this
represents in the soil for comparison with other references on arsenic
concentrations in soils. If the material added remains in the top
centimeter of the soil having a bulk density of 1.0, the concentration
of arsenic in the soil will be 2,100 ppm. Presumably this high concen-
tration would occur only for a short time as instructions call for
washing the material into the soil by intensive watering. Assuming
that ultimately the material will be leached, (however, Stadtherr found
less than 6% of it leached beyond %" with 16" of applied water) and fixed
or stored in the top 10 cm. of the soil the estimated concentration of
arsenic in the soil a short time after application may drop to 210 ppm.
This compares with natural background arsenic contents in soils that
may range from 1-70 ppm (Arnott and Leaf), and thus could be considered
to be a very high arsenic content for soil.
The persistence of this material in the soil and its release in
quantities which may be toxic to plants, or concentrated by them in
toxic quantities depends upon subsequent processes of solution and
storage as fixed into insoluble formSjOr as anions on the anion exchange
complex of the soil, and the subsequent degradation or leaching of the.
arsenic compounds from the soil.
Pei .> i stence in Soi 1
Depending upon solubility of the added arsenic compounds, theymay
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remain as added(while gradually going into solution) for varying periods
of time. Apparently under some conditions despite the low solubility
constants of the materials this solution rate can be fairly rapid. Epps
and Sturgis found that nearly one quarter of the Arsenic Trioxide they
added to a silt loam soil went into solution readily. This may be more
rapid where the soil is more acid, or where the soil is less aerated.
A major aspect of the persistence of the arsenic in the soil will
be in the various chemical processes which occur in the soil after the
arsenic is in soluble form. The arsenic in soluble form from the PAX
will be mainly as arsenate: '
or H AsO. /I
3 * O
This dissociates as a very weak acid in a stepwise fashion in final
dissociation with increasing acidity of the soil. In i> poorly drained
soil with reducing conditions this may be converted to Arsenite:
n
c
In soils that were kept wet for extended periods, Epps and Sturgis found
that the soluble J^s content went up to k.Q ppm by the third week. This
was on a silt loam. This would be at a toxic level to most plants of
greater than 2.0 ppm water soluble arsenic.
An ion Exchange Storage of Arsenic
Anion exchange adsorption of the soluble arsenate may take place
in soils which have a high anion exchange capacity. This would represent
a type of storage which would lend persistence to the arsenic in soil.
In the case of the prescribed addition of PAX '<00 to the soil, the
21. 't9 grams of arsenic added per square meter represents nearly a*»-
v/'Sy'rf-of
equ i valentAarsen ic in anion form if it were all soluble. Considering
-------
a soil with moderate anion exchange capacity, which might be 10 ,
mi 11[equivalents per 100 grams of fine earth, and a bulk density of 1.0,
an estimate of one equivalent of anion exchange capacity per square meter
to a depth of 1 cm. of soil is derived. Dratschev found that clay could
adsorb up to ]% of its weight as arsenate. The amount of arsenic that
would enter into anion exchange storage in the soil will depend upon the
type of clay present, and its amount. Kaolinitic clays typical of mature
soil will have the greatest capacity to adsorb arsenic in the anion form,
and montmori1lonitic clays will have least (Rubins and Dean). The per-
sistence of the arsenic stored on the anion exchange complex will depend
upon the soil pH, and on the types and concentrations of competing anions
present in the soil solution. There is a displacement sequence SOf > CrO,~";>
NO ~~ ;> AsO^ > PO^" V MoO^> l" * Cf * F~* OH ~ in which equivalents
of the first will displace equivalents of the following. Thus additions
of SO., or NO, as fertilizer may displace arsenate that has accumulated
on the anion exchange capacity of the soil. Conceivably a concentrated
addition of POr could do the same. Thus the arsenic could persist for
by '
a long period on the anion exchange complex to be displaced^concentrated
additions of other anions.
The anion exchange capacity of the soil, and the presence of com-
peting anions would be variable from soil to soil, and thus quite
different quantities of storage of the arsenic in thib form may occur.
toMfefriif
The accidental or other changes in anion concentration might be another
unpredictable variable.
Storage of Arsenic in the Soil in Fixed Condition i
Soluble .--ir sonic in the soil may undergo l hi: formation of insoluble
compounds with iron or calcium to become "fixed" in the soil in an
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-5-
analogous manner to phosphorus. Soils high in Iron, high in organic
matter, or high in lime usually have a high capacity to fix arsenic in
insoluble form. (Cooper, et al). These soils are usually the red and
yellow podzolic soils and latosols, or soils high in lime as in arid
areas, or those derived form Limestone. The Hagerstown Soil Series from lime-
stone was found to have a high capacity to fix arsenic in a non-toxic form
by Gile. The arsenic compound in this fixed form has a very low solubility
constant. However this may change with a change in pH, or with oxidation
reduction potential (Keaton and Kardos). Thus, raising the pH of a soil con-
taining arsenic fixed with iron may result in a release of fixed arsenic
into soluble form. Similarly arsenic fixed in a soil high in lime may be
insoluble at neutral pH, but released if the soil is acidified. Conceivably
this could happen with the addition of a sulfur fertilizer. On the other hand,
Kardos has shown that a soil high in soluble arsenic can be renovated by
application of ferrous sulfate which lowers the solubility of the arsenic.
Thus, in general arsenic may be very persistent in soil in which it
is likely to enter a fixed insoluble form. These would be soils high in
organic matter, high in lime, or in iron. Arsenic in this fixed form could
be released into soluble and possible toxic form at some later date bo
•*J
a change in pH and subsequent change in solubility of the fixed form. Pre-
sumable a large quantity of arsenic fixed in a soil could be released in
toxic quantitites by such a change. Bishop and Chisholm have recommended
that the arsenic status of a soil previously treated with arsenic should
be ascertained before attempting to grow arsenic sensitive crops.
Degradation Products
The soluble arsenic derived from the addition of PAX ^00 may in some
situations undergo transformations into much more toxic degradation products.
For example, Epps and Sturgis have noted that if the soil is rendered anaerobic
the arsenates may be reduced to arsenites. Arsenic in the arsenite form is
mticli more toxic to plants. This could happen where l:he material had been
placed on a soil that later became seasonably
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-6-
flcoded or anaerobic. The original compounds would become more soluble,
and the reduction to arsenite from arsenate take place.
A degradation sequence in anaerobic soils can proceed further to
arsine by some molds. Such a sequence under reducing conditions by
Anonymous in the Chem. Eng. News as follows:
Arsenite • #•• Methylarsonic acid r-
dimethylarsinic acid ; ^ dimethyl arsine.
Challenger described this sequence of react!or-s earlier, and showed how
if temporary oxidation conditions arise the dimethyl arsine might be
oxidized to CC" and arsenate.
Thus depending upon subsequent changes bringing about anaerobic
conditions to a soil having a high content of fixed or stored arsenic,
this might be transformed into compounds of much highs,- toxicity. This
could occur under flooding, or where fill material was placed over a
soil, or where construction might take place over the soil. Thus it
would be wise to know where large quantities of arsenic has been added
to soil as with PAX kQO to avoid such possible undesirable transformations,
Physical Concentration
The arsenica 1 compounds added in the PAX ^00 product could possibly
be concentrated by physical processes occuring in the soil or in soil
management practices.
Wind blowing surface soil may cause surface drifting of the soil '
in which arsenicals have been added and thus concentrate them in the
drifting material. This has been found to occur sufficient in amount
to cause a noticable increase in arsenic contents in plants grown on
such drifted soils according »-o lacobs et al.
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-7-
Surface runoff of water and accompanying sheet erosion of surface
soil may accumulate and deposit arsenic rich surface soil downslope
from the application area. Conceivably such deposition could occur in
anaerobic environments such as wet meadows and swamps and further
accentuate the concentration by detrimental degradation products such
as arsines being formed.
Soil management practices which would tend to accumulate surface
soil layers in localized deposits may result !n local concentrations of
arsenic rich soil. For example if soil were scraped from a surface for
some reason and piled in local accumulation or fill, vegetation sub-
sequently grown there might.be enriched with arsenic. Vacuum devices
used to collect leaves from lawns might concentrate surface arsenic rich
soils if they were dry and dusty. An example of such Accumulation by
a lawn mower accumulating clippings and associated surface soil has been
described by Buck.
These possibilities of physical processes concentrating soils enriched
with arsenic and depositing them in still more concentrated situations
introduces another unknown element in the control of the distribution
of the added arsenic.
Biological Concentration
Vegetation growing in arsenic treated soils may accumulate arsenic.
This accumulation will be mostly in the foliar parts of the plants
(Jacobs). Foraging animals might utilize the browse or herbage grown
upon such soils, and if confined in some way to this forage be subject
to undesirable concentrations of arsenic. Jacobs et al reported foliar
contents up to 19 ppm in potatoes.
Home vegetable gardens inadvertently placed on soils which had
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-8-
previously been treated with arsenicals in the large amounts specified
for the PAX kOQ product could ...ither high concentrations in the foliage.
The effect of such past arsenical additions in soil raising the vegetative
uptake would be more noticeable on sandy soils and less on heavy textured
soils as indicated by the work of Gile.
Isensee et al working with model ecosystems, aquarium tanks with food
chains extending from mud to plants to aquatic animals, found that arsenicals
(Cacodylic acid and dimethylarsine) were accumulated more readily by organisms
low in the particular food chain established in thejr model. However there
was a low magnification in organisms higher up this food chain. PAX kOQ
does not add arsenicals of the types used in this work, but some of the
degradation products under anaerobic conditions could be of this type.
Machlis in original work and a literature review noted that where arsenic
was high in the soil or nutrient medium the arsenic content would rise up
to limiting toxic amounts in the plant. These limits are different for
different species. He found for example 12 ppm in Sudan grass (Sorghum
vulgare var. sudanense), and 1.2 ppm, for beans (Phaseolus vulgaris var.
hum?Us) suppressed growth. Daniel found that the level at which Arsenic was
toxic in soil depended upon the phosphorus content and speculated that
Arsenic toxicity to plants was a phosphorus' deficiency problem.
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-9-
Summary
This report has been confined to the possible problems associated
with the addition of arsenious oxide and lead arsenate in the quantities
prescribed for the use of PAX ^00 3 year crabgrass control. The following
is a summary of the main points:
1. Rates of addition of PAX *»00 as prescribed result in arsenic
contents in the soil of up to 2100 ppm if retained within the
top centimeter of the soilfes some studieb indicate)may occur.
If eventual leaching and fixing of this arsenical material in
the top 10 cm. of soil occurs this concentration may drop to 210 ppm.
Normal arsenic background in soils ranges from 1-?0 ppm.
2. The arsenic added to a square meter of soil if entirely con-
verted to an ion form would occupy the an ion exch?r,yc capacity
present to a depth of 1 cm of that soil.
3- Soil usually has a high capacity to retain arsenic either as
fixed, that is bound in insoluble compounds; or adsorbed on the
anion exchange capacity of the soil. The literature indicates
that up to 8000 Ibs. of arsenic trioxide could be retained in
the top 9 inches of an acre of soil.
k. The arsenicals added in PAX kOO will go into solution as
arsenates in well drained soils and possibly arsenite in poorly
drained soil. Solution will be more rapid in acid soils and in
poorly drained soils.
5. Mature soils that are heavy textured and characterized by
Kaolinitic clays will adsorb large quantities of arsenate on the
anion exchange complex. This may be subject to later displacement
by other anions such as sulfate and nitrate.
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-10-
6. Soluble arsenic in the soil may be fixed as compounds of
low solubility in the presence of large amounts of iron or calcium.
The solubility of arsenic in this fixed form is a function of pH.
A change of pH as by liming an iron rich soil high in fixed
arsenic may release large amounts of arsenic in soluble form.
7. Soils will vary widely in their capacity to store arsenic
in fixed form. Light textured, low organic matter, and low iron
or calcium soils will have the lowest cape-Ities to fix arsenic
in insoluble storage.
8. Degradation products of the added arsenic compounds may be
particularly toxic if the soil is anaerobic (i.e. due to flooding,
paving, or filling). In these situations dimethylarsine and arsine
may result due to micro organism activities in the anaerobic
environment. These are much more toxic than the original arsenicals,
9. Physical concentration of the arsenic rich soils by erosion
and deposition may result in concentration and accumulation in
new locations.
10. There may be concentration of arsenic in the foliage of plants
growing on soils in which arsenic content has become locally
enriched. Animals browsing or grazing this foliage may thus pick
up large amounts of arsenic.
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-11-
Recommendat ions
1. Due to the high application quantity of the PAX 400 material
and the obvious high concentration of arsenic resulting in the
soil from this application, and the uncertainties of later changes
in the soil with possible rendering of the arsenic in available and
toxic forms to plants or animals it is recommended that this pro-
duct be used only with instructions for °xtreme care.
2. Where use is necessary, it would be best to have the application
carried out under the advice and responsibility of a person knowledgeable
of the possible persistence and deleterious transformations that may
occur in the soil at the location.
3. A record should be kept of all applications of the PAX ^00
materials so as to avoid future alterations of treated soil which
may tend to concentrate or transform the arsenical compounds into
more toxic amounts of forms. This will be increasingly important
as multiple applications of PAX J»00 are made in the same area.
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-12-
Bibliography
Anon. 1971. Trace metals; unknown, unseen pollution threat. Chem.
Eng. News. July 19, 1971 p. 29~33.
Arnott, J.T. and Leaf, A.L. 1967. The determination and distribution
of toxic levels of arsenic in silt loam soil. Weed Science 15:2
121-124.
Bishop and Chisholm. 1962. Arsenic accumulation.- Canadian Jour, of
Soil Science. k2: 78-80.
Challenger, F. 1947- Biological methylation. Science progress.
35: 396-416.
Cooper, H.P., et al. 1932. Soils differ markedly in their response to
additions of Calcium arsenate. South .Carolina Expt. Sta. 45th
Ann. Report. See page 27.
Daniel, W.H. I960. Arsenic toxicity - current progress. Proc. North
Central Weed Control Conf. 17:25.
Epps, E.A. and Sturgis, M.B. 1939- Arsenic compound toxic to rice.
Soil Science Soc. of Amer. Proc. 4:1939 215-218.
Gile, P.L. 1936. Effect of different colloidal soil material on the
toxicity of calcium arsenate to millet. Jour. Agr. Res. 52: 477-491.
Isensee, A.K. et al. 1973. Distribution of alkyl arsenicals in a model
ecosystem. In Press - submitted to Jour, of Environmental Quality
1973.
Jacobs, L.W. et al. 1970. Arsenic residue toxicity to vegetable crops.
Kardos, L.T. et al. Investigations of the causes and remedies of the
unproductiveness of certain soils following the removal of mature
trees. Washington Agr. Exp. Bui. Vol. 41 page 25.
Keaton, C.M. and L.T. Kardos. 1940. Oxidation - reduction potentials
of arsenate - arsenite systems in sand and soil mediums. Soil
Science 50:3 189-207.
Machlis, L. 1941? Accumulation of arsenic in the shoots of Sudan Grass
and bush beans. Plant Physiology 16: 521-544.
Stadtherr, R.J. 1963- Studies in the use of arsenicals for crabgrass
control in turf. Ph.D. thesis - University of Minnesota. 117 pp.
Vincent, C. 1944. Vegetable and small fruit growing in toxic ex-orchard
soils of Central Washington. Wash. Agr. Exp. Sta. Bull. 437-
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SECTION III
TURF MANAGEMENT ASPECTS
Report to PAX Arsenic Advisory Committee
May 14, 1973
A. E. Hiltbold
Weed Problems for Which PAX is Used
Vigorous, well managed turfgrass is a thing of beauty and pleasure
as a home lawn, on a playing field, golf course, or in the park. Recent
trends of suburban living, increased income and leisure time have en-
hanced the desire for attractive and useful turf. Research has expanded
rapidly in selection and adaptation of grass species, nutritional and
cultural requirements, and pest control. The wide array of herbicides
introduced during the past twenty years has greatly improved the con-
trol of weeds in turf, yet there is not the ideal herbicide applicable
to all situations.
PAX 3 Year Crabgrass Control (Reg. No. 3234-3, Dec. 14, 1970) is
used primarily for control of smooth crabgrass (Digitaria ischaemum
Schreb.), large crabgrass (Digitaria sanguinalis L. Scop.), and annual
bluegrass (Poa annua L.) in established turfgrasses such as Kentucky
bluegrass (Poa pratensis L.), red fescue (Festuca rubra L.), and
bentgrass (Agrostis sp). The herbicidally active ingredient of the
PAX product is the arsenic provided by As203 (25.11%) and PbHAsO^ (8.25%),
functioning as a preemergence material applied at the currently recommended
rate of 20 lb/1000 ft2, providing the acre equivalent of 181 and 43 Ib.
total As and Pb, respectively. This rate may be reduced to one-third
for annual maintenance after the first year application at full rate.
Weeds generally invade where turf is thin or bare soil is exposed
by heavy traffic, improper fertilization or mowing, or by poor soil
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—2—
moisture conditions. Crabgrass and Poa annua make unpleasant contrasts
of color, texture, and height in the desired turf and also contribute to
the thinning of the turf through competition. Poa annua is widely dis-
tributed in United States, appearing with germination of seed in the fall
and during mild periods in the winter and spring. Most vigorous growth
occurs on moist, fertile soil, but it persists in areas of low fertility
and soil compaction. Seed is produced during most of the growing season;
the seedheads are unsightly, difficult to mow, and contaminate adjacent
areas. During the mid-to late-spring, competition from Poa annua retards
the growth of the established turf. With onset of hot, dry weather, Poa
annua dies rapidly, leaving a patchy, unthrifty appearance. Extensive
die-back of Poa annua occurs even in the northern Uri-ted States, making
its management as a turfgrass impractical.
Crabgrass commonly begins its growth period in late spring, taking
over areas left by dying Poa annua. Smooth crabgrass is prevalent in
northeastern United States while large crabgrass is most abundant in the
mid-Atlantic and southeastern states. Both species grow rapidly with
abundant moisture, fertility, and light during the summer, causing
severe competition of desirable turfgrass and unattractive contrasts of
i
color and texture in the turf. Seed are produced from mid-summer until
the plants are killed by frost. The dead crabgrass areas in the turf
are ugly during the fall and provide the access for germinating Poa annua
in the next cycle. Light enhances germination of both Pjja^ annua and
crabgrass in areas of thin turf.
Turf weeds are seldom controlled by a single procedure. Most weed
control programs stress management for better turf cover and the use of
herbicides. A comprehensive look.at turf weed control methods would
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-3-
include the use of weed-free seedbeds, weed-free propagation materials,
prevention of weed germination or emergence with preemergence herbicides,
reducing weed growth and development with management or herbicides,
regular mowing to destroy weeds intolerant of mowing, preventing seed
set, and destroying the established plants (15).
Control of crabgrass requires prevention of seed set for several
years. Germinating seedlings can be eliminated through competition,of
dense growth of the established turf and with use of preemergence herbi-
cides.
Effectiveness of PAX 3-Year Crabgrass Control and the
Availability and Effectiveness of Alternative Control Measures
PAX functions as a preemergence herbicide with considerable selectivity.
The dissertation research of Stadtherr (42) is probably the most compre-
hensive study of PAX 3-Year Crabgrass Control available in the literature.
When PAX was applied at the recommended rate of 25 lb/1000 ft2, the
product provided complete control of crabgrass the first year and re-
sidual control exceeding 90% in each of three succeeding years, with no
visible injury to bluegrass. The lethal effect of PAX on crabgrass: was
associated with germination and emergence of the radicle. However, it
was possible to seed bluegrass on a loamy soil immediately after appli-
cation of PAX at the recommended (IX) rate without injury to the seeded
bluegrass. On two other soils some reduction of stand occurred when
seeding was done on the day of PAX application. Stadtherr found the in-
jury by arsenicals to be due to injury of plant roots without appreciable
translocation of arsenic to the above-ground parts. For example, established
crabgrass did not absorb sufficient arsenic to kill the plants. Roots
and .stolons failed to grow into PAX-treated soil. The long period of
-------
-4-
residual activity of PAX was associated with resistance to leaching of
arsenic from the soil surface. In controlled leaching experiments
with PAX applied to the surface of two soils, less than 6% of the toxic
substances of PAX or their equivalent arsenicals moved below the 1/2"
depth after leaching with 16" of water.
Campbell and Quinlan (5 ) compared five preemergence herbicides
including PAX for crabgrass control in Kentucky bluegrass. In com-
parison with sesone (2-(2,4-dichlorophenoxy, ethyl sodium sulfate),
neburon (l-butyl-3-(3,4-dichlorophenyl)-l-methylurea), alanap 1-F
(1% N-l naphthyl phthalamic acid), and chlordane (octachloro-4, 7-
methanotetraliydroindane), PAX at 25 lb/1000 ft2 was the only material
that gave good control of crabgrass throughout the germinating period.
A continuation of the work the following year compared the PAX treatment
with lead arsenate at 10 and 20 lb/1000 ft2. Results were not out-
standing, but these treatments gave considerable reductions in number
i
of both crabgrass species.
Both pre- and postemergence herbicides were compared for crabgrass
control in mixed turf in southern California (53). A single application
f\
of PAX at 25 lb/1000 ft on March 1 gave complete control of crabgrass
throughout the summer. Slight turf injury was noted one week after
treatment but this was followed by improved color. Alanap 1-F was nearly
r\
as effective as PAX but required three applications of 18 lb/1000 ft
each. Other preemergence herbicides reduced crabgrass numbers but were
far below the efficacy of PAX. The data showed the necessity for appli-
cation ahead of crabgrass seed germination. The persistence of PAX and
the short period of activity of the synthetic organic herbicides work to
the advantage of J'AX in this situation. Among postemergence herbicides
DSMA (disodium mcthanearsonatc) at 6.7 oz/1000 ft^ and PMAS (10% phenyl
mercuric acetate) at 2.5 O/./JOOO ft2 reduced crabgrass populations but
several carefully timed applications were required.
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-5-
One of the most widely recommended preemergence herbicides is DCPA
(dimethyl tetrachloroterephthalate). Watschke (48) evaluated various
experimental herbicides in comparison to DCPA for crabgrass control in
i
Kentucky bluegrass and creeping red fescue turf. DCPA at 10 Ib/A applied
in May provided essentially complete control of crabgrass without injury
to the bluegrass and only slight thinning of the fescue. Engel and
Bussey (14) compared DCPA at 12 Ib/A, siduron (l-(2-methylcyclohexyl)-3-
phenylurea) at 12 and 18 Ib/A, bensulide (0,0-diisopropyl phosphoro-
dithioate S-cster with N-(2-mercaptoethyl) benzenesulfonamide) at 10 Ib/A
as preemergence herbicides applied to Kentucky bluegrass turf in late
April. All herbicides attained one or more ratings of 90% crabgrass
control or higher. No turfgrass injury was observed with use of these
herbicides.
Daniel do) listed the crabgrasses and Poa annua among those plants
sensitive to arsenic. He points out the tolerance to arsenic of established
turfgrasses such as Kentucky bluegrass, bentgrasses, and redtop. Even
seedlings of these species survive arsenic applications that are toxic
to crabgrass. PAX at 25 lb/1000 ft2 (equiv. to 5.16 Ib As/1000 ft2) was
compared with calcium arsenate (equiv. to 3.2 Ib As/1000 ft2) and lead
arsenate (equiv. to 5 Ib As/1000 ft2) for reduction of crabgrass with
similar success. Calcium and lead arsenates were effective in controlling
Poa annua in turf, where these arsenicals were compared with numerous
experimental herbicides in 1955-56 (2l). It was concluded .that for control
of Poa annua in fine-leaved fescues and bentgrasses, 2.75 to 4.6 Ib As/1000 ft ,
i
concentrated in the soil surface, offered the greatest degree of success.
Frceborg and Daniel (19) have related the arsenic susceptibility of Poa
annua fo temperature and light conditions and to level of extractable
-------
-6-
arsenic in the soil during germination. At various levels of applied
toxicity was more pronounced at 30 C than at the lower temperatures. At
conclusion of the growth period, 30 days after application of As203 and
, ' I
seeding', dilute acid-extractable arsenic was measured in the soil, using
Bray P-l extractant (0.03 N NIfyF + 0.025 N HC1). At. rates of applied
As£03 up to 1280 ppm As in the soil, approximately 2.5% appeared in the
dilute acid extract. With 30 C growing temperature, Poa annua was killed
with extractable arsenic levels of 14.5 ppm As, and severely stunted and
chlorotic with 8 ppm As. These results suggest that to maintain control
of Poa annua at 30 C the concentration of weak acid extracts should be
in the range 8-15 ppm As. At lower temperatures approximately 20-45
ppm As was required.
Translation of these levels of extractable soil arsenic to rates
of application for weed control is difficult because of the locallization
of applied arsenic in the soil surface and its slow rate of dissolution
and movement into the soil with leaching. Water solubilities of As£03
and Ca3(AsO^)2 are 2.04 and 0.013 g per 100 ml water at 25 C, respectively.
Water solutions in equilibrium with solid phases thus contain 15,450 ppm
As in the case of As2C>3 and only 49 ppm As in the case of CagCAsO^^.
Arsenic concentrations in soil solution would be affected also by
equilibria with soil minerals such as kaolinite and hydrous oxides of
iron and aluminum. In soil immediately below the applied arsenic, where
grass weeds germinate, solution concentrations must approach the saturation
level.
Partial control of Poa annua can be achieved by management favoring
a dense tiurf in lace summer prior to germination of annual bluegrass.
Suppression of annual bluegrass with lead or calcium arsenate has been
-------
-7-
practiced for a long time. Calcium arsenate is considered one of the
most effective materials available; however, the development of a toxic
level for weed control often reduces the established turf or makes re-
seeding unsuccessful. The activity of calcium arsenate for Poa annua
control is decreased by high levels of phosphorus in the soil (31).
Trial and error have been relied on in determining treatment rates.
Jagschitz (28) compared bensulide, lead arsenate, and calcium
arsenate for preemergence control of Poa annua in Colonial bentgrass
(Agrostis tenuis Sibth.) putting green turf. The.herbicides were applied
annually at the rate of 0.34, 24, and 4.8 lb/1000 ft2 for bensulide, lead
arsenate, and calcium arsenate, respectively, for a 4-year period. After
several years of these treatments good control of foa_ annua was obtained.
Among the more recent preemergence.herbicides, benefin (N-butyl-
N-ethyl-ot,a,a-trifluoro-2,6-dinitro-p-toluidine), bensulide, DCPA, and
nitralin (4-(methylsulfonyl)-2,6-dinitro-N,N-dipropylaniline) can prevent
germination of annual bluegrass. However, they have not demonstrated
broad effectiveness nor sufficient control. They seem to have little
merit in cooler, humid regions where annual bluegrass may survive from
year to year. While their damage to established turf may not exceed
that of the arsenates, they can be expected to inflict undesirable amounts
of injury on sensitive species such as bentgrass (13).
In summary, PAX is an effective herbicide for crabgrass and Poa annua
control. It is more persistent than any of the synthetic organic herbi-
cides, guaranteeing weed control for a 3-year period following a single
application. Additional advantages are offered in its control of various
broadleaf weeds, white grubs, and earthworms in turf. Inorganic arsenicals
are currently the only herbicides providing gradual, selective control
-------
-8-
of Poa annua in closely mowed perennial turf such as on golf greens.
Granular form of calcium arsenate is presently the most widely used
arsenical for this purpose. Professionals in turf research, golf course
superintendents, and numerous home owners have attested to the effective-
ness of PAX and the arsenical approach to turf weed control. However,
other herbicides are available for many situations. These materials are
more demanding as to their rate and time of application and control a
more limited spectrum of weeds for shorter periods of time. The PAX
product offers economy in the cost of material and infrequency of appli-
cation.
Behavior of Arsenic in Soil
Concern with arsenic in agricultural soils of tae United States stems
from crop injury associated with long-term usage of high rates of lead
and calcium arsenate for insect control. Lead arsenate was used for many
years in apple orchards to control codling moth. It has been estimated
(2) that 20% of all the lead arsenate used in United States was used in
eastern Washington. The peak use came in 1943 when applications in
Washington averaged 50 pounds of arsenic per acre of bearing orchard. In
1948, DDT replaced lead arsenate for insect control. While established
orchards seldom showed toxic effects of accumulated spray, replanted
apple, pear, and peach would'not grow in old orchards. This injury was
readily apparent during the 1930's when extensive removal and replanting
of orchards was done. At this time crop injury was observed in the South
as a result of soil arsenic accumulations from calcium arsenate applied
for boll weevil control in cotton. Dorman and Coleman' (13) estimated
the amount of calcium arsenate applied at from 3 to 10 pounds per acre,
-------
—9—
with as many as 6 applications per season, depending upon the size of the
i (
cotton and insect infestation. Probably not more than 30 pounds per acre
were applied annually (11 Ib As/A). While cotton tolerated considerable
arsenic levels, injury was observed in-rice ( 16 ), cowpeas and oats
( g ) grown on treated soil following cotton. Analyses of soil samples
i
collected from all regions of United States and parts of Canada (4,22,29,24,37,
I
39,49,50 ) indicate that arsenic occurs in all soils regardless of pesti-
cide application. Amounts found in soils receiving no arsenical treat-
ment range up to 14 or 18 ppm As (49,4,39 ) or may average as much as
13 ppm As ( 50 ). A recent survey of arsenic contents in more than 500
soil samples from Alabama"( 24 ) had a frequency distribution of soils
with 14% containing less than 1 ppm As, 46% with 1-4 ppm As, 22% with
4-7 ppm As, 14% with 7-10 ppm As, and 4% with more than 10 ppm As. These
. samples were selected from among those submitted for soil test and fertil-
izer recommendations for cotton, with the objective of determining the
current arsenic levels in fields presumably treated with calcium arsenate
in the past. The data indicate that these fields have not received ap-
preciable calcium arsenate or else that extensive loss of arsenic has oc-
J
curred through erosion, crop removal, or leaching below the plow layer.
The more extreme concentrations of arsenic occur in orchard soils
where levels in excess of 100 ppm As have been reported (4,22^37,49 ).
Woolson et al ( 50 ) found arsenic residues averaging 165 ppm As in sam-
ples of 58 surface soils with history of arsenic application. Washington
orchard soils (10 samples) averaged 627 ppm As, with one as high as 2,500
ppm As. Significantly greater amounts of arsenic occur in soil beneath
the trees, compared to soil between the trees, as a result of spray drip
( 37,50). Analysis of four commercial orchard sites in Oregon in 1945
-------
-10-
showed as much as 116 ppm As and 377 ppm Pb in treated soil, amounting to
20 to 30-fold increases in arsenic and 13 to 40-fold increases in lead
as a result of 20-25 years of lead arsenate spraying (30).
Where records of past usage of arsenicals are available, recent
determinations of arsenic residues in soil indicate the element to be
highly persistent in soil. The level of arsenic established in soil (126
ppm As) with annual applications of lead arsenate remained essentially
constant during 5 succeeding years without further addition ( 34 ). Ar-
senic levels injurious to red pine in forest nursery soils were estimated
to be little changed from those established 35 years previously when
As203 was used for white grub control ( 44 ). The recovery of applied
arsenic in soil of Indiana orchards was nearly complete ( 50 ), indicating
very little arsenic leached or lost. On the other hand, arsenic con-
centrations established with lead arsenate in 1935 for white grub control
in turf ( 38 ) underwent continuous decline during the following 15-year
period. The rate of loss was related directly to arsenic concentration
in the soil. The gradual decline of grub control during the period was
associated with a corresponding decline in soil arsenic. Leaching of
arsenic has been found to be a significant loss process in soils with low
I
contents of active iron and aluminum. Losses of applied arsenic from
sandy surface soils in the Netherlands were directly related to the amount
of arsenic in the soil, with an average half-life of 6.5 years (45 ).
Much of the arsenic lost from the upper 20 cm of soil was found in the
20-40 cm depth, although net loss of applied arsenic occurred continuously.
Leaching was concluded to be an important factor in dissipation of toxicity
from high rates of sodium arsenite applied to a loamy sand soil in New
Jersey (18 ). Complete inactivation of the 75 Ib As per acre application
-------
-11-
was observed in the upper 4 inches of soil during the 30-month sampling
period. At the other extreme, McGeorge ( 35 ) observed the complete
retention of arsenic within the upper 4 inches of ferruginous Hawaiian
soils sprayed with sodium arsenite equivalent to 3.75 Ib As per acre for
a 5-year period, despite rainfall averaging 200 inches per year on flat,
porous soil surfaces. Arsenic applied as methanearsenates over a 4-year
period for weed control in turf on a sandy loam soil in Alabama was re-
covered in large part from the upper 6 inches oZ soil, but significant
leaching .into the 6-12 inch depth was observed (29 ). Soils differ
widely in those properties affecting arsenic retention or leaching, and
those properties similarly affect the capacity of soil to inactivate toxic
applications of arsenic.
Crafts and Rosenfels (9 ) found that red soils had greater
capacities for reducing arsenic toxicity than soils of other colors in
California. Similarly, Cooper et al ( 8 ) in South Carolina showed
that coarse-textured gray soils such as the Norfolk and Durhum series
were seriously affected by relatively light applications of calcium arsen-
ate, whereas fine-textured dark soils such as Cecil, Greenville, and
Davidson series were not affected, even at high application rates. Dorman
and Coleman ( 13 ) applied rates of calcium arsenate up to 1600 Ib per
acre prior to planting cotton on soils varying in texture from sandy loam
to clay. Only on Ruston sandy loam were, cotton yields depressed by
arsenic during 4 years of cropping after application. The fourth year
yields showed the 400 Ib rate of calcium arsenate was completely inacti-
vated and much of the toxicity of the 1600 Ib rate was lost. Gile (20)
compared the effects of colloidal material .from 36 soils and subsoils on
the toxicity of calcium arsenate in greenhouse pot experiments. He con-
cluded that the resistance of a soil to calcium arsenate injury depends
-------
-12-
on the quantity of colloid present and the specific resistance of the
colloid, the latter being dependent upon the quantity and reactivity of
the iron present. Recent attempts to characterize the chemical forms
!
of arsenic in soils ( 29,50,51) indicate that most of the residual
i
arsenic is bound as insoluble iron'and aluminum compounds.
i i
Over the range of soil pH from 4-8 the predominant arsenate ion is
H2As04~ with HAs04= increasing with pH above 7. With mildly reducing con-
ditions in the pE 4-8 range arsenious acid (H3At,03) becomes stable (17).
Addition of iron oxide to an arsenate-arsenite system results in oxidation
of arsenite to arsenate with a subsequent increase in the redox potential
(32). These chemical factors in aerobic soils favor the transformation
of reduced forms of arsenic to the predominant arsenate form. Most soils
contain sufficient reactive iron and aluminum to precipitate arsenate in
•very insoluble forms ( 51 ). The time required for added arsenate to
equilibrate with these insoluble forms varies with rate of application
and the soil content of reactive iron and aluminum, but generally is
marked by rapid decline of water soluble arsenic and more gradual shift
i
of arsenic into the iron fractions. When arsenic is displaced from field-
weathered, high arsenic soil by leaching with phosphate, the more soluble
aluminum arsenates are removed, concentrating the less soluble iron ar-
senates (31).
Microbiological transformations of arsenic are known to occur. Quastel
i
and Scholefield ( 40 ) reported the microbiological oxidation of arsenite
to arsenate in soil. The course of arsenite oxidation was found to follow
the typical log growth curve, with oxygen uptake in agreement with the
reaction NaAs02 + H20 + 0 -> NaH2AsO^. Addition of 0.1% sodium azide
completely inhibited arsenite oxidation. Upon enrichment of the microbial
-------
-13-
population with arsenite-oxidizing species, subsequent applications of
arsenite were oxidized rapidly and without the initial lag phase. Green
(23) isolated bacteria, B_. arsenoxydans and B^. arsenreducens, from
solutions of arsenite in cattle dipping tanks. These fecal bacteria were
found capable of oxidizing and reducing arsenic and were enriched in the
0.1% sodium arsenite of the dipping tanks. Microbiological reduction
i
of arsenate with evolution of arsenical gases was reported by Thorn and
Raper ( 46 ). In addition to numerous strains of Aspergillus and
Scopulariopsis found to evolve the odor of arsine, other active fungi
were isolated from arsenic-toxic field soils. In view of this capability
of soil fungi it was concluded that accumulation of arsenic in soil may
be expected to occur only under massive amounts or under special con-
ditions unfavorable for development of a varied microflora. Later studies
i
•by Challenger and co-workers (3, 6 ) verified the conclusion of rather
I
widespread capability for arsine evolution among fungi and also identified
the gaseous products. Fungi were grown on bread cultures containing 0.1%
of As203» Na2HAsO^, CH^AsOCONa^ disodium methanearsenate, (Ct^^AsCKONa)
sodium cacodylate, C^HyAsOCONa^ sodium propylarsonate, and others. Cul-
tures were aerated and the evolved gases absorbed and determined. Strains
of A. niger, A., glaucus, j^. brevicaulis, Penicillium no tat urn and £.
chrysogenum were active on one or more of these arsenicals. Trimethylarsine
((CH3)3As) was the most common gaseous product, accounting for loss of
70% of the As203 during a 24-month period. In all cases the arsenic was
reduced to the +3 oxidation state and all substituent oxygen atoms replaced
by methyl groups. With the methanearsonates and propylarsonates the
evolved aryine contained the original alkyl Intact: trJmethy.1 arsine tind
dimethyl-n-propylarsine. Zussman et al ( 54 ) reported the production
-------
-14-
of a volatile arsine by the dermatophyte Trichophyton rubrum when grown in
arsenate-containing media. Arsenite did not serve as a substrate for
arsine production. While only aerobic microorganisms have thus far been
identified in production of tzethyl arsihes, losses of arsenic by volatil-
ization from anaerobic soils have been reported (16, 41, 52). Woolson
and Kearney (52) found extensive volatilization of arsenic from aerobic
soils treated with cacodylic acid, and even greater losses from anaerobic
soils. The volatile product was considered dimethyl arsine, unstable and
readily oxidized in air to the oxide or to cacodylic acid. The ultimate
fate of the arsenic was concluded to be metabolism to arsenate and in-
activation by soil iron compounds. Oxidation of the methyl substituents
of arsenic has been reported to occur slowly in soil ( 12,47,52 ) with
liberation of C02 and arsenate..
Reduction of ferric iron associated with bacterial growth in submerged
soils may be implicated in the observed sensitivity of rice to arsenic
residues in soil from use of calcium arsenate in cotton. While no injury
of cotton occurred with use of the arsenical, frequently toxicity appeared
I
after the soil was flooded during growth of rice (41). Reduction of iron
arsenate at the low prevailing redox potential would be expected to increase
. the concentration of soluble arsenate and arsenite. Similarly, the tox-
icity of As203 used for weed control in forests of the eastern United
States was found to be greater on wet, poorly drained soils than on well
drained sites (33).
Plants generally absorb and translocate relatively small amounts of
arsenic into above-ground parts. McLean et al (36) investigated the
potential hazard of vegetable gardening on soils formerly in lawns treated
with lead arsenate for white grub control. Field plots were established
-------
-15-
on Sassafrass loam in New Jersey, with rates up to 1000 Ib of lead arsenate
i
per acre Incorporated in the -upper 4 inches of soil 7 days before plant-
ing a variety of vegetables. Arsenic analyses of the harvested produce
• i
showed less than 1 ppra As in all plants. On a former orchard site con-
taminated from arsenic sprays 10 years previously, the greatest concen-
tration of arsenic observed in vegetables was less than 2 ppm As in onion
tops, despite the soil arsenic concentration of 233 ppm. Oregon orchard
soils with arsenic contents elevated 20 to 30 times original level by
accumulated spray residue produced a variety of forage and vegetable
crops with arsenic contents increased only 1.3 to 3.0 times over those
from adjacent low arsenic soils ( • 30 ). Root portions of the plants
were more affected by soil arsenic than were tops, being increased 4-15
times over control level. However, the edible parts of plants grown in
' sprayedr-over soils contained on the average less than a tenth of the legal
tolerance for arsenic on fruits and vegetables. Williams and Whetstone
(49) determined arsenic contents of numerous plant species growing on
soils with accumulated arsenic and others without arsenic histories. In
untreated soils various vegetable and weed species contained less than
2 ppm As. In a Sassafrass sandy loam with 270 ppm AS in the upper 3
inches, orchard grass and wild carrot contained 2 ppm As or less. Mustard
was the only species containing appreciable arsenic' 34 ppm in roots
and less than 1 ppm As in tops. The arsenic contents of lawn grasses
ranged up to 2 ppm As on soils treated repeatedly with As£03 and lead
arsenate to establish levels from 150-550 ppm As in the soil over several
years. Johnson and Hiltbold (29) reported arsenic contents of field crops
grown on a sandy loam soil containing residual arsenic from methanearsonate
applications in turf. With arsenic levels in the surface soil ranging
up Lo 28 ppm As no effects on crop yields were obtained, but arsenic
-------
-16-
residues were found in harvested material. Arsenic uptake was related
to soil arsenic concentration and differed among crops. Seed of cotton
and soybeans accumulated the highest concentrations of arsenic, up to 9
ppm As. Vegetative material of sorghum was in an intermediate group,
and the winter forage legumes and grasses were in the lowest arsenic
group containing 2 ppm As or less. The low As content of corn grain
provided an interesting contrast with the oilseed crops. Differences
in arsenic uptake by warm- vs. cool-season crops was postulated to be
related to their rates of transpiration. A similar effect of season
was observed by Benson (1) with barley growing in greenhouse pot experi-
ments with arsenic-contaminated soils. Sand cultures with high rates of
lead arsenate severely curtailed the growth of barley in summer but had
little or no effect in winter. Jacobs et al (27) found the order of
crop tolerance to arsenic to be potatoes > peas > sweet corn > snap beans
grown on Plainfield sand in Wisconsin after rates up to 643 Ib As/A were
i
I
applied as sodium arsenite. While yield reduction of the latter 3 crops
occurred at arsenic concentrations of as low as 10 ppm As in this soil,
arsenic concentrations in the edible portion of these crops was less than
1 ppm As. Flesh of potato tubers contained up to 0.5 ppm As and only
the peelings showed significant arsenic contamination (up to 84 ppm As).
A subsequent survey (43) of 18 Wisconsin potato fields known to have been
treated previously with sodium arsenite as a vine killer in potatoes
showed that while arsenic levels in soil ranged from 2.2 to 25.7 ppm As,
the arsenic content of potato tuber peelings was only 0.2-2.6 ppm As
and up to 0.6 ppm As in tuber flesh. Deuel and Swoboda (11) studied the
i
yield and arsenic content of cotton and soybeans as indicators of the
toxicity of As2C>3 applied to 2 soils. While 50 Ib As/A was sufficient
-------
-17-
to decrease the vegetative growth of cotton in Amarillo fine sandy loam,
as much as 500 Ib As/A was required in the Houston Black clay. An in-
ternal arsenic concentration of only 4.4 ppm As in the plant tissue caused
a growth reduction of cotton on both soils. Only 1 ppm As in the tissue
of soybean plants induced a growth reduction.
The similarity of phosphorus and arsenic, and the possibility of
applying phosphorus to ameliorate toxicity of arsenic in soils has at-
tracted considerable attention. Hurd-Karrer (25) conducted nutrient cul-
ture experiments to determine the effect of phosphate on toxicity of
arsenic to wheat. She suggested that arsenates would be non-toxic if the
P:As ratio were more than 4:1. Results of Clements and Munson (7) sup-
ported the concept of antagonism of phosphate on arsenate absorption.
Phosphorus in culture solution was found to effectively inhibit absorption
.of pentavalent arsenic but not in reducing the toxicity of the element
within the plant. Jacobs and Keeney (26), however, found that increasing
rates of phosphorus aggravated arsenic toxicity in Plainfield sand and
resulted in increased arsenic uptake by corn. Tissue concentration of
arsenic was about 10 times higher in corn grown on Plainfield sand than
on Waupun silt loam with equal levels of applied arsenic. Similar results
were reported by Woolso^. et al (51) for the Lakeland sand and Hagerstown
silt loam. Application of phosphorus equal to arsenic in Lakeland sand
increased the toxicity to corn over that from arsenic alone. In Hagerstown
silt loam phosphate reduced arsenic toxicity. When available P and As
were determined by extraction of the soil it was found that better plant
growth was associated with P:As ratio of 6.8 than with P:As = 0. 7 or 3.3,
supporting the conclusions of Hurd-Karrer. However, increasing phosphate
resulted in increased arsenic contents of the plants despite their
i
improved growth.
-------
-18-
In summary, arsenic is an ubiquitous constituent of plants, ranging
from trace levels to perhaps 40 ppm As in certain severely injured plants.
Arsenic is not extensively translocated from roots to tops and the nature
of root injury to plants seems to preclude large uptake of arsenic. Fur-
thermore, the threshold for arsenic injury in above-ground parts of plants
is low; thus restricted growth limits arsenic.accumulation in harvested
portions. In order for most soils to sustain available arsenic concen-
trations sufficient to induce Injury, extreme ccntents of total arsenic
are usually required. Because of extensive adsorption and precipitation
in insoluble form, arsenic availability decreases rapidly in soil. Leach-
ing functions in some very sandy soils to slowly move arsenic into deeper,
more clayey subsoil. Microbiological transformations occur in both
aerobic and anaerobic soils to produce methyl arsines that probably ac-
.count for appreciable losses of applied arsenic from soils. There is no
evidence of biomagnification of arsenic in the environment.
-------
Literature Cited
1, Benson, N. R. 1953. Effect of season, phosphate, and acidity on
plant growth in arsenic™toxic soils. Soil Sci. 76:215-224.
2* "Benson, N. R. 1968. Can profitable orchards be grown on old
orchard soils? Washington.,State Hort. Assoc. Proc. 64:109-114..
3. Bird, M. L.., F. Challenger, P. T. Charlf.cn and J. 0. Smith. I94S
Studies on biological methylation. 11, Action of Moulds on
inorganic and organic compounds of aroenic. Biochem. J. 43:78-83.
4. Bishop, R. F. and D. Chesholm. 1962. Arsenic accumulation in
Annapolis Valley orchard soils. Canadian J. Soil Sci. 42:77-80.
5. Campbell, R. W. and L. R. Quinlan. 1957. Crabgrass control in
bluegrass. Proc. North Central Weed Control Conf. 14:29-30.
6. Challenger, F. 1947. Biological methylation. Science Progress
35:396-416.
7. Clements, H. F. and J. Munson. 1947. Arsenic toxicity studies
in soil and in culture solution. Pacific Science 1:151-171.
S. Cooper, H. P., W. R. Paden, E. E. Hall, W. B. Albert, W. B.
Rogers, and J. A. Riley. 1931. Effect of calcium arsenate
on the productivity of certain soil types. 44th Annual Report
S. C. Exp. Sta. 28-36.
9. Crafts, A. S. and R, S. Rosenfels. 1939. Toxicity studies with
arsenic in 80 California soi.ls. Hilgardia 12:177-199.
10. Daniel, W. H. 1953. Preventing erabgrass in turf areas. Troc.
North Central Weed Cop^rol Conf. 15:35-36,
11. Deuel, L. E. and A. R. Swoboda. 1972. Arsenic toxicity tc cotton
and soybeans. J. Environ. Quality 1:317-320.
12. Dickens, Ray and A. E. Hiltbold. 1967. Movement and persistence
of methanearsonates in soil. Weeds 15:299-304.
.13. Dorman, C. and R. Coleman. 1939. The effect of calcium arsenate
upon yield of cotton on different soil types. Jour. Amer.
Soc. Agron. 31:966-971.
14. Engel, R. E. and C. W. Bussey. 1972. The effect of three experi-
mental herbicides on control of erabgrass and turfgrass species
balance. Proc. Northeastern Weed Sci. Soc. 26:197-200.
15. Engel, R. E. and R. D. Ilnicki. 1969. Turf weeds and their
control. in_ Turfgrass Science; Hanson, A. A. and F. V. Juska,
ed. Monograph No. 14, Amer. Soc. Agron.
-------
16. Epps, E. A. and M. B. Sturgis. 1939, Arsenic compounds toxic to
rice. Soil Sci. Soc. Amer. Proc. 4:215-218.
17. Ferguson, J. F. and J. Gavis. 1972. A review of the arsenic cycle
in natural waters. Water Research 6:1259-1274.
18. Frans, R. E., C. R. Skogley, and G. H. Ahlgren. 1956. Influence
of soil type on soil sterilization with sodium arsenite.
Weeds 4:11-14. '
19. Freebprg, R. P. and W. H. Daniel. 1970. Atomic absorption to
measure arsenic rates controlling Poa annua L. Proc. North
Central Weed Control Conf. 25:84-85.
20. Gile, P. L. 1936. The effect of different colloidal soil materials
on the toxicity of calcium arsenate to millet. J. Agric. Res.
52:477-491.
21. Goetze, N. R. 1958. Poa annua control in turf. Proc. North
Central Weed Control Conf. 15:36-37.
22. Greaves, J. E. 1934. The arsenic content of soils. Soil Sci.
38:355-362.
23. Green, H. H. 1919. Behavior of bacteria towards arsenic. South
African J. Sci. 15:369-374.
24. Hiltbold, A. E. 1968. Arsenic content of cotton soils in Alabama.
Research Report, Proc. Southern Weed Conf. p. 188.
25. Hurd-Karrer, A. M. 1939. Antagonism of certain elements essential
to plants toward chemically related toxic elements. Plant Physiol.
14 :9-29.
26. Jacobs, L. W. and D. R. Keeney. 1970. Arsenic-phosphorus interactions
in corn. Soil Sci. and Plant Anal. 1:85-93.
27. Jacobs, L. W. , D. R. Keeney, and L. M. Walsh. 1970. Arsenic residue
toxicity to vegetable crops grown on Plainfield sand. Agron. J.
: 62:588-591.
• . i'
28. Jagschitz, J. A. 1970. Chemical control of Poa annua L. in turf-
grass and the effect of various chemicals on seed production.
Proc. Northeastern Weed Control Conf. 24:393-400.
29. Johnson, L. R. and A. E. Hiltbold. 1969. Arsenic content of
soil and crops following use of methanearsonate herbicides.
Soil Sci. Soc. Amer. Proc. 33:279-282.
30. Jones, J. S. and M. B. Hatch. 1945. Spray residues and crop
assimilation of arsenic and lead. Soil Sci. 60:277-288.
i
31. Juska, F. V. and A. A. Hanson. 1967. Factors affecting Poa annua
L. control. Weeds 15:98-101. i
-------
32. Keaton, C. M. and L. T. Kardos. 1940. Oxidation-reduction potentials j
of arsenate-arsenite systems in sand and soil mediums. i
Soil Sci. 50:189-207. . ' • !
!
i
33. Leaf, A. L. and R. E. Smith, Jr. 1960. Herbicidal value of arsenic j
trioxide in eastern United States. Weeds 8:374-378. j
i
34. MacPhee, A. W., D. Chisholm, and C. R. MacEachern. 1960. The ;
persistence of certain pesticides in the soil and their effect on i
crop yields. Canadian J. Soil Science 40:59-62. !
1 • ' • ' ' ' i
35. McGeorge, W. T. 1915. Fate and effect of arsenic applied as a ;
spray for wee'ds. J. Agr. Res. 5:459-463. ;
36. McLean, H. C., A. L. Weber, and J. S. Joffe. 1944. Arsenic content
of vegetables grown in soils treated with lead arsenate. J. Econ.
Entomol. 37:315-316. I
• . • i
j
37. Miles, J. R. W. 1968. Arsenic residues in agricultural soils of i
southwestern Ontario. J. Agric. Food Chem. 16:620-622. j
38. Neiswander, C. R. 1951. Duration of the effectiveness of lead
arsenate applied to turf for white grub control. J. Econ.
Entomol. 44:221-224. |
i
39. Olson, 0. E., L. L. Sisson, and A. L. Moxon. 1940. Absorption of J
selenium and arsenic by plants from soils under natural conditions. !
Soil Sci. 50:115-118.
40. Quastel, J. H. and P. G. Scholefield. 1953. Arsenite oxidation j
in.soil. Soil Sci. 75:279-285. :
i
41. Reed, J. F. and M. B. Sturgis. 1936. Toxicity from arsenic
compounds to rice on flooded soils. J. Amer. Soc. Agron. ' j
28:432-436.
I
42. Stadtherr, R. J. 1963. Studies on the use of arsenicals for crabgrass I
control in turf. Ph.D. Dissertation, Univ. of Minnesota. j
43. Steevens, D. R., L. M. Walsh, and D. R. Keeney. Arsenic residues !
. in soil and potatoes from Wisconsin potato fields - 1970. j
Pest. Monitoring J. 6:89-90. j
I
44. Stone, E. L. and T. Greweling. 1971. Arsenic toxicity in red pine !
and the persistence of arsenic in nursery soils. USDA Forest j
Service "Tree Planters Notes" Vol. 22, No. 1. •
t
45. Tammes, P. M. and M. M. de Lint. 1969. Leaching of arsenic from
soil. Neth. J. Agric. Sci. 17:128-132. j
. ' i
46. Thorn, C. and Raper, K. B. 1932. The arsenic fungi of Gosio.: Science |
76:548-550.
-------
47. Von Endt, D. W. , P. C. Kearney, and D. D. Kaufman. 1968. Degradation
of raonosodium methanearsonic acid by soil microorganisms. J. Agric.
Food Chem. 16:17-20.
48. Watschke, T. L., J. M. Duich, and D. V. Waddlngton. 1972. Evaluation
of preemergence chemicals for crabgrass control in 1971. Proc.
Northeastern Weed Sci. Soc. 26:201-203.
49. Williams, K. T. and R. R. Whetstone. 1949. Arsenic distribution in
soils and its presence in certain plants. Tech. Bui. 732 U.S.D.A.,
Washington, D. C. 20 pp.
50. Woolson, E. A., J. H. Axley, and P. C. Kearney. 1971. The chemistry
and phytotoxicity of arsenic in soils: I. Contaminated field
soils. Soil Sci. Soc. Amer. Proc. 35:938-943.
51. Woolson, E. A., J. H. Axley, and P. C. Kearney. 1973. The chemistry
and phytotoxicity of arsenic in soils. II. Effects of time and
phosphorus. Soil Sci. Soc. Amer. Proc. 37:254-259.
52. Woolson. E. A., and P. C. Kearney. 1973. Persistence and reactions
of ^C-cacodylic acid in soils. Environ. Sci. Technol. 7:47-50.
53. Youngner, V. B. and T. F. Fuchigami. 1956. Control of crabgrass
with chemicals. So. Calif. Turfgrass Culture 6:No. 4.
54. Zussmah, R. A., E. E. Vicher, and I. Lyon. 1961. Arsine production
Trichophyton rubrum. J. Bact. 81:157.
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SECTION IV
EFFECTS ON FISH AND WILDLIFE
THE THREE-YEAR PAX CRABGRASS CONTROL PRODUCT:
EFFECTS ON FISH AND WILDLIFE;BIOCONCENTRATION
Eugene H. Dustman
Introduction
In duscussing the role which the Three-Year Pax Crabgrass Controll
i
product may play in producing an effect on animal's, it is fitting to
proceed from the general to the specific. Much of the information basic
to an understanding o£ the material! in this section, or, indeed, any
portion of the Committee'3 report pertaining to environmental consider-
ations, must come from various sections of the report dealing with the
chemical and physical! characteristics of arsenic, its toxicologicasl
properties, and its effects on and behavior in soils, plants, and
animals.
throughout the course of this assignment there has been the constant
urge to extend one's self beyond the limits of the Committee assignment,
and to address the much larger problem of arsenic in the environment.
This, of course, transcends the responsibility of the Committee; therefore,,
a true and accurate assessment of conditions resulting from application
of the Pax material cannot extend much beyond the limits of the area; to
which it is applied unless other, and surely more important, sources of
arsenic and lead are considered.
Arsenic is a ubiquitous substance in our environment. It occurs
in many chemical combinations, some organic, some inorganic. It also
occurs in elemental form. Its chemical combinations under natural
conditions remain largely unidentified and poorly understood because
the current most sensitive analytical methodology does not make their
-------
separation possible. In studies of-the significance of arsenic in
animals, plants, and the biosphere generally, the literature is replete
with measurements of total arsenic; yet it is believed that the levels
ait which araenicals are bound in animal tissues is proportional to their
toxicity (25), and toxicity generally is related to the valence of the
arsenic (31).
Pentavalent arsenic is generally less toxic than the trivalent
form (U8); organic forms are generally much less hazardous than the
inorganic forms (30). Frost (19) points out that factors such as the
degree of absorption into the cells, the rate of metabolism, and the rate
of excretion vary with circumstances and cause variations in toxicity.
He uses a striking example to support the view that the levels at which
arsenicals are bound in tissues is proportional to their toxicity: At
their respective 11)50 leve^8 °f 700, 16, and 0.08 mg/kg tryparsamide,
benzenearsonic acid, and benzenearaenoxide produced similar 1 eve Its of
arsenic in rabbit tissues. The same held for other animals. He concluded
that target enzymes in the rabbit, although far more susceptible to
trivalent (benzenearsonic acid and benienearsenoxide) than to pentavalent
(tryparsamide) arsenicals, bind a similar level! of arsenic at point of
death. These differences clearly relate to the rate at which the
E
arsenicals are excreted.
Good general orientation to the subject of arsenic is to be> had by
referring to publications by Frost (19) and Schroeder and Balasaa (48).
Arsenic is found in soils, meet foods, many waters, almost all plants
and pliant products, and in most animal tissues. Two forms occur in
man's environment, pentavalent and trivalent. Biological activitie*
-------
in these valence states differ markedly. Pentavalent arsenic as arsenate
i
(inorganic arsenic acid or its salts) is nontoxic in normal concentra*-
tions, is excreted rapidly, largely through the kidneys, probably does
not accumulate to any great extent in human tissues, is a normal) constit-
i
uent of food and may (possibly) perform some physiological function.
Schroeder and Balasaa refer to it as biogenic arsenic. Most enzymes are
not inhibited by it, and it can substitute for phosphate in some
phosphorylases. Human daily intake is in the range of UOO - liOOO micro-
grams. However, as Frost (19) points out, "Although As*^' compounds are
more toxic than their As** analogues,, after autoxidation an excess of
either would be expected to intefere with phosphorous metabolism. Such
a mechanism may account for the additive toxicity of different arsenicals."
Trivalent arsenic as arsenite (inorganic arsenous acid and its- salita)
is the principal form produced commercially. It is toxic^ it chelates
woith dithiol groups and inhibits those enaymes dependent thereon. It
accumulates in animals, is a contaminant of soils and foods through ita
use in herbicides and other pesticides and performs no known physiolog-
ical function. Oxidation of trivalerit arsenic to the pentavalent form
occurs slowly in the upper layers of the earth's crust and in animals.
Various workers have either suggested of concluded that pentavaQlent
arsenicals are reduced in vivo to the toxic trivalent form (22, 27).
Until such time as this matter is resolved, there remains the fundamental
question in arsenic metabolism of whether arsenicals accumulated in body
tissues can be stored as relatively innocous residues. And of much
interest is the recent work of McBride and Wolfe referred to in Chemical
amd Engineering News (9). These workers have found that through the
-------
action of anaerobic methanobacteria arsenic is converted into the highly
i • .
poisonous dimethyl arsine, which may behave in aquatic systems in much
the same manner as methylmercury. With methyl cobalamih serving as the
methyl donor, As*-* (reduction! A»** (arsenite) (methylation) methyll
arsonic acid (reduction) dimethyl arsinic acid (As*) (reduction)
dimethyl) arsine (As )•
It has long been known that natucal arsenate may be reduced to toxic
compounds (AsH3) by heat or by the action of certain algae and molds (19,
48).
lexicological Considerations
Although many different species of animals are exposed to arsenic
when the arsenicals are released into the environment, detailed toxico—
logical! investigations have been confined largely to man, a variety of
his domestic animals, and common laboratory forms which lend themselves
well to detailed experimentation and observation. The findings made
through studies of these forms relate generally to many other forms.
Oehme (38) and Lisella et ali. (32:) offer abbreviated accounts of the
mechanisms of inorganic arsenic toxicity. Oetime's discussion occurs
under the headings "absorption", "distribution", biotransformation",
i
and "excretion".
Absorption: Certain forms of arsenic may be absorbed through the intact
skin. Necrosis and ulcerations may appear at the site of contact; amd
cell division may be inhibited and nuclear abnormalities occur. Absorp-
tion Crom the digestive tract is dependent upon solubility. Finely
divided powders are more completely absorbed than coarse ones. Gastric
juices may enhance solubility, especially the carnivores with their
-------
highly acid digestive tracts. Soluble compounds of arsenic are well
absorbed through the digestive tract and all mucous surfaces including
the lungs (by inhalation). Some victims may exhibit gastrointestinal
disturbance; others may show nervous raanisfestations.
Distribution in body: After absorption, 90 - 95% of the inorganic arsenic
is found in red blood cells in combination with hemoglobin; that in serum
is bound to proteins. Within 2H houra it rapidly leaves the blood (the
rat is a notable exception) and goes to the Liver, kidney, lung, wall of
the gastrointestinal tract, and spleen. Smaller amounts may be found in
muscle and nervous tissue. In about 2 weeks, or with continuous exposure,
arsenic will begin to build up in skin, hair, and bones. Chronically
poisoned dogs have four to six times more arsenic in hair than in liver
per unit of weight. Arsenic binds tightly to organic sulifhydryl groups
of the protein fraction of the respective tissues (enzyme inhibition)
and is only slowly released. Inorganic arsenic passes across the pHacenta
as demonstrated in the human fetus (16).
liotransformation: Widespread damage, is caused by arsenic combining
with the sulfhydryl groups of proteins. Inhibition of these enmymes
causes a breakdown in cellular metabolism. Serving as a substitute for
phosphorous, arsenic also uncouples oxidative phosphorylation in the
lliver mitochrondia, thus discouraging the production of energy. Other
enzyme systems also are affected. Though relatively stable, the thio-
arsenic compounds may be oxidised to arsenoxides and then to other
oxidation compounds.
Excretion: Inorganic arsenic is excreted mostly by the liver and the
kidneys. Most of the arsenic excreted in the urine from a single dose
-------
will appear within the first 4 days. In man, arsenic excretion begins
2. - 8 hours after exposure, and it may still be found in small amounts
after 10 days. Up to 70 days may be required for complete elimination
after repeated administration of 'arsenic. A smaller amount of arsenic
may be eliminated in feces.
Acute Toxicity of Lead Arsenate, Arsenic
Trioxide, and Certain Other Arsenicals
Lead arsenate (PbHAsO^) and arsenic trioxide (AS203> (also known as
arsenic oxide and arsenous oxide) are the principal ingredienta in the
Pax product. An examination of toxicity measurements for these compounds
is in order. Those measurements associated with certain other arsenicals:
are included for comparative purposes.
The LE>5Q method for measuring toxicity••had not been developed when
inorganic arsenicals were having their heyday as insecticides in the
early 1900's; thus the older toxicity measurements are not strictly
comparable with modern-day LDcg readings. Nonetheless, these earlier
measurements are useful and enlightening and in some instances the only
ones available. The following material summarizes some of the more
meaningful acute toxicity measurements as I was able to unearth them in
the literature. The information on domestic and laboratory forms is,
given to provide some indication of what might be expected to affect wild
animals even though distantly related.
Arsenic Trioxide
Mammals
The U)5o for tin.- rat was 385 mg/kg (283 mg, of As) when given an
-------
encapsulated dose of arsenic trioxide in a 4- grasshopper bait (59); only two of
twenty-four died, others went off feed.
The minimum lethal dose of arsenic trioxide for chickens was 75 mg/kg
-------
8
when it was mixed in fine powdered form with a food mixture (57).
Fishes
The tolerance level of pink salmon fry exposed for 3 days to arsenic
tripxide in aerated sea water-closely approximated 9.3 ppm (26). Exposure
for 10 days in aerated sea water to arsenic trioxide followed by transfer
to pure running sea water indicated a tolerance level between 2.6 and
5.3 ppm for both periods. Even after initial concentrations (method did
not employ a continuous flow system in which concentration would be held
constant) of 5.3 and 9.3 ppm had remained in aquaria for 22 days, statis-
tically significant kills resulted in less than 3 days, indicating that
danger of arsenic trioxide poisoning can persist for some time even
though the arsenic trioxide had apparently changed to a> form not detectable
by the analytical! method used.
Lead Arsenate
Mammals
The minimum lethal oral dose of lead arsenate given in pelleted
form to domestic rabbits was 200 mg/kg (40 mg of As) (8). The same dose
also killed wild hares but death was longer delayed.
The lethal dose for sheep was 3.9 g when lead arsenate was given SUB
a single oral dose. Death occurred on the 12th day CO.
Three pairs of sheep weighing 80 - 100 pounds each were fed 1, 0.5,
and 0.25 g of lead arsenate per day. The two sheep on the li g dosage
died within 7 days; one. of the sheep receiving 0.5 g/day died after 35
days; one ol Liu- animals receiving 0.25 g died at the end of 35 days. (35).
-------
Birds
The lethal dose of lead arsenate for the chicken was 0.1 - 56 g when
given in a single oral encapsulated dose (54). Death occurred over a
span of 2 - 27 days.
Sodium Arsenite
A value judgment such as the one to be made on the Pax product
should have the benefit of readings on the :«atsitivity of aquatic organ-
isms to the principal components of the material. Other than for acute
toxicity measurements on pink salmon (26) I have been unable to find
such determinations. Rather than leave such a serious void, I am includ-
ing information on acute toxicity of sodium acsenite which has been
assembled largely by Pimenteli (*5). I hasten to add, however, that
sodium arsenite, a compound commonly used for aquatic weed control, ia
more soluble than either of the Pax arsenicals and is roughly 9 to 11
times more toxic to mammals and two times more toxic to birds than
arsenic trioxide. One must take this into account as he reads the materi»-
ail given below. Sources of Pimentel's information are given.
Mammals
The LD5Q for the rat was 10 - 50 mgAg(28); and W: mg/kg (2k mg of
As) as determined by Done and Peart (17) f and for the mouse, 51 mgAg (36)
when sodium arsenite was given in single oral encapsulated doses.
The lethal dose of sodium arsenite for the white-tailed deer was
*» cc of arsenic solution when given as a single ora-l dose(*).
The. lethal dose of sodium arsenite for th« cow was 1! - * g and
tor the dog 0.05 - 0.15 g when given as a single oral dose (10).
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10
Birds
Mallard ducks tolerated 8 mg/B&y of sodium arsenite for a period in
which the total dose reached 973 mgAg in the birds (55).
The minimum lethal dose of sodium arsenite for the chicken was 37,5
mg/kg when mixed in fine powdered form with ai food mixture and given in
1
pelleted form (57).
t
Fishes
LCc for various fishes
Exposure Time
Species (hours) ... (ppm) Source
Lake emerald shiner 2* ^.5 Swabey and Schenk (51)
Spot tail minnow 2k 15 Boschetti and
McLoughlin (3)
Bluegilli Z* 58 Cope (12)
Rainbow trout 24 100 Cope (12)
Rainbow trout 48 36.5 FWPCA (20)
Bond (2) reported sodium arsenite to be safe (for fish) at dosages
of % - 4 ppm in soft waters and 5-6 ppm in hard waters..
Rainbow trout (U>50 = 60 mgAg) and bluegills (11)50 =
were relatively tolerant of sodium arsenite compared with other herbicides
i
(15).
Cope (15) reported that a dosage of 4 ppm of sodium arsenite caused
kidney and liver damage in bluegills.
Sodium arsenite applied at 5 ppm for the eradication of submergent
aqiuatic vegetation in ponds had no effect on rainbow trout or brook trout
populations (29).
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11
Molluscs and Arthropods
The minimum lethal dosages (ppm) producing a kill of fish-food
organisms exceeding 25% are the following: Daphnia, 3.0; Eucypris, 6.0;
Hyallella, 2.5; Culex, Aedes, and Anopheles, 6.0; and Chironomua, 10.0(60),
The 2.4-hour LC^Q for stonef ly nymphs (Pteronarcys calif or nica>) waa
140 ppm (47).
The 48-hour ECjQ (immobilisation value at 60 degrees F) for water-
fleaa (Simocephalius serrulaitus)and Daphnia pulex uas 1,400 ppb and
1,800 ppb, respectively (47).
Johnson (29) reported that 3 to 8 ppm of sodium arsenite killed
filamentous algae and submerged aq.uatic plants in ponds, but had no
effect on the numbers of pond invertebrates such as chironomid larvae,
beetle larvae and adults (Haliplidae),true bugs (Nodonectidae and
Dystiscidae), mayfly nymphs, damselfly nymphs, dragonfly nymphs, and
amphipods. Walker (58), however, reported that treating ponds with sodium
arsenite at dosages from 2.5 to 2.0 ppm caused ai 50% reduction of midges,
waterbugs, and snails.
The 24-hour LC^Q for stonef ly nymphs (Pteronarcys) was 1160 ppm (11).
Phytoplankton and Zooplankton
Sodium arsenite at 4 ppm did not affect the number of phytoplankton,
but did cause drastic reductions in xooplankton (14).
Lethal Residue Levels
Residue levels in tissues and organs which are indicative of
lethality are a boon to the one who is attempting to determine the cause
of. death of an animal. Unfortunately, these levels Usually do not rest
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12
within narrow limits. As a general rule of thumb, 10 to 15 ppm on ai
wet weight basis in the liver and kidney is indicative of arsenic
poisoning if clinical signs, necropsy findings, and history are compat-
ible (5). However, as Hatch and Funnell (24) discovered in their
I
studies of cattle which had died of arsenic poisoning, arsenic levels
in the liver and kidney were as low as 1.5 to 5 ppm and as high as 30
j
ppm, wet weight.
Cacodylic Acid
It has already been mentioned that inorganic arsenicals are generally
more toxic than organic arsenicals. A number of the organic compounds
are used as herbicides. They usually cause much less of an insult to
the environment because they are less toxic and less persistent than
the inorganic compounds. Toxicity data on cacodylic acid, an organic
arsenical, is presented here for comparative purposes.
Mammals
The LD50 for the rat was 1,280 to 1,400 mgAg to cacodylic acid
when this dosage was fed orally (28).
Fishes
USDI (55) reported no effect of cacodylic acid on longnose killi-
fish at 40 ppm in a 48-hour exposure test.
The U>5o f°r mosquito fish and taillight shiners approached 1,000
ppm for cacodylic acid (41). Largemouth bass, fed for 2 weeks on
mosquito fish exposed to 1,000 cacodylic acid for 2U hours, appeared
to be unaffected by the treatment.
i
Mosquito fish, largemouth bass, and taillight shiners exposed to
i
concentrations of 100 ppm of cacodylic acid for 72 hours survived well.
-------
13
Some mortality was observed when concentrations reached 6311 ppm with
am exposure time of 72 hours (HI).
Amphibians
The 48-hour LCc0 for lufo tadpoles was between 100 and 1,000 ppm
cacodylic acid (41).
Molluscs
Exposure of the eastern oyster to HO ppm of cacodylic acid for 48
hours had no noticeable effect (56).
Arthropods
Cacodylic acid at 40 ppm had no effect on pink shrimp during a 48-
hour exposure(56) .
Two species of dragonfly nymphs (Pantala sp. and Gynacantha nervosa)
exposed for up to 72 hours to 1,000 ppm of cacodylic acid, showed no
noticeable effects (41).
Chansler and Pierce (7) reported that cacodylic acid injected at the
rate of L to 2 ml per injection at 2-inch intervals around the trunk
killed bark beetles (Dendroctonus spp.). ,
Pane Product
The 11)50 for the rat was 625 rog/kS ^l29 mgAg of As) of the Pax
crabgrass control material when it was given as a single oral encapsul-
ated dose (17). This study indicated that the Pax product is more than
twice as toxic as arsenic trioxide when the comparison is made on the
basis of the mg/kg of elemental arsenic.
Horses and cows died after eating grass clippings that were taken
from lawns treated with Pax 3-year Crabgrass Control (6). Using the
Pax preparation containing arsenic trioxide at 27 percent and lead
-------
arsenate at 8 percent plus 0.2: percent heptachlor Buck (6)'determined
i
that grass clippings taken from treated plots contained arsenic levels
that were hazardous to mammals following at period of several months,
after several inches of rain and snowfall, and after the lawn had been
mowed seven times.
' Sublethal Studies
Since arsenicals are used rather freely in animal nutrition as food
additives, a number of sublethal studies have been made to make certain
that chronic effects do not attend such use. Other studies have been
made to determine sites of deposition, rates of excretion, species
differences, etc. A few of these studies will be mentioned here.
Peoples (44) added a solution of AS2C>3 to the diet of three cows
to give levels in the food of 0.0, 0.8, 4.0, and 20 ppm corresponding
to doses of 0.04, 0.20, and 1 mg/kg. During the 8-week feeding period
1^
milk, urine, and feces were analyzed. The animals were sacrificed and
tissues analyzed for arsenic and examined for pathology. No evidence of
gross or microscopic pathological changes were found in the tissues. Mo
arsenic was found in the milk, muscle, brain, or fat. Other tissues at
the highest dose in ppm were liver, 2.10; kidney, 0.90; spleen, 0.60;
skin, 0.25; intestine, 0.30; and bone, 0.16. Most of the arsenic was
excreted in the urinft; about 10% was excreted in the feces.
Groves et al. (23) fed equivalent amounts of arsenic in the form
of Lead arsenate (103.4 g) and arsenic trioxide (29.4 g) to pigs for
283 days. I'ifts were sacraficed at the end of I:lie experiment and autopsies
and tissue analyses w*>re performed. Mo pathological changes wen: noted;
tin- blood picture, appeared normal; and pig weights did not differ
-------
15
significantly. The pig fed lead arsenate contained arsenic concentra-
tions that were roughly proportional to the arsenic intake. The pig •
receiving arsenic trioxide, however, had significantly less arsenic in
the liiver, heart, spleen, and blood than the pig fed lead arsenate.
Typical of animals ingesting lead, the animal given lead arsenate
contained 25.3 ppm of lead in the liver and 192 ppm in bone. Needless
to say, animals ingesting lead arsenate receive a- double insult, both
lead and arsenic.
Cattle and horses reportedly can consume up to 2.0k g of arsenic
trioxide daily without toxic symptoms
Arsenicals and Wildlife Losses
Non-Pax Related Considerationa
Several instances of wildlife mortality or suspected mortality due
to exposure to arsenicals are recorded in the literature. In their
study dealing with the effects of arsenic-treated grasshopper bait on
chickens, Wilson and Holmes (59) prefaced their publication with a
comment on suspected wildlife mortality due to arsenic poisoning. The
grasshopper poisoning campaign in Wisconsin in 1934 resulted in the
application of more than 10,000 tons of poison grasshopper bait in
northern counties. The bait consisted of 100 g sawdust, 1 ounce whey,
)
and k g arsenic trioxide which was broadcast over the land surface for
consumption by grasshoppers. These workers mention that, a number of deer
were found dead in. the woods and around small ponds, the cause of death
not known. Also, an endemic disease appeared among the prairie chickens
which so greatly reduced the number over large areas in the grasshopper
territory th;it only n Ccw individuals could be found when the hunting
-------
16
season began. Farmers and sportsmen attributed the mortality to the
grasshopper bait.
Lilly (31), experimenting with pheasants, fed poisoned grasshopper
bait to this species and concluded that gallinaceous birds are relatively
immune to grasshopper poisoning as recommended and practiced. More
recent work with pheasants and chickens, however, has demonstrated that
these species are notorious for their ability to withstand exposure to
many pesticides, and that species vary greatly in their susceptibility to
pesticides. Such differences must be recognixed and dealt with in what-
ever assessments of effects of pesticides are attempted.
In the spring and summer of 1952, reports of unusual wildlife
mortality in certain areas in the southwestern part of the upper peninsula
of Michigan were received by state wildlife personnel (
-------
17
poisoning. The Tennessee deer had ingested treated vegetation. Use
of the arsenic acid for this purpose constituted a misuse of the material.
Delta Brand Arsenic Acid, USDA Registration No. 295-6, is approved for
use on Bermuda grass lawns to control crabgrass and Dallis grass.
An undated news release issued by the U.S. Fish and Wildlife Service's
Regional Office, Minneapolis, Minnesota*, reports a robin die-off in
south Minneapolis in which birds contained 200 mg of arsenic trioxide,
an ingredient in a; commercial weed killer. It is stated in the release
that the birds probably ate earthworms containing the arsenic material
which had been used to treat the lawns. It is further stated that 5 to
10 mg of arsenic normally would be enough to kill robins.
The Pax Product and Fish and Wildliife
. A letter requesting information on any animal mortality, domestic
or wild, terrestrial or aquatic, which could be attributed to use of the
Pax product was sent to the directors of the fish and game departments
in six western, states. Selection of the states was on the basis of theiir
' I
close proximity to the Pax formulation plant in Salt Lake City, Utah,
and the likelihood of greater use of the Pax product ait these locations.
Information from the Pax Company.on sales volume and distribution of the
product was not supplied in time to make use of it in the selection of
sites of inquiry. Of the three states responding (Nevada, New Mexico,
Wyoming), none had knowledge of animal mortality traceable to the use of
the 'Pax product.
The Pax product as formulated under Registration No. 3234-3 contains
25.11% arsenic trioxide, 8.25% lead arsenate, and 4% ammoniacal nitrogen
derived from ammonium sulfate. The recommended rate of application is
40 pounds per 2,000 square feet. At this rate, 181 pounds of arsenic
-------
18
and 43 pounds of lead are applied per acre with each treatment. For
perpetual control, instructions call for a yearly application of the
same material at a third of the initial rate or a full-rate application
every third year.
It is most unfortunate that no definitive experimental studies have .
been made to obtain information on possible haiards associated with use
of the Pax material. Reliance on chance observations is not an appropri-
ate way to evaluate possible haiards to domestic animals and wildlife.
Suitably designed studies should be conducted to detect possible hazards
if continued use of the Pax product is permitted.
Based on our knowledge of arsenicals, it seems likely that the Pax
product is contributing in some measure to the overall environmental
load of lead and arsenic; but is is not possible at this time to separate
the contribution made by the Pax material from arsenic and lead coming
from other sources. Although the two arsenicals in the Pax product are
relatively insoluble, a variety of factors will lead to a redistribution
of ait least some of the material.
Only in extremely localized and straight-line situations is it now.
possible to relate hazard to use of the Pax product. The loss of horses
and cows due to the ingestion of grass clippings taken from Pax-treated
'*
lawns is a straightforward example of cause and effect (6). Sublethal
poisoning of humans due to inhalation, skin contact, or accidental
ingestion also are readily relatable to exposure (statistics on human
poisoning assembled for the Paw; Review Committee by EPA). The fact
remains, however, that no recorded instances of wildlife losses due to
the use of the Pax product were encountered^unles* the robin mortality
in Minneapolis- was ...such an_ event. Usually, unless poisoned animals
-------
19
remain close to the scene of exposure, extremely expert sleuthing is
required to determine the cause of death. Animals poisoned by arsenic
do not succumb rapidly, thus providing ample time for movement away
from the area of exposure. This coupled with the fact that most wild
animals die without detection would make it appear unlikely that poisoned
animals would be encountered by chance. There is the distinct possibility
that soils of treated areas are rendered so free of the kinds of inverte-
brates on which birds feed (earthworms, grubs and other immature insects,
slugs, snails, etc.) that birds do not forage extensively on treated
lawns. This offers an interesting subject for research. Arsenicals
are commonly used as soil sterilants and to kill earthworms, snails, slugs,
and other unwanted invertebrate animals.
Despite the relatively in situ nature of the more insoluble arseni-
cals, one would expect movement of a portion of the arsenic and lead in
solution atnd by sediment transport. It seems likely that small ponds and
lakes within some treated areas could provide interesting experimental
situations. In his studies on the use of arsenicals for crabgrass control
in turf, Stadherr (50) mentions that the Pax material accumulated in
depressions in an irregular lawn surface and caused dead spots. There is
the distinct possibility that high concentrations of the material may be
found in these depressions and may constitute a real haxard to dogs, cats,
and various species of wildlife that may use such pools for drinking;
there is also the chance that children may, on occasion, wade and play in
such temporary puddles. This matter should be investigated.
-------
iioconcentration
l
Bioconcentration is a term used in the field of pollution ecology
to describe the accumulation of a substance in the body of an organism
which exceeds the level of intake of the substance as it occurs in the
medium in which the animal lives, or in the trophic level(s) which the
i
animal uses as a food source. Some good examples of bioconcentration are
t
to be had by referring to the organochlorine pesticides. Fish may
accumulate residues both from the water that surrounds them and from the
food they eat (1). Cutthroat trout exposed once monthly to a 30-
minute bath in waiter containing 0.3 and 1.0 ppm of DOT had 4 - 6 ppm
in their bodies after 6 to 8 treatments; this represents an increase of
4 - 20 times. Fathead minnows exposed to water containing 0.000015 ppm
of endrin had total body concentrations 10,000 time the amounts in the
water (37). Woodcock fed earthworms containing about 3 ppm accumulated
approximately four times this amount in their bodies in 2 months. Those
fed earthworms containing about 3 ppm accumulated about four times this
amount by the time of death 16 — 52 days later (51). Starting with a>
DDT level in the soil of 9.9 ppm, it reached 1*1 ppm in earthworms and
444 ppm in robins (45)r a quite simple food chain that proved to be
devastating to the robins where DDT was being used to control Dutch elm
disease. ' .
Bioconcentration of Arsenic
In ponds treated by Dupree (18) with sodium arsenite at 4 ppm, the
arsenic concentrations in plankton reached a peak of 6,955 ppm arsenic
trioxide within 27 days after treatment. In two other'ponds that received
8 ppm AsoOj in 1955 and 4 ppm As^O* in 1956, plankton reached a peak of
-------
2-1
8,200 ppm AS2Q- within Ul days after treatment. Sixeable amounts of
arsenic were retained by the bottom muds.'
Cope (13) reported that bluegill concentrated sodium arsenite in a
i
few days from a level of 0.69 ppm in the water to 11.6 ppm in adult
bl'uegills. ; •
Macek (3U) in discussing biological magnification of pesticides
i
in food chains expresses the view that the majority of the herbicides
do not meet the prerequisites for biological magnification, although it
appears that inorganics, such as sodium arsenite, could possibly undergo
biological magnification.
laensee et all. (unpublished manuscript) studied the distribution
Ik
of C labeled cacodylic acid (CA) and dimethylarsine (DMA) among aquatic
organisms in a model ecosystem and concluded that the lower food chain
organisms (algae and Daphnia magna) bioaccunulated more CA and DMA than
did higher food chain organisms (snails and fish). "Amounts accumulated
indicate that CA and DMA do not show a high potential to biomagnify in
the environment. An increase in biomass (primarily algae) over 32 days
largely accounted for a gradual loss of DA and DMA from solution.
Equilibrium between each organism and the external solution was more
important in determining CA bioaccumulation than consumption of one food
chain organism by another." It should be noted that these workers make m
distinction between the arsenic acquired from the water (bioaccumulation)
l .
and the arsenic acquired from the ingestion of the food chain organisms.
Many workas do not make this separation in deal ing with bioconcentration
because it is difficult to determine the manner in which body burdens of
a substance have been acquired.
-------
22
Quite obviously the subject of arsenic bioconcentration needs more
study. On the strength of what is known on this subject to date, it
appears reasonable to subscribe to the idea that arsenic does bioconcentrate
in some animals. Some of the. arsenicals are qjuite persistent in soilsj
some are rather readily taken up and stored by plants and animals in
fairly good quantity; arsenic is readily recycled; what few species of
animals have been studie4 to date, there is evidence of some differences
in sites of storage, degree of binding in tissues and organs, and rates
of excretion. These characteristics coupled with the investigation of a;
variety of species and ecological situations yet untouched will undoubtedly
bring to light a number of deviants.
-------
23
LITERATURE CITED
1. Allison,, D. J., J. Kaillman, 0. B. Cope, and C. Van Valen.
Some chronic effects of DDT on cutthroat trout. Bur. Sport
Fish, and Wildl. Res Rpt. No. 64.
2. Bond, C. E. 1960. Weed control in fish ponds. Oregon Weed
Conf., Proc. 21:25-2,7.
3. Boschetti, M. M. and T. F. McLoughlin. 1957. Toxicity of sodium
arsenite to minnows. Sanitalk 5:14-18.
4. Boyce, A. P. and L. J. Verme. 1954. Toxicity of arsenite debarkers
to deer in Michigan. Mich. Dept. Cons., East Lansing, Mitneo.
Rpt. 8pp.
5. Buck, W. B. 1970. Diagnoses of feed-related toxicoses. J. Am.
Vet. Med. Assoc. 156(10) U434-1443.
6. Buck, W. B. 1972. Hazardous arsenical residues associated with
the use of a lawn crabgrass control preparation. Special—repert_ ,t
prepared fo~r use by "the Pax Review-GemBvittee-j-l-lpp. ),-^Jf^rt^—, /•>•*•-"
/
7. Chansler, J. F. and D. A. Pierce. 1966. Bark beetle mortality in
trees injected with cacodylic acid (herbicide). J. Econ. Ent.
59:1357-1359.
8. Chappellier, A. M. and M. Raucourt. 1936. Les traitements
insecticides arsenicaux. Sont-ils dangereus pour le gibier
et pour les animaux la ferme? Ir± Annales des Epephyties et de
Phytogenetique 11(2):191-239.
9. Chemical and Engineering News. 1971. Trace metals: unknown,.
unseen,pollution threat. Chem. Eng. News, July 1971: 29,30,33.
10.. Clarke, E. G. C. and M. L. Clarke. 1967. Garner's Veterinary
Toxicology. 3rd ed., Williams and Wilkins, Baltimore, p44-54.
11. Cope, 0. B. 1965a. Some responses of fresh-water fish to
herbicides. Southern Weed Conf., 8:439-445.
12. Cope, 0. B. 1965b. Sport fisheries investigations, p51-63. I_n
Pesticide Wildlife Studies, U.S. Fish and Wildlife Service
Circ. 226.
13. Cope, 0. B. 1966. Contamination of fresh-water ecosystem by
pesticides. J. Appl. Ecol. 3(Supplement on pesticides in
the environment and their effects on wildlife): 33-34.
-------
24
14. Cowell, B. C. 1965. The effects of sodium arsenite and silvex on
the plankton populations in farm ponds. Trans. Amer. Pish. Soc.
94:371-377.
15. Crosby, B. C. and R. K. Tucker. 1966. Toxicity of aquatic
herbicides to Daphnia magna. Science 154:289-291.
16. Curry, A. S. 1972. Advances in forensic and clinical toxicology.
Chemical Rubber Co. Press, Cleveland, Ohio, p!85-190.
17. Done, A. K. and A. J. Peart. 1971. Acute toxicities of arsenical
herbicides. Clinical Toxicol. 4(3):343-355.
18. Dupree, H. K. 1960. The arsenic content of water, plankto'n, soil,
and fish from ponds treated with sodium arsenite. Proc. South-
east. Assoc. Game and Fish Commissioners: 132-137.
19. Frost, D. V. 1967. Arsenicals in biology - retrospect and
prospect. Fed. Proc. 26(1) .-194-208.
20. FWPCA. 1968. Water quality criteria. Report of the Nat'l Tec.
Adm. Comm. to Seer, of the Interior, Fed. Water Pollution
Control Adm. USDI 234pp.
21. Gallagher, B. A. 1918. Experiments in avian toxicity. J. Amer.
Vet. Med. Assoc. 54:337-356.
22. Goodman, L. S. and A. Gilman. 1965. The pharmacological) basis
of therapeutics. Macmillan Co., N.Y.
23. Groves, K., E. C» McCulloch, and J. L. St. John. 1946. Relative
toxicity to swine of lead arsenate, lead acetate, and arsenic
trioxide. J. Agr. Res. 73:159.
24. Hatch, R. C. and H. S. Funnell. 1969. Inorganic arsenic levels in
tissues and ingesta of poisoned cattle: an eight-year survey.
Can. Vet. J. 10(5) :117-l2aO.
25. Hogan, R. B. and H. Eagl'e. 1944. The pharmacological basis for the
widely varying toxicity of arsenicals. J. Pharmacol. Exper.
Therap. 80:93-113.
26. Holland, G. A., J. E. Lasater, E. D. Neumann, and W. E. Eldridge.
1964. Toxic effects of organic and inorganic pollutants on
young salmon and trout. Res. Bui. No. 5, Dept. of Fisheries,
State of Wash., 264pp.
2J. Hood, R. D. and S. L. Bishop. 1972. Teratogenic effects ot
sodium arsenite in mice. Arch. Environ. Health 24(l):62-65.
-------
25
2:8. House, W. B., L. H. Goodson, H. M. Gadberry, and K. W. Dockter.
1967. Assessment of ecological effects of extensive or repeated
use of herbicides. Defense Documentation Center, Defense Supply
Agency. AD0824314. U.S. Dept. Com. Nat. Bur. Standards, Inst.
Appl. Technol. 369pp.
29. Johnson, M. G. 1965. Control of aquatic plants in farm ponds in
Ontario. U.S. Fish and Wildl. Serv., Progr. Fish Culturist 27:23-30.
30. Kerr, K. M., J. W. Cavett, and 0. L. Thompson. 1963. The toxicity
of an organic arsenical, 3-Nitro-^-hydroxyphenolarsonic acid.
Toxicol. Appl. Pharmacoli. 5:507525.
31. Lilly, J. H. 1940. The effect of arsenical grasshopper poisons
upon pheasants. J. Econ. Ent. 33(3):501-505.
32. Lisella, F. S., K. R. Long, and H. G. Scott. 1972. J. Environ.
Health 34(5):511-518.
33. Loy, H. W., S. S. Schiaffino, and W. B. Savchuck. 1961. Determination
of arsenic valence by microbiological assay. Ann. Chem. 33(2):
283-285.
34. Macek, K. J. 1970 Biological magnification of pesticide residues
in food chains. _In Proc. Sympos. on the Biological Impact of
Pesticides in the Environment, Environmental Health Services
Center, Oregon State University, Corvallis, p!7-2l.
35. McCulloch, E. C. and J. L. St. John. 1940. Lead arsenate poisoning
of sheep and cattle. J, Amer. Vet. Med. Assoc. 96:321-326.
36. Meliere, K. A. 1959. Cacodylic acid. U.S. Army Engineering
Command, Army Chemical Center (Maryland) ENCR No. 34, June 1959,
AD 318 626.
37. Mount, D. I. and G. J. Putnicki. 1966. Summary report of the 1963
fish kill. Trans. 31st N. Amer. Wildl. and Natural Resources
Conf.:177-184.
38. Oehme, F. W. 1972. Mechanisms of heavy metals toxicities. Clinical
Toxicol. 5(2):151-167.
39. O'Kane, W. C., C. H. Hadley, Jr., and W. A. Osgood. 1917.
Arsenical residues after spraying. New Hamp. Agr. Exper. Sta.
Bui. 183, 62pp.
40. Oliver, E. T. 1966. An ecological study of the effects of certain
concentrations of cacodylic acid on selected fauna and flora.
Dept. of the Army, Fort Detrick, CDTL45644.
41. Oliver, K. H., G. H. Parsons, and C..T. Huffstetler. 1966. An
ecological study on the effects of certain concentrations of
cacodylic acid on selected fauna and flora. Air Proving Ground
Center. Air Force Systems Command, USAF, Eglin Air Force Base,
Fla. 25pp.
-------
26
42. Overby, L. R. and R. L. Frederickson. 1963 Metabolic stability
of radioactive arsanilic acid in chickens. J. Agric. Fd. Chera.
11:378-381.
43. Packman, E. W., D. D. Abbott, and J. W. E. Harrison. 1961. . The
acute oral toxicity in raits of several diet-arsenic trioxide
mixtures. J. Agr. Fd. Chem. 9(*O :271-272.
44. Peoples, S. A. 1962. The metabolic fate of arsenic trioxide in
the lactating bovine. Fed. Proc. 21(2):183.
45. Pimentel, David. 1971. Ecological effects of pesticides on non-
target species. Office of" Science and Technology, Wash., D. C.,
220pp.
46. Reeves, G. 1. 1925. The arsenical poisoning of livestock. J. Econ.
Ent. 18(1):83-90.
47. Sanders, H. 0. and 0. B. Cope. 1968. The relative toxicities of
several naiads of three species of stoneflies. Limnol. Oceanogr.
13:112-117.
48. Schroeder, H. A. and J. J. Balassa. 1966. Abnormal trace elements
in man: arsenic. Arsenic News No. 15: Arsenic Development
Committee 26. Rue La Fayette, Paris 9, 16pp.
49. Seddon, J. R. and A. A. Ramsay. 1933. Toxicity of certain arsenic
and lead compounds for sheep. New South Wales Dept. Agr., Vet.
Res. Rpt. No. 6. 113pp.
50. Stadherr, R. J. 1963. Studies on the use of arseriicals for
crabgrass control in turf. Doctoral Thesis, university of
Minnesota, 117pp.
51. Stickel, W. H., D. W. Hayne, and L. F. Stickel. 1965. Effects of
heptachlor contaminated earthworms on woodcocks. J. Wildl.
Mgmt. 2:9:132-1U6.
52. Swabey, J. H. and C. H. Schenk. 1963. Studies related to the use
of algacides and aquatic herbicides in Ontario. Aquatic Weed
Control Soc. Meeting, Proc. 3:2iO-28.
53. Swiggart, R. C., C. J. Whitehead, Jr., A. Curley, and F. E. Kellog.
1972. Wildlife kill resulting from the misuse of arsenic acid
herbicide. Bui. Environ. Contain, and Toxicol. 8(2) :122-128.
54. Thomas, E. F. and A. L. Shealy. 1932. Lead arsenate poisoning in
chickens. J. Agr. Res. 45(5):317-319.
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27
55. USDI. 1963. U.S. Dept. of the Interior. Pesticide Wildlife
Studies, Circ. 199.
56. USDI. 1966. Bureau of Commercial Fisheries Biological Laboratory.
Bio-assay screening tests on cacodylic acid (Gulfbreeze, Fla.),
Jan. 1966.
57. Van Zyl, J. P. 1929. On the toxicity of arsenic to fowls. 15th
Annual Rpt. of the Director of Vet. Services, Union of S.
Africa: 1189-1202.
58. Walker, C. R. 1962. Toxicological effects of herbicides on the
fish environment. Ann. Air and Water Poll. Conf. (Nov. 12, 1962,
Columbia, Mo.), Proc. 8:17-3U.
59. Wilson, H. F. and C. E. Holmes. 1936. Effects on chickens of
arsenic in grasshopper bait. J. Econ. Ent. 29(5):1008-101U.
60. Zischkale, M. 1952. Effects of rotenone and some common herbicides
on fish-food organisms. Field Lab. 20:18-2U.
-------
SECTION V
TOXICOLOGY
PAX ADVISORY REPORT, SECTION ON TOXICOLOGY
All arsenical compounds are capable of causing injury,to the
animal or human organism. What is not generally understood is the
variation in the toxic potential of the many compounds contained within
the arsenic spectrum. As a rule, inorganic arsenicals are more toxic
than the organics and trivalent forms are more toxic than the pentavalents.
Notwithstanding the well established poisonous nature of arsenic, both
trivalent and pentavalent forms have been used as therapeutic agents in the
treatment of syphilis and certain parasitic diseases with beneficial effects.
Modern application in this regard has replaced arsenicals with more
1,2
efficient and less toxic medicaments.
TOXICOLOGY
Toxic agents induce their effects by physical or by chemical or,
physiologic (enzymatic) mechanisms or sometimes by a combination of
the above. The two fundamental considerations are the action of the
intoxicant on the host and the reaction of the host to the intoxicant. Allied
factors that influence toxic response are: route of entry, dose, particle
size, solubility of the material, and individual susceptibility. Just how
trivalent arsenicals exert their action on the animal organism is not
completely understood, but certain views are held. For example, it is
believed that one of the ways trivalent arsenicals (certain forms more
than others) exert their toxic effect is by inhibiting the pyruvate oxidase
system which is essential for energy transformation within culls. There
is also experimental evidence that certain enzymes, d-amino oxidase,
-------
2.
2-glutamic acid oxidase, monoamine oxidase, and transaminase.are
inhibited in various degrees by trivalent arsenicals; whereas other
enzymes are inactivated. Those enzymes which contain sulphydryl
1, 4, 5
groups are highly susceptible to the action of arsenic. ' ' Wadkins
states that arsenic is also capable of uncoupling oxidative phosphorylation
5,6
in liver mitochondria, thus interfering with ATP formation.
Both of the arsenicals contained within the herbicide product
being reviewed are well known compounds to industry and agriculture.
Arsenic trioxide is a by-product of nonferrous arsenic containing ores
and is encountered in certain insecticides, weed killers, poison baits,
glass making, enamels, alloys, taxidermy, wood preserving, and metal
smelting. Considerable exposure to this compound can occur in the
smelting of lead, copper, cobalt, tungsten, and gold ores containing
metallic arsenic. Smelter workers can experience absorption of
arsenic by way of inhalation, ingestions and skin contact as can be
demonstrated in elevated urinary values for arsenic. Rarely, however,
do these exposures produce signs and symptoms of an acute arsenical
intoxication. The major problems reported in such workers by Pinto et
7 '8
al in the United States and Holmquist in Scandinavia have been related
to manifestations ranging from mild to moderate dermatoses, 'including
primary irritation of the mucous membranes of the nose, mouth and eyes.
Nasal perforation is not unusual. Holmquist's most extensive and careful
study of the cutaneous lesions caused by arsenic trioxide in industry
-------
3.
showed that contact dermatitis was by far the most common ailment
observed among these workmen. He described cutaneous changes as
eczematous dermatitis, toxic dermatitis and combinations of the above.
9
Birmingham et al in 1964 observed similar skin lesions, including
ulcerative changes of skin folds, among the workmen and several
children who lived in a western mining community where arsenic trioxide
from the smelter became a plant and community pollution problem.
Skin changes caused by arsenic trioxide are largely primary
irritant in nature, with a small percentage resulting from allergic hyper-
9
sensitivity. Industrial experience with arsenic trioxide has been generally
good because of hygienic practices as ventilation controls, daily change of
work clothing, use of respirators, and daily showering. Even in plants
with poor hygiene, acute intoxication from inhalation or skin contact with
10
arsenic trioxide is rare.
Acute intoxication from arsenic trioxide generally arises from
./"'*-•
*7-*li
accidental or purposeful ingestion. Clinical signs, symptoms and severity
• ;*.*'
usually parallel the dose, but individual susceptibility can vary. The
affected animal or human, depending upon the dose, displays a variable
time of onset of gastrointestinal signs characterized by dryness and
irritation of the oral cavity, difficulty in swallowing, severe abdominal
pain, nausea, wretching and vomiting, followed by profound diarrhea
similar to that observed in cholera. Direct action of the intoxicant upon
the blood vessels in the bowel induces blood-streaked stools, severe
-------
4.
i
dehydration, exhaustion, and shock. The basic lesion is associated with
increased permeability and dilitation of the small arterioles and capil-
laries. Toxic dosage of trivalent arsenic varies considerably, but it is
highly dependent upon solubility, particle size and, obviously, the
amount ingested. Chronic arsenical intoxication can be expressed in a
number of clinical displays which include gastrointestinal and neurological
effects, kidney and liver damage, and melanosis or pigmentation of the
1,2,4,11
skin. These problems have been surprisingly uncommon in
industry, even in plants where preventive practices were absent.
As to the toxicity assessment of the product in question, both
arsenic trioxide and lead arsenate have a lower order of solubility.
Nevertheless, they are capable of causing toxic effects if sufficient expo-
12
sure occurs. Sollman quoted 0.2 to 0. 3 grams of trioxide as a fatal
dose. Thienes and Haley refer to the fatal dose of arsenic trioxide as
14
approaching 0. 1-0. 2 grams. Done has correctly pointed out the lack
of precise toxicity information associated with arsenicals in general and
trioxide in particular. For example, the LD-50 information may range
15
from 9 to 39 to 500 mg. /kg. Hueper and Payne reported no significant
adverse effects in rats and mice fed 34 p. p.m. of arsenic trioxide in
water for a period of 24 months. Hatch and Funnel state that in cattle
the oral lethal dose of arsenic trioxide is 15 to 45 grams, whereas the
lethal dose of sodium arsenite is 1-4 grams. Calvary et al performed
feeding experiments using dogs to study the chronic effects oi lead acetate,
-------
5.
lead arsenate, and arsenic trioxide. He fed the lead acetate at three
levels, 12. 8, 38.4 and 64 mg. of added lead per kg. of diet; lead
arsenate was fed at 64 mg. /kg. of diet; and arsenic trioxide at two levels,
26. 8 and 107. 5 mg. /kg. of diet. All of the dogs fed arsenic diets
survived. Of 20 dogs fed on different levels of lead, 15 died of lead
poisoning.
14
Done and Peart compared the toxicity of sodium arsenite to
that of arsenic trioxide and an organic arsenical administered to young
rats. This work was done partly because of the lack of information
dealing with comparative acute toxicity data of various herbicides in
experimental animals. They ascertained from their work the following
LD-50s: Sodium arsenite - 42 mg. /kg. , arsenic trioxide - 385 mg. /kg. ,
PAX product - 156 mg. /kg., lead arsenate - 344 mg. /kg., and calcium
arsenate - 100 mg. /kg. These results are in general agreement with the
arsenic poisoning information compiled from (1) The National Clearing
House for Poison Control Centers; (2) Pesticide Regulation Division
accident files; (3) Summary of 62 pesticide accidents investigated (1963-
1966) by Plant Pest Control Division. From 1939 to 1967 there were 184
c'ases involving 202 victims of which 39 fatalities were attributed to
arsenic. Twenty-four of these were due to sodium arsenite; seven to
arsenic trioxide; one to lead arsenate; and seven to other undetermined
arsenical compounds. Three of the 39 cases were suicides. 'All of the
poisonings were due to ingestion. None of the fatalities was attributed
-------
6.
to the product in question or to the more potent ^herbicides marketed by
;
19
the company at that time. In Arsenical Poisoning Informational Data,
January '68-September "72, compiled by the Accident Investigation
Section of the Office of Pesticide Programs (October '72), 29 deaths
were reported. During this same period, PAX Crab Grass Control was
the cause of fatal ingestions in five horses, five cattle and bees. The
cattle and equine fatalities resulted from having fed the animals lawn
clippings which had been treated with PAX crab grass arsenical. From
the data presented by the Poison Centers, including Dr. Done's material
from USDA, it appears that PAX has not caused any human fatalities,
but it has been involved in nonfatal illness of humans and several deaths
in livestock. The 1969 episode involving the death of five horses which
had eaten PAX treated grass has been fully described by Buck in a com-
20
munication obtained for this committee. Postmortem findings in two
of the horses showed arsenic in the liver, kidneys and stomach. Post-
mortem findings were also described in cows -which had eaten grass
clippings from a lawn treated with PAX some five to six months earlier.
Further investigation was conducted by Buck in which PAX treated grass
clippings were fed to a young calf which died in 27 hours. The* arsenical
content of grass clippings in the liver, kidney and rumen were chemically
validated in the laboratory. Two rabbits fed grass clippings from a PAX
treated lawn also suffered fatal toxic effects and showed arsenic in the
liver, kidney, stomach contents and feces.
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7.
j
21
A critique of this report submitted by B. R. Ellison, Research
Director of the PAX Company, took strong issue with severa} statements
made in the Buck report. In short, the company did not accept the
<• /
diagnosis of arsenical intoxication in the horses examined at autopsy.
HAZARDS TO USERS AND APPLICATORS
Most sources of toxicologic data agree that arsenic trioxide and
lead arsenate have a lower toxic potential than several other arsenical
compounds. Up-to-date evidence of the effects of lead arsenate in humans
22
was presented in a cohort study by Nelson et al involving orchard
workers in Wenatchee, Washington, with variable lead arsenate exposure
indices. The study was conducted on 1, 231 individuals who had partici-
pated in a 1938 morbidity survey by the USPHS of the exposure effects of
lead arsenate spray used on the apple trees. Classification included spray
exposure, duration, age and sex. The orchardist group had the highest
exposure; a consumer group had no direct exposure. A third group had
intermediate exposure. Over 97% of the original group was located. For
all study members combined, the standard mortality ratio was 70%. The
cohort group experienced less mortality than the Washington average.
The product in question is considerably lower in arsenic content
than was the case with the other PAX products which poisoned the
animals and which recently have been withdrawn. None the less, the
present product is quite capable of providing toxic insult and tloes constitute
a'hazard where children and pets may have access to it if stored in garages,
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8.
basements, out buildings, barns, etc. The actual application of PAX
Crab Grass Control as prescribed does not constitute a formidably toxic
potential, be cause inhalation and ingestion factors would be minimal.
Body contact while applying the mixture should be avoided, but systemic
toxicity from body contact is not probable. Cutaneous effects.as contact
dermatitis, irritant folliculitis, pyodermas, and ulceration of the body
folds, including the finger and toe webs, could occur if the trioxide is not
removed from skin a few hours after application. Twenty-five percent
arsenic trioxide is entirely capable of producing skin ulcerations, but
the chemical must remain on the skin for several hours. This irritant
propensity is enhanced by the action of sweat.
When the applicator waters in the material, some contact through
displacement onto the applicator's clothing and footgear could occur, but
this does not appear to be a major problem.
HAZARDS TO THE PUBLIC '
It is unlikely that treating plots of land with PAX Crab Grass
Control product would cause systemic toxicity from airborne pollution
with arsenic. It is conceivable that adults or children walking barefooted
in the freshly treated plot and failing to wash soon thereafter could develop
primary irritant ulcerative effects on the skin, particularly b'etween the
toes. This situation was observed in several children in the arsenic
9
pbllution episode in Nevada by Birmingham et al. Further relevant
reference has occurred iti reports from the company under the term
-------
9.
"PAX paws, " as noted in dogs. Such ulcerative phenomena probably
result from the trioxide granules being held in the crevices of the paws.
It is conceivable that a pet could be poisoned from licking its contami-
nated feet, however, the amount involved is small indeed and when this
fact is added to the low solubility and large particle size of the arsenic
^diminishes the chance of systemic effects by this route.
The possibility of children ingesting candy or food which has
been dropped on a treated plot does exist. However, the amount of
*
arsenic which would adhere to an edible material seems insufficient to
warrant great concern.
If it is true, as has been stated, that animals are attracted to
arsenic then it is possible that they could lick or eat the freshly treated
grass with possible ill effects. It has also been stated that the bovine
species is attracted to soil containing arsenic.
COMMENTS
A review of the literature dealing with arsenic, its effects on
pathophysiology, its toxicologic and clinical signs in the animal and
human organism has been made. There seems to be little question
that the two arsenicals used in the PAX Crab Grass Control product
are capable of causing toxicologic response. However, data from Poison
Control Centers, the U. S. Department of Agriculture and other informa-
tional centers have not validated any human fatality from this product.
Animal fatality allegedly has resulted from feeding PAX treated grass
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10.
c\ppings to the livestock. Animals fed PAX treated lawn clippings
under controlled observations did succumb to arsenical intoxication.
The potential hazard to children and pets associated with storing such
products around the house is significant. The possibility of applicators
and the public developing ill effects from this material are remote,
though not impossible. It is conceivable that children and adults could
develop irritant reactions on the skin by walking barefoot or by lolling
around on treated grass while wearing a minimal amount of clothing.
It is already known that dogs can develop ulcerations of the paws because
of the action of the arsenic trioxide, but there was no evidence in the
literature that the dogs died from having experienced such exposures.
As to the question of young children ingesting candy or food which had
been dropped on freshly treated plots, it is unlikely that enough arsenic
would be taken in to be of serious consequence. A remote hazard should
be recognized in the case of the child afflicted with pica, since he might
ingest soils containing high amounts of the freshly treated area.
After reviewing Dr. Buck's excerpt of his paper dealing with
the crab grass control product, one is convinced of his strong feelings
concerning arsenic herbicides in general and the product in particular.
The episodes he described were unfortunate and, indeed, uncalled for;
but they did happen. In Mr. Ellison's rebuttal, I share his criticism
concerning the analytical data presented by Dr. Buck, but found it dif-
ficult to readily agree that the animals probably died from an arsenical
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11.
other than PAX.
As far as safety and health is concerned, it would be preferable
if all arsenicals were used under stricter controls. Even that system,
however, would not remove all of the problems associated with economic
poisons. It is unfortunate that we have to rely on potentially lethal
materials to manage crab grass. However, since their use is permitted
in certain areas of the country and in view of the scientific evidence
available, I find it unwarranted to selectively eliminate this product for
the purpose intended while permitting use of other agents with equal or
more toxic potential.
Donald J. Birmingham, MD
5-8-73
DJB vp
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BIBLIOGRAPHY
1. Buchanan, W. D. Toxicity of Arsenic Compounds. New York:
Elsevier Publishing Company, 1962.
2. Bennett, I. L. , Jr. , and Heyman, A. Heavy Metals. In Principles
of Internal Medicine (5th ed). Harrison, T. R. , et al (eds). New
York: McGraw-Hill Book Company, 1966, pp. 1405-1408.
3. Stokinger, H. E. Section III. Mode of Action of Toxic Substances.
In Occxipational Diseases--A Guide to Their Recognition. Gafafer,
U. S. Public Health Service Publication No. 1097. Washington, D. C. :
U. S. Government Printing Office, 1964.
4. Goodman, L. S. , and Gilman, A. The Pharmacological Basis
of Therapeutics (2d ed). New York: MacMillan Company, 1958.
5. Oehme, F. W. Mechanisms of Heavy Metal Toxicities. Clinical
Toxicology 5(2): 151-167, 1972.
6. Frost, D. V. Arsenicals in Biology--Retrospect and Prospect.
Fed. Proc. 26: 194-207, 1967.
7. Pinto, S. S. , and McGill, C. M. Arsenic Trioxide Exposure in
Industry. Industrial Medicine and Surgery 22: 281-287, 1953.
8. Holmquist, I. Occupational Arsenical Dermatitis. Acta Dermato-
Venereol. (Stockholm) 31 (Suppl. 26): 1-214, 1951.
9. Birmingham, D. J. , Key, M. M. , Holaday, D. A. , and Perone,
V. B. An Outbreak of Arsenical Dermatoses in a Mining Commu-
nity. Arch. Derm. 91: 457-464, 1965.
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10. Pinto, S. S., and Bennett, B. M. Effect of Arsenic Trioxide
Exposure on Mortality. Arch. Environmental Health 7(5): 583-
491, 1963.
11. Vallee, B. L. , Ulmer, D. D. , and Wacker, W. E. C. Arsenic
Toxicology and Biochemistry. AMA Arch. Industrial Health 21(2):
132-151, I960.
12. Sollman, T. H. A Manual of Pharmacology and its Application
to Therapeutics and Toxicology (8th ed). Philadelphia: W. B.
Saunders Company, 1957.
13. Thienes, C. H. , and Haley, T. J. Clinical Toxicology (5th ed).
Philadelphia: Lea & Febiger, 1972.
14. Done, A. K. , and Peart, A. J. Acute Toxicities of Arsenical
Herbicides. Clinical Toxicology 4(3): 343-355, 1971.
15. Hueper, W. C. , and Payne, W. W. Experimental Studies in
Metal Carcinogenesis: Chromium, Nickel, Iron, Arsenic. Arch.
Environmental Health 5; 445-462, 1962.
16. Hatch, R. C. , and Funnell, H. S. Inorganic Arsenic Levels in
Tissues and Ingesta of Poisoned Cattle: An Eight-Year Survey.
Canadian Vet. J. 10(5): 117-120, 1969.
17. Calvery, H. O. , Laug, E. P. , and Morris, H. J. The Chronic
Effects on Dogs of Feeding Diets Containing Lead Acetate, Lead
Arsenate, and Arsenic Trioxide in Varying Concentrations.
J. Pharm. & Exper. The rap. 64: 164-387, 1938.
-------
18. Arsenic Poisoning Information. Compiled from (1) National
Clearing House for Poison Control Centers, (2) Pesticides
Regulations Division Accident Files, (3) Summary of 62
Pesticide Accidents Investigated (1963-1966) by Plant Pest
Control Division.
19. Arsenical Poisoning Information. Compiled by Accident
Investigation Section, Office of Pesticide Programs, October
12, 1972.
20. Buck, W. B. Hazardous Arsenical Residues Associated with the
Use of a Lawn Crabgrass Control Preparation.
21. Ellison, B. R. A Critique of a Report Prepared by Dr. W. B.
Buck, entitled "Hazardous Arsenical Residues Associated with
the Use of a Lawn Crabgrass Control Preparation. " March 19,
1973.
22. Nelson, W. C. , Lykins, M. H. , Mackey, J. , Newill, V. A.,
Finklea, J. F., and Hammer, D. I. Mortality Among Orchard
Workers Exposed to Lead Arsenate Spray: A Cohort Study.
,->
J. Chron. Pis. : 105-118, 1972.
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Discussion
Despite the fairly exhaustive reading and literature research
conducted in our brief span of study of the PAX Company problem, and
considering arsenic history and attitudes toward "arsenic", it would
be surprising if the committee had reached unanimous agreement. In the
first place, it is very clear that the arsenicals involved are quite
toxic to animals and to man if injested in sufficient quantity. There
is also the tendency to enact laws and regulations to try to protect
individuals against the misuse of pesticides and other agricultural
chemicals. The fact that tolerances for arsenic in foods seem to be
almost a part of our culture must also be taken into consideration. On
the other side of the argument, there stands the strong evidence that
inorganic arsenicals play little understood positive roles in biology,
*
possibly as a catalyst for phosphorylations in animals (30) and in
photophosphorylations in plants (31). If ostracized, there will be
little or no incentive to learn more of the benefits inherent in their
safe uses.
Although used successfully as a persistant soil sterilant by
Crafts and Rosenfels (32), without hazard to wild or domestic animals,
the value of arsenic trioxide in horticulture did not end there. The
surprising discovery was made separately that lead arsenate and/or
arsenic trioxide at somewhat lower levels had remarkable value to repress
the germination of crabgrass seed when used at the soil surface. Reports
by McNulty and Rhodes (33) brought this to the attention of the Utah
Cooperative Association, leading finally to the development of a patented
combination of arsenic trioxide with lead arsenate (3). The Utah Co-
operative Association then established the PAX Company to market this
product, which went through many experimental improvements, all regis-
tered for use by the U.S. Dept. of Agriculture. PAX Three-Year Crabgrass
Control products were sold mainly for use on home lawns and were handled
by hardwear and garden stores. In some cases PAX found use on golf
courses. That the product appeared trouble-free and satisfied its buyers
for about 20 years is evident from the testimonials seen in Appendix 1.
Subsequently, calcium arsenate came into widespread commercial
use; for the control of crabgrass and Poa annua on golf courses. The
* [''or roferences, see Section 1.
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p
Chapman Division of Rhodia marketed the product Chip-Cal along this
line. Their investigation and resulting action assured continued use
of tricalcium arsenate on golf courses.
In 1970, New York, Iowa, and other states enacted legislation
providing for the licensed application of inorganic arsenicals. This
action was welcomed by Rhodia and used as a means to advance the sale
and safe use of their products. Meanwhile, the older PAX Company products,
based on arsenic trioxide and lead arsenate, fell into disfavor in many
states, particularly in Iowa where the unfortunate accident recounted
by Buck (2.) had occurred. Governmental efforts to inveigh on the PAX
Company to remove their product from the market in 1970-71 were overcome
by legal defensive action on behalf of PAX, supported by the safety
evidence provided by Done and Peart (l). It then became painfully
evident that 20 years of safe usage did not obviate all possibilities
for misuse of the product, particularly in the chance event of the
feeding of grass clippings to animals. A brief survey of turf management
experts acquainted with the use of calcium and lead arsenates on golf
courses .disclosed that none were aware of poisoning.in animals or humans
stemming from the recommended use of such products. This is somewhat
surprising in that calcium arsenate is somewhat more toxic than PAX.
That the licensed application of such toxic pesticides will reduce
all possible hazards to the public can hardly be denied. On the other
hand, the removal of responsibility for individuals to think for them-
.jselves and to act for the welfare of all, is the essence of democracy.
It costs far less where people manage their own affairs in such matters
than where government intervenes. The views expressed by Drs. Kearney
and Woolson, i.e., "...I don't think we should regulate the ability of
citizens to use a product safely." (Appendix 2) seem to be the crux
of the matter.
The efficacy of PAX lawn care products is evident from the 20-year
sale of the product; also from unsolicited testimonials from homeowners
and go\f course superintendents (Appendix 1.). The PAX products are now
permitted or marketed, so far as our records show, only in certain
western states. Such states have predominantly alkaline soils, quite
different from those in the East. To raise and maintain good turf in
-------
many of the western states is a more difficult problem than in the East.
Fo. this reason and others, consideration might logically be given to
assigning authority to each state regarding the safe uses of inorganic
arsenicals for turf management. It should be recognized, however, that
such household items as aspirin, boric acid, oxalic acid, gasoline, guns,
knives and automobiles are at least as injurious when misused.
Recommendations
The primary recommendation is for further research:
1) To establish better knowledge of the precise values of inorganic
arsenicals for turf improvement.
2) To establish ways to minimize hazards from such uses.
Recommendation is made to support research toward better understanding
of the fundamental role of arsenic in plant biology, its relation to
phosphorus and nitrogen metabolism, particularly to conservation of
essential resources of phosphorus. In view of the long and unique, but
little understood value of lead arsenate as a pesticide, catalyst for
maturation and improved quality of fruits, and for turf management, we
urge further research on its safe uses.
In view of the record, it is recommended that registration of the
single PAX Company Three-Year Crabgrass Control product now registered
be continued in registration with the Department of Agriculture and/or
the Environmental Protection Agency. It is further recommended that those
charged with turf management and regulatory controls of pesticides in
each state again review the overall problems relating to the safe uses of
PAX Three-Year Crabgrass Control, calcium arsenate, and lead arsenate
products for turf improvement. Whereas licensed application seems
appropriate for such products for commercial turf, such as for golf
courses, public parks and grounds, imposition of such restraint seems
inappropriate for home-owners. More prominent label warnings against
feeding arsenical-treated grass clippings to animals should suffice
to reduce hazard of the PAX product for home use.
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APPENDIX I
AFFIDAVIT
State of Utah )
County of Salt Lake)
B. R. Ellison, being first duly sworn, deposes and says:
It Is my understanding that the Committee would like me to fur-
nish them In affidavit and Illustrated form as much of the Information as
possible which Or. Frost asked me for at the time of his recent visit with
me In Salt Lake. Therefore, this affidavit will contain a rather general
discussion on some of the technical aspects of Three-Year Pax Crabgrass
Control, the arsenlcals which It contains, and their behavior on the soil.
From time to time, In our discussion, a comparison was drawn with other
arsenlcals, particularly calcium arsenate, sodium arsenlte, and lead
arsenate.
Dr. Frost wanted Information about country clubs and golf courses
which have treated their entire fareways. Also, he wanted to know If we had
any affidavits or recommendations from golf course superintendents. We have
such Information and it will ba discussed in the affidavit.
Dr. Frost asked me specifically if I had some areas that showed
the encouragement of desirable turf grass plants as mentioned in Dr. Richard
Stadtherr's thesis. I was able to show him such a plot.
Dr. Frost selected four pictures from a number of my slides which
I showed him which he felt should be contained in a report to the Committee.
These are therefore attached as exhibits to this affidavit with an explana-
tion of what they show.
Dr. Frost asked for explanation of what might be done If a person
treated an area with PAX Crabgrass Control and then decided that they wished
to grow something else besides turf In the area. We discussed this and the
discussion will be contained In the affidavit.
GENERAL DISCUSSION OF A TECHNICAL NATURE CONCERNING PAX THREE YEAR CRABGRASS
CONTROL, THE ARSENICALS CONTAINED IN IT AND THEIR BEHAVIOR IN AND ON THE SOIL.
It Is a well known fact that certain crop lands have been taken
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-2-
out of production by the repeated use of arsenicals used as insecticides.
Probably most famous of these damaged soils occur in the orchard areas of
the northwest and some cottonlands in various parts of the country. It is
characteristic of these sotts that arsenical can be found at considerable
depths in the soil, well into the root zone of the plants, and a considerable
reduction In yield is characteristic of these areas and attributed to the
high arsenical content of the soil. The Important thing to realize In these
soils Is that the arsenical did not migrate to these great soil depths by
Itself but rather was cultivated into the deeper layers of the soil. Arseni-
cal compounds, like phosphates, are very tenaciously bound by various fractions
of the soil, some of which are clay particles and organic coilatable materials.
Some turf areas, particularly those that are not receiving adequate amounts
of nitrogen fertilization will accumulate an abnormal amount of thatch or
litter layer. Such areas are quickly recognized on the golf course because
of the watering problems they present. This thatch layer forms a very
efficient water barrier. Fairways with such areas have serious problems of
water management. While the homeowner may not recognize the condition as
readily as the golf course superintendent, it nevertheless exists in some
home lawns. Obviously, if such an area resists the penetration of water, it
also resists the proper washing In of any pesticide material, particularly
PAX Three Year Crabgrass Control. In such an abnormal Uwn, a fairly large
percentage of the arsenical will become fixed in the thatch layer and never
reach the mineral soli at all. A PAX Three Year application in the Fall on
such a lawn would not be washed In. Rather, it would become bound on the
decaying thatch layer. Virtually the entire PAX application might very well
be removed the following Spring If the area were power raked. It is likely
that a sizeable percentage of the PAX application would be removed even by
close mowing with a vacuum type rotary mower.
The ultimate fate of arsenicals placed on the soil surface of a
stabilized soil, such a growing turf, is quite different from that of an
arsenical which is applied year after year on cottonland or In orchards.
For one thing, a rate of arsenical, tremendous by standards of PAX Crabgrass
and Soil Pest Control, Is sprayed on the fruit trees and plants not once in
three years but several times In one season. Although the application is
made to the trees and cotton plants, most of it ultimately reaches the
orchard floor or soil. Later It Is plowed and cultivated under usually too
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-3-
rather substantial depths.
Arsenical* applied to a stabilized soil are usually found within
the first half inch of soil with by far the greatest part of It within the
first quarter inch. If the management of ihls soli promotes a good deal of
growth of micro-organisms, as would be the case with a turf area, there are
a number of microorganisms that are normal and common members of the soil
mlcroflora that produce exogenous enzymes which catalyze the production of
volatile arsenical compounds which pass Into the atmosphere. It Is character-
istic, as determined by many soil staples run by the PAX Company for a ,
number of years, that characteristically approximately half of the arsenical /
is dissipated In the first year after application.
It Is generally concluded by soil chemists that the soil chemistry
and behavior of arsenlcals in the soil Is similar to that of phosphorous
compounds and that it Is likely that arsenlcals and phosphate compounds
compete for positions on the colloidal micelles of the soil.
It Is known that arsenical compounds exert a distinctly stimulatory
affect on certain crops, many of them grasses. Or. Frost and I discussed
the possibility stimulatory affect might possibly be due to the arsenical
compound making available a certain amount of phosphorous as a result of the
arsenical displacing the phosphorous on the soil colloid. I have no informa-
tion on this, but I do have some studies on the reverse situation. It occurred
to me that if there was a mutual competition between phosphorous and arsenical
for a position on the clay particles or other colloidal particles In the soil
that an application of a phosphate material to an area that has previously
received an application of arsenical might result In arsenical damage to
the turf or perhaps Increased weed control simply as a result of making more
of the arsenical available In the soil solution as a result of the phosphate
displacing it from the soil colloids. Both field and laboratory studies are
carried on in an attempt to investigate this possibility.
In the field, heavy applications of arsenic trioxide were made to
a turf area, washed In, and left for a period of one month. These plots
were In three replications. In a month after the Initial application, an
-------
appltcatfon of dI ammonium phosphate was made to one half of each plot and
washed In. The rate of arsentcals applied to the turf was arsenic trioxide
at the rate of 20# per 1,000 square feet. The arsenical was applied alone,
without the fertilizer and insect Icldal materials which characterized the •
product PAX Three Year Crabgrass Control. I think the reason is obvious.
The dI ammonium phosphate was selected because it is a very soluble phosphate.
It was applied at a rate equal to 1# of f^c per 1,000 square feet. No
difference could be detected through the entire season between the two halves
of the three replicated plots.
In the laboratory, a screened, sandy loam, soil was shaken in
flasks that had a saturated solution of arsenic trioxide (actually arsenious
acid). These soils were filtered out of the flasts and leached with saturated
solutions of dI ammonium phosphate. We could detect no liberated arsenic in
the leachate.
Utah soils are generally characterized by having high levels of
phosphate. All turf soils In the country were for years fertilized most
characteristically, and improperly, with a 6-10-4 fertilizer. Most old lawns
contain a very high phosphate level in the soil, no matter In which part of
the country they occur, as a result of this improper type of fertilization
which was charactestic earlier.
Golf courses, likewise, were generally heavily overfertllIzed with
phosphate containing materials. Phosphate levels in the soil on most golf
courses are fantastic. If there was any greet antagonism between arsenic
and phosphate, turf areas should be the last place on which a company should
venture with an arsenical herbicide. Indeed, competitive companies marketing
calcium arsenade or lead arsenade for the control of crabgrass or other weeds
suggest that their product may not work if the soil contains rather large
amounts of phosphates. We do not seem to have inhibition of our combination
of arsenicals as a result of high phosphates In the soils. A Denver golf
club, Green Gables, treated their fairways with great success with our product,
PAX Three Year. The product was very successful in spite of the fact that soil
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-5-
tests showed that the fairways averaged 1,000 pounds of available P20j per
acre. Thirty pounds of available ^2^^, ^or a phosphate loving crop like
alfalfa, Is marginal. If available PjQ$ is below that, most state soil
labs would recommend fertilization with phosphate, but if it was substantially
above thirty pounds per acre, they would not.
Remarkably enough, for areas that have suffered crop damage from
the application of arsenicals, zinc chelate seems to be more effective in
counteracting the effect of the arsenical than phosphate applications.
Arsenicals placed on crop lands that are cultivated and plowed
every year may constitute a serious hazard to such lands. This is largely
because the arsenicals that are applied and later plowed down to six to
eight inches depths, have little chance of escaping. Certainly complex
chemical reactions occur with these arsenicals and some volatile arsenicals
are produced by micro-organisms but when the arsenicats are deep In the soil,
the volatile arsenical Is usually recaptured in some cycling chemical reaction
and it does not escape. A further difference between the application of an
arsenical to the surface of a turf soil as opposed to a cotton crop or an
orchard floor is that the micro-organism activity Is extremely high in the
superficial layers partly because both moisture and nitrogen are usually
readily available at the superficial layers. This, of course, promotes
great micro-organism activity. In the deeper layers of the orchard floor
or the cotton field that has plant detritlous plowed under with the arsenical
until the nitrogen may be extremely scarce, water relatively scarce, and
consequently micro-organism activity is extremely low.
Or. Frost ask me what would happen if a person treated an area with
PAX Three Year Crabgrass Control and then changed his mind and decided to
plant something else. Of course a number of factors would be Involved In
this situation. Plants vary remarkably In their vulnarabi11ty to this com-
bination of arsenicals. We regularly plant and establish bluegrass seeds right
in a PAX application. I don't think that it is necessary to speculate on
the possible fate of agricultural crops since our product Is specifically
designed for established lawns. There Is some Indication, that the
consequences would not ba very serious since a good deal of modern suburbia
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-6-
has moved out on to the truck garden farms of Long Island and such similar
areas which were regularly treated with arsenicals. In these areas they
have managed to establish landscaping, tn fact very beautiful landscaping,
with the minimum of difficulty. There Is approximately 20% of elemental
arsenic In PAX Three Year Crabgrass Control. At a recommended rate of 20
pounds per square feet we would apply approximately four pounds of elemental
arsenic applied per thousand square feet. Soils laboratories generally use
the figure of 100 pounds per cubic foot for soil. If we could persuade
this changable fellow to turn his soil over to a depth of 6 Inches, and
that would not be unreasonable, we would end up with approximately 80 parts
per million of elemental arsenic in the soil which would constitute the
major root zone of most ornamentals. Many soils that grow normal vegetation
have higher natural rates of elemental arsenic than this.
Certainly if we were considering fertilization and discussing the
application of a phosphate rather than arsenical we would not assume that
100% of the phosphate would be available to the plants. Phosphate is quite
regularly fixed in many soils In forms that are unavailable to the plant.
Some soils are so notoriously efficient at fixing phosphate that it is almost
impossible, at least from the economic point of view, to fertilize them
heavily enough with phosphate to grow a crop that does not show phosphate
deficiency. Certainly all soils fix some of the phosphate that Is applied.
We find this to be the case with the arsenicals in our product as well.
Two areas In our distribution area have some soils that are notoriously
efficient in fixing arsenicals. One Is the Arcadia area (« suburb of Los
Angeles) and the other is in the vicinity of St. Joseph, Missouri. In these
areas, even at high rate, we get no control of crabgrass. The dealers in
these areas are alert to the situation and so little difficulty develops.
When a customer buys the product tn these areas and reports poor control,
we refund his money with an apologetic letter pointing out that the
fertilizer in the product did at least justify the spreading of the product.
I do not understand the mechanism of the fixation of the product in these
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-7-
areas but at least the phosphate levels in the soil samples that'we have
had determine from these areas do not run anywhere near the levels found
on some golf courses where our product has been particularly successful.
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-8-
GOLF COURSE APPLICATION
Dr. Frost was particularly Interested in seeing some golf courses
that had treated their complete golf course with our product. Incidently,
at this point I should make it clear that we do not recommend this product
on golf greens. It has been used successfully by a number of superintendents
and Dr. Cornman of the New York State College of Agriculture at Ithlca had
a demonstration application at Nassau County Parks Golf Course. His appli-
cation of our product, along with Dacthal and a number of other leading
crabgrass controls stole the show. Nevertheless we simply do not wish to
be Involved in the liability that could result from the misuse of our product
on a golf green. We are talking about approximately $10,000 worth of turf.
This turf is generally abused In every way conceivable. It is a virtual
miracle for the golf course superintendent to bring it through the season
still alive. When a green dies, the superintendent usually loses his job.
To avoid this, a superintendent cannot be blamed for throwing suspicion
toward the most recent pesticide he applied on his greens. We do not wish
to be in that position but we stand completely ready to back our product
on fairways. Our company does not have a golf course program. Nobody in
the company calls regularly on golf courses and we do not Intend to. A
company must have a whole line of golf course supplies to make it profitable
to devote the time and manpower necessary for a golf course sales program.
We do not even package our product In a convenient size to be used on large
areas of turf. Remarkably enough, each sale to a golf course has resulted
from experimental applications made either by the PAX Company or, in many
cases, research men from the various State Experiment Stations.
The first complete golf course sale resulted in exactly that way.
Dr. Victor B. Youngner and Tosh Fuchigami of the Department of Forticulture
and Ornamental Horticulture at the University of California at Los Angeles
made some crabgrass control applications of an experimental nature on the
15th fairway of the Bel Air Country Club in Beverly Hills. The results of
their application was published In the Southern California Turfgrass Culture
-------
-9-
which was the official organ of the Southern California Turfgrass Council.
It is attached, marked Exhibit I. As you will note, the arsenical content
of the product at that time was the same as it is today. It differs from
the present product in two respects. One Is that the Insect control was
amplified with Chlordane at that time rather than Heptichlor and two, the
fertilizer grade was 7-0-0 rather than todays 't-O-O. You will note that
the rates were excessively high, 3.33 pounds and 2.5 pounds per hundred
square feet respectively. These plots were replicated three times and the
general effect on all six plots was slight turf damage followed by quick
recovery. This was fertilizer burn from the excessively high rate of
fertilizer applied. It is generally a rule amoung turf men, and a very good
one, that no more than one pound of actual N be applied per thousand
square feet at any one time. At the high rate, they were applying 2.33
pounds of actual N per thousand square feet. It was at this point that I
was brought into the PAX Company. My first contribution was to lower their
fertilizer grade to a more acceptable level. Nevertheless, these were rather
historic plots because they remained for a period of four years showing
almost perfect crabgrass control after all of the other plots have completely
faded away. As a result of this, Bel Air Country Club contacted us for a
price to treat all eighteen of their fairways. We supervised their applica-
tion and it was so successful that the following year three of the prestige
clubs In the neighboring area.In Los Angeles treated their complete fairways.
Testimonials of the superintendents of these clubs are Included marked
Exhfblt IK
Golf courses are usually interested in our product for one of two
things. Either crabgrass control, as was the case with the Los Angeles
clubs, or Poa annua control. Remarkably enough fairways that are infested with
Poa annua are very seldom infested with crabgrass, at least this is true in
the West. Poa annua In the West Is a particular problem in golf courses
because since we regularly irrigate our turf areas, the Poa annua is seldom
but under enough stress of heat and moisture to die. Consequently from the
Rocky Mountain states West through California and the Northwest, Poa annua
-------
-10-
is not a true annual, but acts as a weak perennial. Control of Poa annua
In the Mlddlewest and generally the Atlantic seaboard, at least the
Southern part of the Atlantic seaboard, Is a relatively easy matter because
in late July it all dies. It Is a Winter annual In such areas and germinates
again In late August or early September. There are several preemergents
that will prevent Its re-establishment. Some of the best of these are
i
Betasan, Dacthal or Benefln. These kill the seedling shortly after germination.
In those states In which Poa annua acts as a weak perennial, preemergence
controls are not successful. A post-emergence control Is required. It Is
usual on Poa annua Infested golf courses for the Poa annua to be by far the
dominate species. Even though the course was originally planted to perennial
turf, the Poa annua rapidly replaces It. In some sections It comprises 100%
of the turf and it Is no** unusual for whole fairways to be in excess of 90% •
Poa annua. Since Poa annua is shallow rooted and subject to a number of
fungus diseases as well, such fairways can literally die overnight.
Obviously it would be desirable on such courses to get rid of the
Poa annua but the situation is something like riding a tiger. It is impossible
to get rid of the Poa annua all at once because that would leave a bare
fairway — a situation that would be totally unacceptable to the golf course
membership. I am convinced that PAX Three Year is the only product that can
take out Poa annua so slowly on such fairways that the perennial turf can
expand and keep up with the disappearing Poa annua so that at no time do we
leave the fairway bare. The whole process takes approximately three years
and is a matter of understanding the nature of both the perennial turf; the
weed, Poa annua; and the product, PAX Three Year Crabgrass Control. I, or
someone else from the company, most regularly supervises the application on
fairways that are as heavily Infested as this.
Such fairways are to be found on the Salt Lake Country Club which
I took Or. Frost to see. This was the first golf course, In which the
fairways were almost totally composed of Poa annua, that treated all 18 of
their fairways. Again, no attempt was made to sell this club the product.
The club decided to buy as a result of several test plots which I placed on
-------
-11-
thelr 8th fairway. Since the entire club was treated approximately 6
years ago, their fairways are no longer composed almost completely of Poa
annua but Poa annua Is beginning to return to the fairways. The club Is
now In the process of retreating some of the more heavily Infested fairways.
Dr. Frost saw treated fairways into which the superintendent had drilled
Merlon Bluegrass seed because there was not enough perennial turf grass
left to give cover when the Poa annua disappears.
As a result of the sucess of the treatment at the Salt Lake
Country Club, all the other country clubs In our vicinity that had any
kind of budget to work with treated their fairways. Amoung these are
Hidden Valley Country Club, Willow Creek Country Club, Oakrldge Country
Club and Riverside Country Club. Several country clubs In Denver have
treated. The first one was the Green Gables Country Club which treated
their entire 18 fairways. The result of these app!(cations Is given in
reprints from the June 1971 "Rocky Mountain Golf Course Superintendents
Reporter". This Is the official organ of that chapter of the Golf Course
Superintendents Association of America;* The superintendent of Green Gables
Country Club, Ben Struempf, wrote the article. Although his understanding
of the nature of the operation of the product Is somewhat faulty, his
spirit Is good. The fact of the matter is they turn their 18th fairways
from a miserable mess of Poa annua to 18 fairways of good perennial
bluegrass. In this course, they again seeded directly Into the PAX
application with the bluegrass seed because they did not have enough
perennial grass to give any cover when the Poa annua went out.
-------
-12-
PHOTOGRAPH OF RESULTS
From a number of slides which I showed Dr. Frost, he selected
four which he thought it would be desirable for the committee to see. I
have had them reproduced in black and white. I would have had colored
prints made from them, but they would have taken longer than we would had
available. Colored prints could be made available to the committee later
if they so desire them. The first photograph (Exhibit IV) Is a picture
of a plot which I took Or. Frost to see. This plot is ten years old this
spring. It was not put on by anyone In our company. It was put on by the
Extension Agronomist, Lewis Jensen. A number of other materials were used
in this turf area and some of them gave good control the first year, of the
crabgrass. However, their was no control the second year. I have heard that
it Is the object or at least It was the object of the registration section
when it was contained in the USDA, to remove all long residual hermicides
from the market. If long residual is a sin, we are certainly guilty. Our
name implies it, our results confirm it. I repeat, the plot that Dr.
Frost saw was ten years old. At the time, our grass was just beginning
to break winter dormancy and green up. The location is one of our city
parks and the turf care in the city parks is virtually non-existent. The
so called-turf in the city park consists mainly of weedy grasses, dandelions,
crabgrass, etc. Of course, at this time of year it Is too early for crabgrass
to be showing. Crabgrass germinates in our area most regularly about May
20th. Nevertheless the plot was completely obvious because of the superior
nature of the turf. The grass was practically all perennial bluegrass In
the plot whereas the rest of the area, which had been treated with various
chemicals at the same time our plot was treated was covered with a so called
turf consisting of a weed patch with the sprinkling of various kinds of
grasses, some of them very undesirable. I showed Dr. Frost this plot in
response to his request to see an area in which the PAX seemed to promote
the growth of good grasses as Dr. Richard Stadther claimed in his thesis.
I think the demonstration was convincing and I can repeat it in any part
-------
-13-
of the country. The picture was taken In late July, three years after the
original application. Nothing was ever done to this turf area In the way of
retreatment of fertilization. I am pointing to the extremely straight
line of crabgrass control which exists even after three years. This Is
another plain Indication that the arsenicals are strongly bound to the soil
and do not move. The crabgnass In the foreground Is so luxuriant it looks
almost like good turf. It has not yet begun to seed. Indeed, It is so
luxuriant that It Is covering up a lot of the other weeds that are present
such as dandelion, etc. Our product by actual count gets approximately 85%
control of dandelions and it can be mlnipulated to give 100% control.
Nevertheless this does not appear on our bag for the simple reason that if
you tell a customer that you give dandelion control they expect very close
to 100% control and 85% control Is not acceptable. It Is a benefit that
they notice and enjoy however, because it was customers that originally told
me that the product gave dandelion control. I had not noticed it. I did
go out and put on plots, however, and confirmed it. The remaining three
pictures marked V, VI and VII are all taken of the Salt Lake Country Club
and show the original Poa annua plots which I applied. The pictures were
taken fairly early in the spring. The winter had been an open winter as is
frequently the case In Salt Lake City. During such a winter, the shallow
rooted Poa annua suffers seriously from drout Injury. The deeper rooted
perennial bluegrasses are able to obtain enough moisture to grow and so green
up earlier. The Poa annua Is still distinctly yellow from Its winter Injury
and so the dark bluegreen plots of perennial Kentucky bluegrass show up
very plainly. Certainly the most Interesting plot of the three, which were
meant to be three replications Is In the left center of the picture. This
was the first plot I applied. I was chagrined to find that my spreader was
not working properly and that most of the material was coming out of one side
of the spreader. I examined the spreader carefully but could not see what
the difficulty was. The plot was already ruined and so I continued with the
spread while my assistant returned to town to buy a new spreader. The plots
in the picture are three years old. The Poa annua had not disappeared from
the plots completely until the fourth year. -The plot in the left middle of
-------
the picture, which was not properly applied, proved to be the most interesting
plot of the group. As you can see, perennial bluegrass established only
where the PAX went and where the PAX did not go the Poa annua maintained its
hold. Please note how straight the lines of the plots are. There is no
tendency for this vigorous growth of perennial Kentucky bluegrass to Invade
the Poa annua under conditions of high phosphate and excessive watering which
is characteristic of most golf courses, perennial grasses simply cannot compete
with Poa annua without chemical help. It Is Interesting to notice that in
the background Is the rough. Because the rough is characteristically neglected
and not heavily fertilized it has a good growth of perennial grass on it.
Poa annua Is nowhere near as sensitive to arsenical treatment as crabgrass.
By the fifth year, the plots are beginning to fail and Poa annua Is beginning
to reinvade. This is shown in the picture marked Exhibit VI. These plots
are thirty feet square. I am standing In the middle of a plot that is five
years old. The previous fall (the fourth year) the half of the plot on the
left hand side of the picture was retreated at half rate (ten pounds per
thousand square feet). One can see that on the left the bluegrass is main-
taining Itself without invasion from the Poa annua whereas the right half is
beginning to be reinvaded with Poa annua after having been free. Of course
when a whole fairway Is treated and the Poa annua is destroyed, it can be
expected to hold a considerably longer period than three years simply because
there is not a ready source of seed to reseed the areas. But the chemical
inhibition from the arsenical begins to fail noticeably by the end of the
fourth season when relatively small areas are treated that are surrounded
by heavy growth of Poa annua. The photograph marked Exhibit VII shows the
selectivity of the treatment but It shows an Improper use of the material.
It Is a'-photograph of a corner of a plot. Poa annua Is extremely sensitive
to arsenical very early in the Spring or. late in the Fall. This plot was
applied late In the Fall. Grass was still growing vigorously, but the end
of the season was approaching. The Poa annua died very quickly and bare
areas developed. As can be seen, the perennial bluegrass Is doing extremely
well in the treated area. Nevertheless, the Poa annua has died so quickly
that the perennial turf is unable to keep up. If an entire fairway was
-------
-15-
treated in this way, it would most certainly be out of service for the
entire season. That is of course what happens when sodium arsenite or some
of the other techniques are used to control Poa annua on a fairway.
Subscribed and sworn to before me
this 25th day of April, 1973-
/?.
" flollary g&bl ic
Residing at Salt Lake
City, Utah
-------
EXHIBIT
Excerpts from Southern California Turfgrass Culture, Volume
6, No. k, October 1956. This publication is the official organ of
the Southern Turfgrass Council. This excerpt is a complete article
written by Dr. Victor B. Youngner and Tosh Fuchigami of the Depart-
ment of Floriculture and Ornamental Horticulture, University of
California at Los Angeles. The residual control which the two sets
of replicated plots of Pax supplied in this experiment resulted in
the first entire golf course application with our product. No at-
tempt was made to sell the Bel Air Country Club the product. We
did agree to supervise the application.
The product used in these tests was essentially the same as
the product we are marketing today except the amount of nitrogen
in the product has been reduced from the original 7-0-0 to the pre-
sent k-Q-Q. Also, Heptichlor was substituted for Chlordane as the
insecticide.
It is interesting to note that penetration into the subsoil of
arsenical is so poor and so slow that it is an ineffective control
for white grubs. Vertually no control of white grubs is obtained
with an application of any arsenical that season although reasonably
good control may be obtained for the following season. To obtain
quick control of white grubs and lawn moth larvae one must use a
material that penetrates more rapidly than arsenicals.
-------
Southern California Turfgrass Culture
CTOBER. 1956
VOLUME 6- NUMBER 4
WEEP CONTROL ADJACENT TO GRASSED AREAS
M. H. Kimballl
Boysie Day
Chester L. Hemstreet^
Turfgrass managers are nearly always responsible for
maintenance of flower beds, plantings of trees and shrubs,
paths, or small drainage channels, in addition to actual
areas of lawns. Control of weeds in such areas, in gravel
and flagstone walks, in parking areas and patios adjacent
to turf is a serious problem. Machine methods are not
adaptable to most situations and chemical methods are
often hazardous to adjacent turfgrass and ornamentals.
The roots of trees and shrubs are often present, limiting
the use of soil-acting chemicals and foliage sprays that
leave toxic soil residues. *
There are a large number of chemical weed killers
commercially available. Some are general weed killers
while others control only certain weeds. Some may be
used safely in the presence of other plants in specific
instances, but the resistance of most ornamental species
to the newer herbicides is not known.
Soil Sterilants
N'hen properly applied soil Sterilants are not hazardous
to nearby turfgrass. Leaching carries the chemicals pre-
dominantly downward with very little lateral movement.
The principal hazard is to trees and shrubs having roots
extending into treated areas, ^'here distance from trees
is considerable -- 30 to 50 feet or more - it is advanta-
geous and relatively safe to use permanent soil steri-
lants. Single treatments of the urea herbicides (CMU or
DCMU), chlorates, borates, arsenicals, or combinations
of these materials control all vegetation for several
seasons and may be renewed periodically at relatively
low cost. These cherr.icals are leached into the soil by
rainfall or irrigation. They are toxic to all plants and
will be" picked up by roots and transported to trees and
shrubs where systemic injury may result. For long-term
sterilization CMU may be used at rates of 20 to40 pounds
per acre, borax or chlorate-berate mixtures at two to four
pounds per 100 square feet, and borascu at four to eight
pounds 'per 100 square feet. These chemicals are applied
dry or may be dissolved and sprinkled or sprayed on the
soil surface. Treated areas should be sprinkler-irrigated
(avoiding runoff) to take the chemical into the soil.
I Cxleiision Ornamental Horticulturist, University of California.
! An v.l. I'11,in l I'liytluluijiM, llnivnisily ol California, Riverside,
t Form Advisor, Agricultural Extension Service, San Bernardino
County.
Fumigants
Fumigants may often be used to advantage to control
perennial weeds near turf plantings. Control by fumiga-
tion is only temporary, however, as no toxic materials
remain in the soil and recontamination can occur immedi-
ately. Fumigation kills the roots of trees and shrubs in
treated areas, but this is a "pruning" action, killing the
roots contacted. There will be no systemic injury due to
absorption of chemicals. If large areas of the root zone
are treated, resulting in root killing, the plants may suf-
fer from lack -of ability to absorb sufficient water.
Methyl bromide at one pound per 100 square feet
applied under well-sealed tarps and held for 24 hours
controls such weeds as nutgrass and bermudagrass, and
in addition kills most weed seeds. Methyl bromide is
very poisonous and must be handled with caution. In-
jections of two ounces of carbon bisulfide in holes six
inches deep and twelve inches apart control deep-rooted
perennials such as wild morning glory. The vapors of
carbon bisulfide are highly explosive. Ethylene dibromide
and DD control nutgrass, oxalis, and other tuberous or
bulbous species when injected at the rate of one-half
ounce per hole with twelve-inch spacings and four to six
inches deep.
Vapam — a new liquid fumigant — may be used to
control bermudagrass and other perennials. The material
is used at the rate of one quart per 100 square feet. To
fumigate an area Vapam is mixed with water and sprinkled
or sprayed on the soil surface then leached in by sprinkler
irrigation. Depth of fumigation may be controlled by the
amount of water used before application and to carry the
chemical into the soil. To kill the roots and rhizomes of
deep-rooted weeds deep leaching is needed. For control
of shallow species such as bermudagrass less water is
required. Excellent control of shallow-rooted perennials
above tree or shrub roots has been obtained by first
thoroughly soaking the soil and then while it is fully-
wet, applying the Vapam. Leach it immediately 'into the
soil by sprinkler irrigation. Apply only enough to carry
the material two to four inches deep, normally about
1/4 inch of water.
Results with Vapam are most reliable when the
chemical is uniformly diluted in the irrigation water
and soaked to the desired depth. One way to do this is
to meter the Vapam into the water of a sprinkler system
(CONTINUED NEXT PAOE)
-------
CONTROL OF CRABGRASS WITH CHEMICALS
Victor B, Youngner and Tosh Fucbigami
Department of Floriculture and Ornamental Horticulture
University of California at Los Angeles
Chemical control of crabgrass has been the subject of
many investigations in recent years. As a result of this
numerous preparations are now available for the control
of crabgrass infestations in established turf.
Tests of several crabgrass herbicides were conducted
on the 15tb Fairway of the Bel-Air Country Club of Los
Angeles during the summer of 1956. The area used for the
tests had been heavily and uniformly infested with hairy
crabgrass, Digitaria sanguinalis, in 1955. The turf in the
area consisted of a mixture of bermuda, bluegrass, bents,
and fescues. Both pre-emergence and post-emergence
materials were used in this test. Seven chemicals, ap-
plied at various rates and schedules, and a check plot
made a total of 14 treatments as shown in the table. The
chemicals used were:
1. Pax AR-76, 8.25% standard lead arsenate, 25.11%
arsenous oxide, 0.35% technical chlorodane
2. Alanap 1-F, 1% X-l naphthyl phthalamic acid
3. Crag Herbicide 1 - 90% 2,4-dichlorophenoxyethyl
sulfate
4. PMAS - 10% phenyl mercuric acetate
5. Standard lead arsenate with Milorganite
6. 18.90% disodium methyl arsonate anhydrous
7. Experimental herbicide 140 - 20% Sodium Arsono-
acetate.
All treatments were randomized in 4 replications. Each
plot was 100 square feet in size.
The first application of pre-emergency materials was
made on March 1, 1956, before crabgrass had begun to
to germinate. Crabgrass seedlings in the two-leaf stage
were first observed March 22, 1956. The first post-
emergence herbicides were applied at this time.
Phenyl mercuric acetate applications were begun when
the seedlings were small as observations have shown
this to be the most effective period- for the use of this
material. Disodium methyl arsonate and Experimental
herbicide 140 were first applied at the time of peak crab-
grass germination.' Turf injury and discoloration notes
were taken one week after treatments. Estimates of the
number of crabgrass plants surviving each treatment were
made by counting the number of plants found in four one-
square-foot plots taken at random in each treatment.
These counts were made twice during the summer, June
18, and September 13.
The results of this experiment are presented in the
table below:
CRABGRASS CONTROL IN TURF WITH VARIOUS CHEMICAL TREATMENTS
TREATMENTS
RANKED ACCORDING TO
EFFECTIVENESS-
JUNE 1956 READINGS
1. Pax AR-76. Pre-
emergence
1 application
2. Pax AR. 76 Pre-
emergence
1 application
3. Disodium methyl arsonate
Post-emergence
2 appl ications
4. Alanap 1-F.
Pre-emergence
3 applications
5. PMAS.
Post-emergence
3 appl ications
6. Alanap 1-F.
Pre- emergence
•\ applications
7. Alanap 1-F.
Pre-ernergencc
3 appl ications
APPLICATION
DATES
March 1
March 1
May 14, 23
March 1
April 1
May 15
March 22, 29
April IS
March 1, 29
May 14
June 22
March 22
May 14
Jun. 22
APPLICATION
RATE PER
100 SO. FT.
3.33 Ibs.
2.5 Ibs.
0.67 oz. in
1 gal. water
1.8 Ibs.
0.25 oz. in
1 gal. water
1.8 Ibs.
1.8 Ibs.
NUMBER OF CRABGRASS PLANTS
PER SQ. FT. AVERAGE OF 4
REPLICATIONS
JUNE 18, 1956
0.06
0.06
0.56
1.06
1.19
1.56
1.56
SEPT. 13, 1956
0.00
0.00
11.25
1.56
10.81
2.50
22.31
REMARKS
Slight turf injury noted 1 week after
treatment. Followed by improved
color
Same as above
No torf injury or discoloration
No turf injury. Improved color 1 week
after treatment
No turf injury or discoloration
No turf injury. Improved color 1 week
after treatment
Same as above
-------
' ' I It \ II (. K \ SS
10 \ 1 1(01. TIM » I.S
I OK l'»"»(.
IMPROVED TURF QUALITY
RESULTING FROM
CHEMICAL TREATMENT
TO
DESTROY CRABGRASS —
The crabgrass population estimates as presented in
this table show that a number of chemicals are now avail-
able which will greatly reduce crabgrass infestations
with little or no injury to the desirable turfgrasses. The
great "turf improvement which was obtained is shown in
the accompanying photograph.
Several additional observations should be mentioned.
All pre-emerpence materials must be applied before any
crabgrass seed germinates for best results. In southern
California this should be no later than early March. Sev-
eral applications of post-emergence herbicides must be
made to obtain good kill of crabgrass. A second series of
post-emergence herbicide treatments should be made in
late summer to kill new crabgrass plants from late ger-
minating seed. Improved turfgrass color and growth was
obtained from the Pax and Alanap 1-F in addition to an
excellent control of crabgrass.
In addition to this series of tests a small test of Du-
Pont Crabgrass and Chickweed Preventer (Neburon) was
made in an adjacent area. This material arrived too late
to be included in the regular test. Unfortunately, by this
time crabgrass seed had begun germination. Nevertheless
population counts showed this material to be an effective
herbicide for crabgrass. It was applied in a single appli-
cation at the rate of 0.8 oz. for 100 square feet of turf.
8. Crag Herbicide 1.
Pre-emergence
4 applications
9. Standard lead arsenate +
Mi lorg unite, '-'re-emergen-
ce • 1 application
10. Oi sodium methyl arsonate
Post-emergence
3 applications
1 1. Crag Herbicide 1.
Pre-emergence
4 applications
12. Experimental Herbicide 1.
Post-emergence
5 applications
13. Disodium methyl arsonate
Post-emergence
1 application
14. Check. No treatment
l'..S.D. at Probability of
March 1, 29
May 14
May 23
March 1
May 14, 23
June 22
March 29
May 14, 23
June 22
May 14, 23
June 1, 7, 22
May 14
0.30 01. in
1 gal. water
1 1 oz. lead
arsenate + 4 Ib
Ibs. Milorganite
0.67 ot. in
1 gal. water
0.30 oz. in
1 gal. water
0.5 oz. in
1 gal. water
0.67 oz. in
1 gal. water
2.31
4.50
5.44
11.00
12.25
12.31
23.88
3.86
11.06
17.13
20.50
32.81
45.31
65.44
95.94
32.90
No turf injury or discoloration
No turf injury or discoloration.
Improved color
No turf injury
Same as above
Same as above
Same as above
I
A difference between treatments greater than 3.86 for the June counts and 32.90 lor the September counts is
significant ot 5?u Probability level. (
.~ . t '
-------
EXHIBIT I I
The "Rocky Mountain Golf Course Superintendent's Reporter",
Volume 6, No. 6, published June 1971. This publication is the
official organ of the Denver Chapter of the Golf Course Super-
intendents Association of America. It is an article by Ben
Struemps, Superintendent of the Green Gables Country Club in
Denver. He describes how he converted his fairways from a turf
containing approximately 80% Poa annua to a turf containing less
than 10% with the use of Pax Three Year Crabgrass Control. I
personally supervised the application. It was extremely success-
ful and as a result several other country clubs in the Denver area
have treated with Pax.
-------
THE
ROCKY MOUNTAIN
GOLF COURSE
SUPERINTENDENTS
REPORTE
Volume 6, Number 6
JMK«, 1971
POA ANNUA
CONTROL
Ky BEN SFRUEMPF
In April, 1970, as the .-irw uiprrintendm! at Green Gables
Country dub, Dover, G'torado, ! WHS informed Ihst the Club's
matt trying problem was. the annual loff of turf duu ro Poa trilt.
With approximately 80% /'« in fairwf ys, lees, and gieens
Our June Host, Ren Struempl, Uluitralts where
100% t'oa Aimua thrived last year. The area has almost
completely jilted in with bluefraa through Ben's efforts.
the first problem was selecting the best course of action for our
Club. One method would be to disregard the health oi existing
hlue grass and maintain for Poa. After looking at the merits
of thin method, we looked for a better method to cure the sum-
mer wilt, since Poo is a fair weather friend, more susceptible
to 'isease and having a hard winter will kill it as easily as beat
and drought Another possibility wts to use so'Jum arsenite
and burn off three fairways a year and renovate completely.
*Viih thn knowledge that the members would never accept Jus
method, we decided on the one remaining alternative which
was to remove the Poa and leave the existing perennial blue-
grass. After reasoning this far, we still had otiier considera-
tions as to the type of product to i se for this course. Growth
reUrdants and seed head prevents lives were ruled out as too
slow {or fairways and not jafe for grrens at present. Pr-
emergencc chemicals were decided by our committee as too
slow for fairways but the only safe means for greens. Trical-
calcium arsenute was disregarded as too fast with the large
amount of Poa that we had. Our final decision was to use an
intermediate product: Pax ihree year compound of lead arse-
nate and arsenical oxides. This product offered a slow post
emergence control (one to t*o ;xars to kill existing Poa and
three years of p;e-eiwrgence control).
Our program ran as follows: On April 15, 1»70, at #16,
we started over-seeding with a blue grass mix (10% Windsor,
15% Menon, 15'A Fylking. 15% Delta, 15% Newport, 15%
Park -nd 15% Commor.) and aerifying all fairways on the
course. On May 18, we started our Pax treatment. Note that
the time of application is important to achieve the desired re-
sults. An early application on lush growing Poa or a late ap-
pricalion in hot weather will give a more rapid kill. Ideal tim-
ing foi a slow kill is to apply just after seeds heads have form-
ed. Pax was applied at half rate one day, watered in, and the
othei half the follownfc day for uniformity. A Scott's drop
spreader was useo for spread-no. We dropped phosphates from
our fertiiuer program in 1970, and will keep it out in tlw fu-
ture w our soil test average 2.0* Ibs. a -lilaHe pht^phate
per acre.
On September 21, we started our second over-seed of the
cou/se. As a newcomer to Denver I made a rnisuke in tim-
ing both over-seedings. The April 15 seeing was early and
did not germinate until mid-July and the fall seeding was la'r
and
-------
EXHIBIT III
Superintendents of prestige country clubs in the Beverly Hills
and Bel Air area of Los Angeles. All of these clubs are exceptionally
wealthy clubs and beautifully maintained. Brentwood Country Club and
Hillcrest Country Club treated their entire golf course after seeing
the excellent results obtained from the treatment at Bel Air Country
Club.
-------
there's nothing like
for golf course
crabgrass contro!
that lasts and
lasts and lasts!
Here's what these experts say:
MAJOR FRED BOVE, Superintendent of Brentwood Country Club,
Brentwood. California says: "Two yea.i ago we decided to treat the
entire 18 fairways with PAX alter viewing the years of residual
contnl which PAX demonstrated at several top country clrbs in
Southcin California. And now the overall success of Pax exceeds
99% in elimination of existing crabgrass. Not unly that, there was a
big reduction o1 annual wueds Lnd "if. nitrogen shot in the aim
was a welcome asset to the application."
-
JOE MARTINEZ, Superintendent of the Bel Air Country Club, Bel Air.
California says: "You don't have to tell me anything about PAX.
I found it so effective that I have incorporated it into my
maintenance program. I use it annually foi sput treating and re-
treating tees and aprons as necessary. I went through three year<,
of almost total crabgrass control after just one application of PAX to
16 fairways. That initial expenditure was extremely worthwhile
and is all it took to convince me."
.•*.:
•
WRITE TODAY FOR MORE INFORMATION:
Pax Company, Dep! 100
580 West 13th South. Salt Lake City 15, Utah
Name
Adilres.-
CHARLES (CHUCK) FRIDAY, Superintendent of H Merest Country
Club, Los Angeles, California says: "I've been at Hillcrest for 36
years and have been waiting for something like PAX all that time.
I decided to make an 18-fairway application of PAX in March, 1962
The crabgrass control so far has been excellent. I'd say it's been a
good 98% kill."
That's what the experts think and say about PAX.
PAX is the ideal crabgrass control for golf courses. It's simple and
easy to apply on a large-scale basis and the results are
extremely effective.
You can cover an entire 18-hole golf course in |usl 3V? days
using just five men and two tractor towed spreading machines
City
State
-------
EXHIBIT IV
At the time of Dr. Frost's visit, he wanted to see a plot
that had been treated with Pax Three Year Crabgrass Control which
encouraged the growth of desirable grass species as mentioned in
the thesis by Richard Stadther. I took him to the plot shown in
the photograph. This plot was applied by the Extension Agronomist,
Lewis Jensen, of the Utah State University. It was applied in
Liberty Park in Salt Lake City. I had nothing to do with the ap-
plication. It was applied at standard rates. I am photographed
on the plot four years after its application pointing to the
extremely sharp line of crabgrass control which this product gives.
Plots on each side of the Pax plot are treated with various other
crabgrass control materials, but have long since lost any weed
controlling abilities which they had. The plot is not ten years
old and is still plainly discernable. Dr. Frost was able to see
it, even though crabgrass has not germinated in our area. He
was able to discern it because of the more desirable turfgrass
species which were growing on the plot than in the contiguous turf
areas.
-------
-------
EXHIBIT V
Or. Frost ask to be taken to a golf course that had treated
its fairways with Pax. I took him to two. Unfortunately our season
is very late and the turf is just breaking dormancy. Both country
clubs which we went to, fn fact all country clubs in our area, were
treated with Pax Three Year Crabgrass Control',so long ago that they
are now in the process of retreating.
Three plots are shown in the photograph. At the time of the
photographs, the plots were four years old. The plot i,n the middle
left of the picture is probably the most interesting of the plots
because the spreader was not working properly at the time that it
was applied. Most of the material came out of one side of the
spreader with the result that some areas were overtreated and other
areas received no treatment at all.
Perennial bluegrass filled in the treated areas but was never
able to compete with the Poa annua which did not receive the treat-
ment .
The photograph was made fairly early in the season. When
Salt Lake has an open winter, Poa annua suffers rather severly from
drout injury because it is shallow rooted. This was an open winter
and the Poa annua is showing the drout injury. The perennial blue-
grass which has come back is deep rooted and therefore is not showing
winter drout injury. That is the principle reason why it has gheened
up and is growing so much earlier.
No attempt at reseeding was made although in this area actual
counts in the turf showed that the perennial Kentucky bluegrass plants
were running approximately five plants per square foot. At no time
was this turf left bare. The Poa annua went out slowly and the
bluegrass filled in as the Poa annua went out.
-------
-------
EXHIBIT VI
In the early Fall of the fourth year of the original applica-
tion of the plots, I retreated the left hand half of one plot at
half rate or ten pounds per thousand square feet of the product.
The photograph shows me standing at mid-line of that plot. These
plots are thirty feet by thirty feet. The untreated half on the
right is beginning to fail and one can see that Poa annua is
beginning to reinvade the untreated area. This shows that even a
vigorous perennial bluegrass turf cannot compete with Poa annua
without chemical help on the average golf course fairway.
-------
-------
EXHIBIT VII
This photograph shows the selectivity of the product but
nevertheless the product has been misused in this area. This shows
a corner of a large plot. Poa annua is extremely sensitive to ar*
senicals early in the Spring and late in the Fall. If the applica-
tion is made during these times, the Poa annua dies very rapidly
leaving a heavily infested area virtually bare. Such a treatment is
not practical on a heavily infested fairway. The desirable thing
is to avoid killing the Poa annua and merely shift the factors of
competion in favor of the deeper rooted perennial bluegrass. This
is done because the major effect of arsenicals in the soil is to
restrict the division of the cells of the root meristems. As the
result of this, the roots do not grow and form root hairs. Since
the root hairs are the major site of uptake of both minerals and
water, the Poa annua, with its shallow root system, is maintained
under almost constant moisture and nutritional stress. Under these
conditions, the perennial bluegrass of whatever variety, is able to
compete successfully with the Poa annua and replace it. This is the
only way I know to treat a heavily infested fairway without leaving
bare areas or making the fairway unplayable for the balance of the
season.
-------
-------
APPENDIX II
1? Rosa Road
Schenectady, N.Y. 12308
April 6, 1973
Writing on behalf of the EPA PAX Company Arsenic Advisory Committee,
inay I seek your help and advice? PAX Ihree-year Crabgrass Control
(25. U $ arsenic trioxide with 8.25 % lead arsenate), although not now in
use in New lork, is permitted for use on hone lawns as well as golf
courses in some western states. Our assignment is to assess the
nossible hazard from this product in particular, but with some view to
related products such as calcium arsenate and lead arsenate for turf
improvement.
Can you provide instances in which the use of such products has caused
measurable toxicity or other adverse effects in animals or humans?
Thup far, we have been unable to find substantial evidence for such
poisoning.
to tho labels, grass clippings after such treatment are
not to be fed. At least one poisoning from accidental feeding of
PAXX treated clippings was reported to have led to death in horses.
One would think that clippings from treated golf courses would have
caused similar problems. Have you heard of any such? Do you know of
any proven hazard to any species from turf improvement arsenical
products ?
If you can possibly do so, please respond promptly. Our deadline
comes soon.
Thanks for your help.
Yours sincerely, , -
''...:' / '
Douglas V. J*rost » Chairman __
PAX Company Arsenic Advisory Committee
-------
EXECUTIVE SECRETARY
WILLIAM H.DANIEL
Department of Agronomy
Purdue University
Lafayette, Indiana 47907
Room 2-303. Lilly Hall
Phone: 317-49-41195
April 10, 1973
PRESIDENT
IOI1N DUN LAP
Oakwnod Club
Cleveland, Ohio
,44121
VICE PRESIDENT
LOUIS I-:. MILLER
Louisa ilk4 Country Club
Louisville. Kentucky
•40206
TREASURER
CHARLES L. RIIYKERD
Department of Agronomy
Purdue University
Lafayette. Indiana
47P07
DIRECTORS
DAVID I-T.ARIS
Country Club of Peoria
1'coria, Illinois
61614
JOHN HTZUERALD
Ccnturv Tuio Distributors, Inc
Cincinnati, Ohio
45241
PAUL MORGAN
Brown's Run Country Club
Midcllctown. Ohio
4S040
ROBERTSCOBEE
Kiley Lawn and Golf
Equipment Corporation
Indianjpolis, Indiana
46268
DUDLEY SMITH
Silver Lake Country Club
Orland Park, Illinois
60462
JAMES.TIMMEKMAN
Oichard Lake Cmintry Club
Oichard Lake Michigan
.48033
THEODORE WOEHRLE
Oakland Hill Country Club
Birmingham, Michigan
4S010
EX-OFFICIO
LEE RECORD
I'.S.G.A. Green Section
Crystal Lake. Illinois
60014
Dr. Douglas V. Frost
17 Rosa Road
Schenectady5New York
Dear Dr. Frost:
12308
I appreciate getting your inquiry of April 6 concerning arsenic
on turf areas.
I have worked with arsenicala since first coming to Purdue in
1950, have hundreds of kodachrome slides showing the results of
using arsenicals to control crabgrass, goosegrass, chickweed,
etc. Have written numerous articles recommending and proposing
its use for turf managers on professionaly managed turf. And, I
currently believe that the granular formulations, such as Chip-
Cal 49$ tri-calcium arsenate should continue to be permitted for
use on professionally managed turf areas.
I recall about 1958 when the PAX Company had all the pre-emergent
market in Indiana. They sold eight car loads of material in the
state that year. By 1965 they had withdrawn their sales in Indiana
because other products were preferred by homeowners and were safer
for homeowners.
I recall Vaughan Seed Company selling one million pounds of granu-
lar Pre-Kill to homeowners about 1960-61. They had two complaints -
one a refund of money, one a replacement of product, but they also
stopped production for homeowners.
The Farm Bureau of Indianapolis sold Stopps. This also was changed
to a less toxic form - all before EPA came along.
I have every reason to encourage EPA to continue to allow pro-
fessional turf managers to use arsenics on professionally managed
turf areas, such as golf courses. We have no companies that are
now recommending arsenicals for home lawns, or for novice use.
The Chipman Company is the only one surviving out of eight that
used to sell calcium arsenate. They have a good educational program
and two professional turf managers.
Note the enclosed leaflet. They should be encouraged to stay in busi-
ness for if they go we will lose a Poa annua control program now in
practice on over 1,000 golf courses having achieved Poa annua removal
.•I ntin-/'rt>Jii organization supporting turf research and education.
-------
Dr. Douglas V. Frost
April 10, 1973
Page 2
and there are at least another 1,000 in the process of removing
Poa annua with arsenicals. I am not for Chipraan, but I am in-
terested in having Poa annua-free golf courses, and feel our
society needs good turf for its leisure time and recreational use.
There is no glory in having Poa annua on a golf course when citi-
zens need the outdoor recreation.
Know you will have trouble finding cases of arsenic damage to man
and animals. The literature says - the body will excrete arsenic,
and the history of the workers in arsenic mining and in chemical
manufacture shows no cases of excessive damage even to workmen in
the plant.
Hy personal experience of more than twenty years working intimately
with golf courses across the United States is that we have no evi-
dence of damage to animals, nor continued damage to persons. Sure,
there have been a couple of mistakes where a man got a temporary
response. For example, one man quit smoking after unwisely using
excessive powdery forms of calcium arsenate years ago before he
could get the granular formulation. But, that same man still uses
granular forms now. We no longer reconmend powdery formulations,
although they could be purchased at half the cost per acre treatment.
Good luck on your research towards finding evidence of toxicityl The
beauty of the program is it is so widely successful and such limited
damage that the program stands as one of those that should be kept.
Therefore, I strongly favor the continued permit to use calcium ar-
senate in a granular formulation by professional turf managers on
professional turf areas as a good procedure which deserves EPA con-
currence, and has current, adequate education and research behind it.
Trust this is helpful.
Cordially
Yours for Better Turf,
William H. Daniel
WHD:kh Turf Research & Extension
Enc. Chip-Cal leaflet
-------
UNIVERSITY OF RHODE ISLAND
KINGSTON • R. I. 02881
College of Resource Development • Department of Plant and Soil Science
April 10, 1973
Mr. Douglas V. Frost, Chairman,
PAX Company Arsenic Advisory Committee,
17 Rosa Road,
Schenectady, N.Y. 12308
Dear Mr. Frost:
I have worked with arsenicals of many kinds in the
herbicidal field since the late 1940's. I have never
personally encountered, nor have I had first-hand knowledge
of, any accidental poisoning as a result of the use of
arsenicals.
I do recommend inorganic arsenicals, such as tricalcium
arsenate, regularly for weed control purposes and don't feel
that there is currently a substitute for certain purposes.
I hope this information is helpful to you.
Sincerely,
C.R. Skogley
Professor of Agronomy
Plant & Soil Science
CRS:lp
-------
COOPERATIVE EXTENSION
NEW YORK STATE
Cornell University • State University of New York • U.S. Department of Agriculture
Chemicals-Pesticides Program
Caldwell Hall, Ithaca, N. Y., 14850
(607) 256-3283
April 11, 1973
Douglas V. Frost, Chairman
PAX Company Arsenic Advisory Committee
17 Rosa Road
Schenectady, NY 12308
Dear Mr. Frost:
I have your letter of April 6 concerning possible hazards of arsenic on
turf. Possibly you are famliar with the fact that calcium arsenate can be
used in New York State on turf for the control of poa annua in prescription
programs with a "B" permit. This material was originally excluded from use
but was later allowed under prescription type programs primarily because
no substantial evidence of injury to the environment or animals in the
environment could be found. We were unaware of any problem resulting from
the feeding of golf course grass clippings to animals. In the event such
were the case, it would seem logical that a restriction on such use might
be employed as is the case on several of our agricultural commodities.
I am sorry that I am unable to come up with anything that would be
helpful to you.
Very truly yours,
i James E. Dewey
^ ytxtension Program Leader
" Chemicals - Pesticides
JED/gmw
CHEfcUCAlS'PESTIOOeS
NEW TURK MOC8AM
New Y"ik St.M" Cnl
GmrH!l! UniVftrr.ily,
s. Now York Mali; Collyqn of Hum.'iri f '.•)!
. County Cov<:ming Hndins. ;trvi Umlc'J
y, ,rri'l N'.-W (••
-------
RUTGEPS UNIVERSITY The State University of New Jersey
COLLEGE OF AGRICULTURE AND ENVIRONMENTAL SCIENCE
P. 0. BOX 231 Department of Soils and Crops
New Brunswick, New Jersey 08903
(201) 247-1766 Ext. 1427
April 12, 1973
Dr. Douglas V. Frost
17 Rosa Road
Schenectady, New York 12308
Dear Dr. Frost:
In answer to your request on the dangers of arsenate treatments
such as "Pax", I have had no direct association or knowledge of
•injury to animals or humans from use of these chemicals (Ca
arsenate, lead arsenate, and "Pax") on turf during my 26 years
in my position.
Since there is great concern about keeping animals away from
arsenic-treated turf and most of the use has occurred on golf
courses where grazing animals are scarce, use of arsenates on
turf has not created ready occasion for such incidents.
It is my understanding that New Jersey is currently considering
chemical bans, restricted use and licensed use. I have no idea
where arsenates will fall in this program.
The arsenates are the only efficient type of herbicide for control
of annual bluegrass in closely mowed turf such as occurs on golf
courses of the Northeast. However, I have no interest in this
type product for home lawns because of the hazard and the fact
that annual bluegrass and crabgrass can be controlled by means
other than arsenates.
I trust these comments are helpful.
„ f . } J
^^- ,-
Sincerely yours, &&.-•«.' „ f . J , ££<-*+. . > -j, J 2.{- : IP'* _/ / 9? 3
Ralph E. Engel
Research Professor in
Turfgrass Management
jc
-------
Unttufrattg at $ at onto
TORONTO 181. CANADA
DEPARTMEN^ OF BOTANY - ^-j x, >Ltf3£iA^_ <5K>Vv5'~_ Te I . 4'6-928-3534
April 23, 1973
Or* Douglas V. Frost,
Chai rman,
EPA PAX Company Arsenic Advisory Committee,
17 Rosa Road,
Schenectady, New York 12308
Dear Sir:
Regarding your inquiry for information on environmental
contamination by heavy metals. My doctorate study involved an
assessment of metal fallout from a nickel refinery and a zinc-
lead smelter and subsequent accumulation in vegetation.
Associated with the zinc-lead smelter I found elevated
levels of Zn, P_b_, Se, As, Sb, Cd and Cu.
Associated with the nickel refinery I found elevated
levels of Ni, Cu, Co, Se and In.
This data may be obtained from my doctoral thesis:-
Roberts, T. M. (1972) The Spread and Accumulat Iion
-------
Page 2
I hope that this information will be of use. I would
be grateful for any reprints of your study.
Yours sincerely,
I. M. Roberts,
Lecturer
TMR/ad
-------
UNITED STATES DEPARTMENT OF AGRICULTURE
AGRICULTURAL RESEARCH SERVICE
NORTHEASTERN REGION
AGRICULTURAL RESEARCH CENTER
Beltsville, Maryland 20705
May 7, 1973
Subject: EPA PAX Co. Arsenic Advisory Committee
To: Douglas V. Frost
Consultant, Nutrition Biochemistry
17 Rosa Road
Schcnoctudy, New York 12300
In response to your letter of April 6, 1973> ve know of no instances
where PAX has caused toxicity problems when used in the recommended
manner. Likewise, we know of no instances where any turf improvement
product has caused toxic problems when used as directed. It is our
opinion that the PAX product, containing 25.11$ As2C>3 with 8.25$ lead
arsenate for crabgrass control, should probably be allowed to be used.
As with any economic poison, there is always the possibility of misuse
by people, but I don't think we should regulate the ability of citizens
to use a product safely.
The lead inclusion in this product does not seem to be great enough to
prevent the use of PAX on turf. The placement of warning statements in
a more prominent position on the label may help in preventing accidental
poisonings, particularly from grass clippings. Other than that, if
the pesticide is watered in, like it's supposed to be, we can see no
further problems with the material.
E. A. Woolson
Analytical Chemist
Pesticide Degradation Laboratory
Agricultural Environmental
Quality Institute
Philip'"CO Kearney \)
Leader
Pesticide Degradation Laboratory
-------
COOPERATIVE EXTENSION
NEW YORK STATE
Cornell University • State University of New York • U.S. Department of Agriculture
Chemicals-Pesticides Program
Caldwell Hall, Ithaca, N. Y., 14850
(607) 256-3283
May 8, 1973
Douglas V. Frost, Chairman
PAX Company Arsenic Advisory Committee (EPA)
17 Rosa Road
Schenectady, NY 12308
Dear Mr. Frost:
I have your letter of April 14 and regret that I have delayed so long in
my response. However, I tried to determine whether or not there were any
restrictions specifically listed for materials which might be used on turf.
I was unable to find any restrictions for such uses.
Restrictions and limitations are quite common on many of our pesticides
and particularly for those that might be used on forage crops or for use on
crops which sometimes might be used as livestock feed.
It would not seem out of order to me for such restrictions to be placed
on products which are used for the treatment of turf. We have had an
occasional inquiry requesting information about the possible use of grass
clippings from sod farms as a possible livestock feed. However, because of
the nature of the compounds being used, chlorinated hydrocarbons like DDT,
dieldrin, and chlordane, we warn them against this practtce due to the
accumulation in the animal even when extremely small residues might be
present. We have had no inquiries that I can recall from golf courses, but
if this is a possibility then a warning against such practice might be in-
cluded as part of the label. ;
v...
ery truly yours,
James . Dewey
Extension Program L'eader
Chemicals - Pesticides
JED/graw
CHEMICAl 5-PESTICIDES
N[W YOtK KOCBAM
N.-w f.,ik ;;i;ilr Cnllfijo nt Af|Mr.iltur«; ;mcl Lite Sncncou. New York Sl.ilo Cnllngi; nf Human Ecology, ami New York Si:ito Votcrinaiy C-.lk-qo :il
O-iM'-ll Uinv.-c.ily. Cin.p.'ialivi! I <|,-MMMU Av.ocialion:. County Governing UoiJir;:.. and United fJl:M*'K hopnrlmi-iil r>l Aijnculturu. t:oop<:f,'itin(j.
-------
April 6, 1973
Mr. George J. Butler
The Western Area Occupational
Health Laboratory
N.I.O.S.H.
Post Office Box 8137
Salt Lake City, Utah 84108
Dear Mr. Butler:
Mrs. Fran Brogan of the Cincinnati office referred me
to you concerning a question dealing with the use of arsenic in Salt
Lake City. I am currently serving on an E. P. A. advisory com-
mittee having to do with the use of a product called PAX Crab Grass
Control. This material is made in Salt Lake City and is used in
considerable quantity in that area. Are you aware of any complairrts
concerning the use of. this material for crab grass control in resi-
dential areas? The company has provided us with considerable
information, but I thought it a good idea to contact the Salt Lake City
office simply to learn whether any complaints had filtered into the
N.I.O.S.H. office at Salt Lake.
By way of introduction, many of my years were spent in the
Division of Occupational Health and, thus, I am calling upon you for
privileged information in case such is at hand. There will be no need
for you to contact the company, as they have provided us with con-
siderable data so far.
Thanking you in advance for any effort this request may
cause.
Sincerely,
Donald J. Birmingham, M. D.
DJB vp Professor
-------
F
DEPARTMENT OF HEALTH. EDUCATION, AND WELFARE
PHS, HSMHA
NATIONAL INSTITUTE FOR OCCUPATIONAL SAFETY AND HEALTH
WESTERN AREA OCCUPATIONAL HEALTH LABORATORY
P. O BOX 8137
SALT LAKE CITY. UTAH 841O8
April 11, 1973
Donald J. Birmingham, M.D.
Professor
Wayne State University
Gordon H. Scott Hall
of Basic Medical Sciences
540 East Canfield Avenue
Detroit, Michigan 48201 '
Dear Dr. Birmingham:
•
Your introduction was unnecessary since your name is quite familiar to
me from your past association with the Public Health Service and your
contributions to the field of dermatology.
I, like many other amateur gardeners here in the Salt Lake Valley, am
aware of PAX Crab Grass Control, but I have never personally experienced
any problems with the use of the chemical. I have also asked some of
the staff at this facility who also use the material but there replies
were as negative as mine. In addition, I contacted Salt Lake County
and Utah State Health Department representatives to see if they had
any record of complaints about PAX products, but neither one of the
agencies had knowledge of any problems attributed to its use in the
community.
I hope that this information will be of some use to you and if I can be
of any further assistance, please feel free to contact me.
Sincerely yours,
--
Georgef Jf Butler
Sr. Sanitary Engineer
Coordinator, DTS/SLC
1*1
b
9
\
-------
PERSONS mo APPEARED BEFORE THE COMMITTEE:
Mr. W.B Robins, Manager, The PAX Company.
Mr. Donald B. Holbrook, Jones, Waldo, Holbrook and McDonough, Attorneys and
Counselors, Salt Lake City, Utah.
Alan K. Done, M.D., Pediatrician and Toxicologist, Medical Division, Food
and Drug Administration, Washington, D.C.
E.A. Woolson, Ph.D., Analytical Chemist, Pesticide Degradation Laboratory,
Agricultural Environmental Institute, USDA, Beltsville, Md.
William Buck, D.V.M., Professor, Toxicology Section, Veterinary Diagnostic
Laboratory, Iowa State University, Ames, Iowa.
PERSONS WHO RESPONDED TO LETTERS FROM COMMITTEE MEMBERS«
George J. Butler, Sr. Sanitary Engineer, Western Area Occupational Health
Laboratory, NIOSH, PHS, HEW, Salt Lake City.
Bernard Ellison, Research Director, PAX Company, Salt Lake City.
William H. Daniel, Ph.D., Professor, Turf Research, Dept. of Agronomy,
Perdue University, Lafayette, Indiana.
Ralph E. Engl, Ph.D., Research Professor, Trufgrass Management, College of
Agriculture and Environmental Science, Rutgers University,
New Brunswick, N.J.
C.R. Skogley, Ph.D., Professor, Agronomy, University of Rhode Island, Kingston, R.I.
William B. Buck, see above.
Douglas I. Hammer, M.D., Human Studies Laboratory, Division of Health Effects
Research, National Environmental Research Center, EPA,
Research Triangle Park, N.C.
John V. Lagerwerff, Ph.D., Soils Scientist, USDA-ARS, Beltsville, Md.
Philip G. Kearney, Ph.D. and E.A. Woolson, Ph.D., Agricultural Environmental
Quality Institute, USDA-ARS, Beltsville, Md.
M. Norman Anderson, Anax Lead and Zinc, Inc., Boss, Mo.
T.M. Roberts , Ph.D., Institute of Environmental Sciences and Engineering, Univ.
of Toronto, Toronto, Canada.
Glen E. Gordon, Dept, of Chemistry, University of Maryland, College Park, Md.
James E. Dewey, Entomologist, Chemical Pesticides Program, Caldwell Hall,
Cornell University, Ithaca, N.Y.
I'alter Durniak, Cornell University Cooperative Extension Agent, Schenectady
County, N.Y
EPA
RTP
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