SUBSTITUTE CHEMICAL PROGRAM
INITIAL SCIENTIFIC
MINIECONOMIC REVIEW
PARATHION
JANUARY 1975
U.S. ENVIRONMENTAL PROTECTION AGENCY
OFFICE OF PESTICIDE PROGRAMS
rttos^JCRITERIA AND EVALUATION DIVISION
— **. WASHINGTON, D.C. 20480
EPA-540/1-75-001
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This report has been compiled by the Criteria and
Evaluation Division, Office of Pesticide Programs,
EPA, in conjunction with other sources listed in
the Preface. Its contents do not necessarily
reflect the views and policies of the Environ-
mental Protection Agency, nor does mention of
trade names or commercial products constitute
endorsement or recommendation for use.
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GENERAL CONTENTS
Page
List of Figures vi
List of Tables vii
Preface xi
Part I. Summary 1
Part II. Initial Scientific Review 12
Subpart A. Chemistry 12
Subpart B. Pharmacology and Toxicology 55
Subpart C. Fate and Significance in the Environment 139
Subpart D. Production and Use 212
Part III. Minieconomic Review 252
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FIGURES
No.
1 Production Schematic for Parathion 18
2 Major Photodegradation Products of Parathion 24
Analytical Scheme for Chlorinated (Nonionic) and Organophosphate
Residues 25
Major Photodegredation Products of Parathion 36
vi
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TABLES
No. Page
1 Raw Materials and By-Products in the Manufacture
of Parathion 17
2 Suggested Formulations for Parathion Emulsifiable
Concentrates 33
Other Photodegradation Products of Parathion 37
4 Dietary Intake of Parathion and Total Organo-
phosphates 42
5 Average Incident and Daily Intake of Parathion. ... 43
6 Percent Distribution of Parathion Residues by Fiscal
Tear in Different Quantitative Ranges 45
7 Summary of U.S. Tolerances for Parathion and/or
Methyl Parathion on Raw Agricultural Commodities. . 48
8 Acute Oral Toxicity of Parathion for Rats 58
9 Acute Toxicity of Parathion for Rats Via Routes
Other Than Oral 59
10 Chronic Oral Toxicity Test in Rats Fed Parathion. . . 62
11 Acute Oral Toxicity of Parathion to Mice 64
vii
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TABLES (Continued)
No.
12 Acute Toxicity of Parathion to Mice—Routes Other
Than Oral 66
13 Acute Oral Toxicity of Parathion to Guinea Pigs ... 67
14 The Toxic and Teratogenic Effect of Parathion
Given Intraperitoneally to Rats on the llth
Day of Pregnancy 89
15 Percentage of Chromosomal Changes at Metaphase of
Male Guinea Pigs After Parathion (0.05 tng/testical)
Treatment 99
16 Susceptibility of Man and Other Animals to Single
Oral Dosts of Parathion 101
17 The Susceptibility of Man and Other Animals to
Repeated Oral Doses of Parathion 102
18 Acute Toxicity of Parathion to Fish 142
19 Common and Scientific Names of Fish Used in Controlled
Toxicity Tests With Parathion 143
20 Comparative Toxicity of Parathion and Malathion
Insecticides to Centrarchids 143
21 Toxicity of Three Organophosphate Insecticides
to Bluegill and White Rats 144
22 E^5Q (immobilization) Values (ppb) of Three Organo-
phosphate Insecticides to Zooplankton 152
23 LC50 Values (ppb) of Three Organophosphate Insecti-
cides to Benthic Invertebrates 153
24 Acute Toxicity of Parathion to Avian Species 158
viii
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No. Page
25 Common and Scientific Names of Birds Used in Con-
trolled Toxicity Tests With Parathion 158
26 Avian Oral Toxicity (5 days) 159
27 Effect of Age on Parathion Toxicity in Mallard Ducks. 160
28 Effects of Intravenous Injections of Parathion on
Hematocrit of Ducks and Quail 161
29 Parathion - Summary of Registered Uses by Crops,
Application Rates, and Rate and Time Restrictions . 214
30 Pest Insects and Mites Against Which Parathion is
Recommended (in alphabetical order by common
names) 219
31 Registered Uses of Parathion Emulsifiable Liquid
(4 Ib active ingredient per gallon) - Crops and
Other Uses, Pests, Dosage Rates and Use
Limitations 222
32 Registered Uses of Parathion Emulsifiable Liquid
(4 Ib active ingredient per gallon) - Crops and
Other Uses, Pests, Dosage Rates and Use
Limitations 231
33 Estimated Uses of Parathion on the U.S. by Regions
and Major Crops (1972) 243
34 Parathion Uses in California by Major Crops and
Other Uses (1970-1973) 246
35 Use of Parathion in California in 1972, by Crops,
Applications, Quantities, and Acres Treated .... 247
36 Use of Parathion in California in 1973, by Crops,
Applications, Quantities, and Acres Treated .... 249
ix
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No^ Page
37 Results of Parathion Application on Sorghum
Midge 259
Results of Parathion Application on Sorghum
Greenbug 261
39 Results of Parathion Application on Wheat
Greenbug . 263
-iO Results of Parathion Application on Corn Insect
Pests . 264
41 Results of Parathion Application for Wireworm
Control 265
42 Results of Parathion Application on Strawberry
Tarnished Plant Bug 267
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PREFACE
The Alternative (Substitute) Chemicals Program was initiated under
Public Law 93-135 of October 24, 1973, to "provide research and testing
of substitute chemicals." The legislative intent is to prevent using
substitutes, which in essence are more deleterious to man and his environ-
ment, than a problem pesticide (one that has been suspended, cancelled,
deregistered or in an "internal review" for suspected "unreasonable
adverse effects to man or his environment"). The major objective of the
program is to determine the suitability of substitute chemicals which
now or in the future may act as replacements for those uses (major and
minor) of pesticides that have been cancelled, suspended, or are in litiga-
tion or under internal review for potential unreasonable adverse effects
on man and his environment.
The substitute chemical is reviewed for suitability considering all
applicable scientific factors such as: chemistry, toxicology, pharma-
cology and environmental fate and movement; and socio-economic factors
such as: use patterns and costs and benefits. EPA recognizes the fact
that even though a compound is registered it still may not be a practical
substitute for a particular use or uses of a problem pesticide. The
utilitarian value of the "substitute" must be evaluated by reviewing its
biological and economic data. The reviews of substitute chemicals are
carried out in two phases. Phase I conducts these reviews based on data
bases readily accessible at the present time. An Initial Scientific
Review and Mini-Economic Review are conducted simultaneously to determine
if there is enough data to make a judgment with respect to the "safety
and efficacy" of the substitute chemical. Phase II is only performed if
the Phase I reviews identify certain questions of safety or lack of benefits
The Phase II reviews conduct in-depth studies of these questions of safety
and cost/benefits and consider both present and projected future uses of
the substitute chemicals.
The report summarizes rather than interprets scientific data
reviewed during the course of the studies. Data is not correlated from
different sources. Opinions are not given on contradictory findings.
This report contains the Phase I Initial Scientific and Mini-Economic
Review of parathion (0,)-dimethyl 0-p-nitrophenyl phosphorothioate).
Parathion was identified as a registered substitute chemical for certain
cancelled and suspended uses of DDT. Where applicable, the review also
identifies areas where technical data may be lacking so that appropriate
studies may be initiated to develop desirable information.
The review covers all uses of parathion and is intended to be
adaptable to future needs. Should parathion be identified as a substitute
for a problem pesticide other than DDT, the review can be updated and made
readily available for use. The data contained in this report was not
intended to be complete in all areas. The review was coordinated by a
XI
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team of EPA scientists in the Criteria and Evaluation Division of the
Office of Pesticide Programs. The responsibility of the team leader
was to provide guidance and direction and technically review information
retrieved during the.course of the study. The following EPA scientists
were members of the review team: George Bagley (Chemistry), team leader;
Jeff Conopask (Economics); E. David Thomas (Registered Uses); Ralph C.
Wright (Registered Uses); William Burnam (Pharmacology and Toxicology);
Elsie Kelley (Pharmacology and Toxicology); Howard Kerby (Fate and
Significance in the Environment); Richard Tucker (Fate and Significance
in the Environment).
Data research, abstracting and collection were primarily performed
by Midwest Research Institute, Kansas City, Missouri (EPA Contract #68-01-
2448). RvR Consultants, Shawnee Mission, Kansas, under a subcontract to
Midwest Research, assisted in data collection. Monsanto, a manufacturer
of parathion, made scientific recommendations and additions to this report.
The recommendations of the following National Environmental Research
Centers, EPA Office of Research and Development have also been incorporated:
Southeast Environmental Research Laboratory, Athens, Georgia; Pesticide
and Toxic Substances Effects Laboratory, Research Triangle Park, North
Carolina.
xii
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PART I. SUMMARY
CONTENTS
Page
Production and Use 2
o
Pharmacology and Toxicology J
Food Tolerances and Acceptable Intake 7
Environmental Effects 7
Specific Hazards of Use 9
Limitations in Available Scientific Data 10
Efficacy and Cost Effectiveness 10
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This section contains a summary of the "Initial Scientific and
Minieconomic Review" conducted on parathion.
Production and Use
Parathion (0,0-diethyl 0-£-nitrophenyl phosphorothioate) is manu-
factured by a synthesis processing involving three reactions:
PS
25
4C2H5OH
S
II
C12
S
It
2(C2H50)2PSH
HC1
(1)
(2)
(C2H50)2PC1
Na
NaCl
(3)
Parathion
The chemical properties of parathion are similar to those of its
methyl analog (methyl parathion). Parathion is oxidized enzymatically
to paraoxon (0,0-diethyl 0-p_-nitrophenyl phosphate), a reaction inti-
mately associated with parathion1 s biological effects. The oxidation
of parathion to paraoxon can also be effected by chemical action of
atmospheric oxygen; atmospheric oxidation is accelerated by ultraviolet
radiation.
Hydrolysis of parathion virtually destroys all insecticidal
activity. Fifty percent hydrolysis of parathion is achieved in 2.7 hr
in aqueous solutions at pH 9 and 70°C; in 17 to 20 hr at pH 1 and 70°C;
and in 690 days at pH 1 to 5 and 20°C. Fifty percent hydrolysis of
paraoxon requires 9.2 days in aqueous solution at pH 10 and 25 °C.
Parathion is commercially available in a large number of registered
formulations and in many physical forms, including emulsifiable con-
centrates, wettable powders, dusts, granules, and aerosol formulations
containing only parathion or parathion in combination with other active
ingredients.
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Parathlon has a very broad spectrum of effectiveness against in
sects and mites. Tolerances for parathion residues have been estab-
lished on about 100 raw agricultural commodities.
The estimated domestic production of parathion in 1972 is 14
million pounds. About 10 million pounds (as active ingredient) were
used in the United States in 1972. A review of available data on farm
use of parathion for the period 1966 to 1972 indicates an upward trend
of 2%/year in the usage of parathion in agriculture. Two of the previous
domestic producers of parathion, however, have discontinued production
of this insecticide since 1972. There is no assessment possible on
the ability of industry to increase parathion supply.
Essentially all domestic usage of this pesticide is agricultural.
Parathion is registered and recommended for use on a large number of
domestic crops, including fruit, nut, vegetable, and field crops.
Domestic crops on which parathion was used in 1972, listed in de-
creasing order of the quantity used, are: cotton, sorghum and small
grains; deciduous fruit and nut crops; vegetable crops; corn; citrus
fruits; tobacco; and numerous other crops, each of which account for
a relatively small portion of the total usage.
The 1972 domestic use pattern, by geographical region and in
decreasing order of use, is estimated to be: West South Central ('ncl/hom?
and Texas); Southwest (California, Arizona, Hawaii, New Mexico, and
Nevada); Southeast; West North Central; East South Central; Northwest;
and Northeast. Slightly more than 10% of all parathion used in the U.S.
in 1972 was applied in California on almost 100 different crops.
Pharmacology and Toxicology
Parathion is a highly toxic pesticide, as evidenced by studies
with laboratory and domestic animals, fish, other aquatic life, avian
species, wildlife and humans.
The literature on clinical cases of acute parathion poisoning in
man is extensive. In nearly all instances, however, the amount iagested,
inhaled, or adsorbed was unknown. An oral lethal dose is estimated to 'e
l-to-2 mg/kg of body weight; the largest nonfatal dose reported is 6.4 mg/kp,
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A 167e inhibition of RBC cholinesterase has been produced in man at a
dosage level of 0.1 mg/kg/day over a 42-day period, while the ingestion
of 7.5 rag/day of parathion for 9 days produced a reduction of plasma
cholinesterase of 27 to 327..
The major cholinergic effects produced by parathion poisoning are
weakness, nausea, vomiting, excessive sweating, headache, excessive
salivation, difficulty in walking, miosis, and muscle fasciculations.
Electroencephalographic (EE6) changes resemble those seen in epileptics.
There have been a few controlled investigations of the dermal ef-
fect of parathion on humans. No certain conclusions have been drawn
from skin tests related to rates of absorption. Paraoxon, the oxida-
tion product of parathion, however, does not appear to be hydrolyzed in
the skin. In the controlled studies reported, the exposure of hand,
forearm or whole body (nude) to relatively high concentrations of
parathion had little adverse effect. Exposure to parathion vapors for
3 hr did not significantly reduce plasma cholinesterase activity.
The hazard from inhalation is said to be three times greater than
from oral ingestion. Unfortunately, the test results that were re-
viewed do not report the actual concentration of parathion in the air
that was being breathed. RBC cholinesterase and plasma cholinesterase
depressions of 98 and 83%, respectively, were reported for subjects
exposed to fumes from parathion.
The acute toxicity of parathion to male rats is presented below:
Route of entry Measurement
Oral LDso (mg/kg)
Intraperitoneal LD50 (mg/kg)
Dermal LD50 (mg/kg)
Inhalation LC5Q (1 hr)
LC50 (4 hr) (mg/4)
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The collective data indicate that parathion is highly toxic to all
species tested thus far by all routes of administration. There is usually
a lesser degree of toxicity produced by dermal exposure than by other
routes. The vehicle is very important in dermal toxicity tests. Episodes
of acute toxicity are more likely to occur in nature than are chronic
poisonings. The pathology of chronic toxicity is similar to that found in
acute episodes. The young are more susceptible than the mature organisms.
In rats, males appear to be less susceptible than females. The symptoms
and mechanisms of physiological action in all species are essentially the
same. Cholinesterase depression is a sensitive clinical measurement.
Pathological damage appears to be minimal even in chronic exposures.
There is little available literature regarding parathion's effect on
reproduction. Most of the reported studies were conducted on wild avian
species (ducks, pheasants, and partridges). Findings indicated that 5-to-
10 ppm of parathion had little effect, if any, on egg production, fertility
or progeny growth. There was no indication that parathion residues occur
in the egg.
There were only two studies found on the mammalian teratogenesis of
parathion. Although they showed that parathion caused a reduction in the
number of fetuses and an increase in the number of resorptions, they
provided little evidence that actual malformation of the fetus occurs
as a result of parathion exposure. The data suggests that parathion
does not produce specific teratogenic effects.
A large number of papers have been published regarding the effect
of parathion on the normal development of avian embryos. Various
deformities have been produced when eggs are immersed in parathion or
the pesticide is introduced into the yolk sac. Investigators have
reported lordosis of the neck, celosomia, retardation of the axial
skeleton, disorganized vertebral musculature, light edema, achondroplasia
and abnormal leg position. Parathion reportedly acts as an antimitotic
substance that markedly effects cell division. Generally, the dosage
of parathion was relatively high before deformation of the embryo
occurred.
The available data concerning the effect of parathion on crustaceans
is meager. The normal length of oyster larvae, however, is reported
to be greatly depressed by 1-ppm parathion in water.
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Treatment of tissue cultures with parathion does not permit
prediction of the'activity that would be produced in the intact organism.
In a study with HeLa cells (a human malignant cell line) paraoxon was
less toxic than parathion, and nitrophenol was as toxic as parathion.
Furthermore, relatively high amounts of parathion have to be used in
tissue culture to produce a definitive response. There is little
difference between malignant and nonmalignant cell responses to
parathion.
There is practically no available literature on the induction of
chromosomal abnormalities by parathion. However, abnormalities have
been induced by parathion in mitotic chromosomes of the guinea pig.
No references were found on the oncogenic effect of parathion.
Parathion had no clear effect on chemically induced tumors.
The following major points can be stated regarding the metabolism
of parathion:
1. Parathion is readily adsorbed through the skin, from the
stomach and the lung.
2. It becomes widely distributed throughout the body but does
not accumulate at any site and causes no effect other than
the irreversible binding of paraoxon to cholinesterase.
3. The major metabolites of parathion that are excreted are
aminoparathion, jj-nitrophenol, diethylphosphorothioic acid,
ethylphosphoric acid and sulfate.
4. The biotransformation of parathion involves two distinct
phenomena: activation and detoxification.
5. Parathion is enzymatically oxidized to paraoxon by the mixed
function oxidase system.
6. Microsomal oxidation of parathion requires NADP!^, oxygen,
potassium chloride and magnesium ion for maximum activity.
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Food Tolerances and Acceptable Intake
Tolerances for parathion have been established for about 100 raw
agricultural commodities in the United States; all but one are in the
0.1 to 1.0 ppra range. The tolerances for parathion and methyl para-
thion are the same. When both chemicals are present, the tolerances
apply to the combined total of methyl parathion and parathion.
The acceptable daily intake (ADI) for parathion has been set at
0.005 mg/kg body weight.
Environmental Effects
Parathion is toxic to fish and wildlife; product labels carry a
warning that wildlife in treated areas may be killed. A brief summary
of the acute toxicity of parathion to fish, anthropods and avian species
is as follows:
LC50 for Fish (ppm)
Bluegill 24 hr 0.141
Bluegill 48 hr 0.047
Golden shiner 24 hr 0.931
Greenfish 24 hr 0.155
Mummichog 48 hr 0.15
Stripped mullet 96 hr 0.125
Tilapia 96 hr 0.375
LC5Q for Anthropods (ppm)
Amphipod (Gammarus lacustris) 24 hr 0.012
Amphipod (Gammarus lacustris) 48 hr 0.006
Stonefly (Claassenia sabulosa) 24 hr 0.0088
Stonefly (Pteronarcella badia) 24 hr 0.008
Stonefly (Pteronarcys californica) 24 hr 0.028
Stonefly (Pteronarcys californica) 48 hr 0.011
Stonefly (Pteronarcys sp.) 48 hr 0.011
Waterflea (Daphnia pulex) 48 hr 0.0004
Waterflea (Daphnia sp.) 48 hr 0.00076
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Oral LD5Q for Avian Species (rag/kg)
Chukar partridge 24.0
House sparrow 1.3-3.4
Japanese quail 6.0
Mallard duck 1.0-2.1
Pheasant 12.4
Pigeon 2.5
Quelea 1.8
Red-winged blackbird 2.4
Starling 5.6
Parathion is universally.recognized as being highly toxic to bees.
Studies of the toxicityof parathion to bees (Apis me 1 lifer a) by direct
topical application and by exposure to parathion containing solutions,
vapors and surface deposits have shown this pesticide to be highly
toxic by all routes tested.
The reports reviewed during this study indicate that parathion would
permit survival of beneficial insects in some predator-parasite systems.
For example, the LD5Q of parathion to the English grain aphid (Macrosiphum
aenae) is 1.8 Ug/g, while the LDjo for two of the aphids most numerous
ubiquitous predators (Hippodamia convergens and Nabis americoferus) are
40 and 21 ug/g, respectively. Such a favorable relationship, however,
does not exist in all systems.
The available data also indicate that parathion is extremely toxic
to aquatic fauna, but relatively nontoxic to the lower aquatic flora.
A number of aquatic microorganisms degrade parathion. Many of these
organisms also preferentially sorb and thus accumulate parathion from
aqueous media. This sorption process may be independent of life pro-
cesses; sorption rates of live and dead organisms showed little differ-
ences.
Only limited data was found on the presence of parathion in the
air. One study reported on the parathion content of air inside and out-
side the homes of workers occupationally exposed to this insecticide.
The results indicated that parathion was present in the atmosphere,
thereby exposing the total population of the area. The presence of
parathion residues in the air raises important questions, including the
origin of such residues, their relationships to parathion use and
handling patterns in the area, their persistence and transport patterns
in air, and their significance to human and environmental health.
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The persistence of parathion in the natural aquatic environment is
apparently markedly affected by microbial activity. One study indicated
that without microbial activity, parathion would remain in the environ-
ment for several months; in biologically active (aerobic or anaerobic)
environments, it would be degraded in a matter of weeks.
Other investigators have concluded that it is unlikely that water
in deeper soil strata could become contaminated with insecticidal resi-
dues from the upper agricultural soil layers, or that parathion could
contaminate underground water supplies beneath any of these soils by
leaching under normal rainfall conditions.
Laboratory, field, and monitoring data on the residues and fate of
parathion in the soil show that the persistence of this chemical varies
considerably, depending upon a number of factors. Parathion residues in
the soil degrade by chemical hydrolysis as well as by microbial action.
The half-life of parathion in soil has been shown to be as short as 1.5
week. In the case of heavy soil contamination, parathion residues have
been shown to persist for at least 16 years.
Parathion is strongly adsorbed by organic matter. Once adsorbed
the chemical becomes unavailable for insecticidal action, and appears
to be protected to a degree against degradation. No data is available
on the fate of such adsorbed parathion residues; it is not known whether
they eventually degrade, or if and under what conditions they might be-
come reactivated by desorption. No information appears to be available
on the fate of the initial degradation products, especially £-nitrophenol
and aminoparathion, or on the effects of these degradation products on
organisms other than mammals and insects.
The two most important environmental transport mechanisms for para-
thion appear to be volatilization and surface runoff while absorbed on
solids.
No data were found on the biomagnification of parathion.
Specific Hazards of Use
The only major hazards associated with the registered uses of para-
thion that have been documented by this review are its acute toxic hazard
to man and, to a lesser degree, its acute toxic hazard to many of the
other higher organisms. Data were not found that documented the associ-
ation of this hazard with any specific use of parathion.
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Limitations in Available Scientific Data
The review of the scientific literature was based on available
sources, given limitations of time and resources. Data was not found
in a number of pertinent areas:
1. The mechanism of tolerance to chronic parathion administration.
2. Chronic inhalation toxicity of parathion, based on cholinesterase
inhibition and on unmistakable signs of toxicity.
3. The fate of parathion residues adsorbed on organic matter or
other soil colloids.
4. The fate and effect in the environment of the major degradation
products of parathion, especially 2.~n^tr°Phen°l an<* amino-
parathion.
5. The persistence and fate of parathion residues in water,
especially under field conditions.
6. The origin, presence, persistence and significance of
parathion residue in air.
7. Parathion metabolism and residues in and on nontarget plants,
and regarding the effects of these residues on wildlife feeding
on such plants.
8. Effects on ecosystems.
Efficacy and Cost Effectiveness
Parathion is registered for a wide variety of crops and pests;
yield changes and efficacy data have been reported for numerous crop-
pest combinations. However, because of inherent limitations in crop-test
data, only order-of-magnitude estimates of economic benefits can be made.
Parathion was reported to be effective when used on cotton to
control the bollworm and boll weevil, but was much less effective for
control of the tobacco budworm. The budworm is more resistant to
parathion than to methyl parathion. The results of one yield test
showed economic gains by the use of parathion on cotton of $93.98/acre.
10
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Effective control of the sorghum midge was achieved with parathion.
However, economic effects ranged from a loss of $10.00 to a gain of $5.00
per acre. Rate and timing of application were important to the effect on
sorghum yield.
Parathion also controls the greenbug on sorghum. Reported yield
changes were variable, ranging from a loss of 458 pounds to a gain of
1,083 pounds per acre; economic benefits ranged from a loss of $12.80 to a
gain of $23.80/acre. Some phytotoxicity was observed, however, when high
rates of parathion were used, and thus adversely affected yields from
some varieties of sorghum.
Greenbug control on wheat ranged from 88% to 92%; economic benefits
ranged from $5.70 to $17.00/acre from the use of parathion.
In two out of three tests conducted in Virginia, parathion greatly
reduced the amount of damage to peanuts caused by the southern corn
rootworm. A control was not used in the third test, and there was no
explanation for not using it. Economic benefits for the one test
reporting yields amounted to $26.50/acre.
One application of parathion effectively controlled the European
corn borer and Western corn rootworm, with benefits ranging from $5.40
to $143.30/acre.
Application of parathion to control the Pacific wireworm on po-
tatoes resulted in reductions of 78% to 95% in the amount of culls.
Economic benefits varied from a loss of $103.00 to a gain of $108.70/acre.
Economic benefits for control of the potato aphid amounted to
$87.90/acre. For the potato leafhopper, benefits were $504.50/acre.
Parathion applied to lima beans at the time of first bloom resulted
in good control of Lygus hesperus and increased yields significantly.
Economic benefits for one test were $236.70/acre.
The economic benefit for control of the pea aphid in one test was
$67.50/acre.
Two applications of parathion appeared to provide satisfactory
control of the tarnished plant bug on strawberries. The economic bene-
fits ranged from $527.70 to $905.70/acre.
Cost effectiveness on a limited statistical basis was demonstrated
for four major crops including three major cotton pests, two sorghum pests,
one wheat pest, and two corn pests. Additional data were presented on
three potato pests and three vegetable/fruit pests.
11
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PART II. INITIAL SCIENTIFIC REVIEW
SUBPART A. CHEMISTRY
CONTENTS
Page
Synthesis and Production Technology 13
Physical Properties of Parathion 16
Analytical Methods 20
Composition and Formulation 30
Wettable Powders 30
Dusts 31
Emulsifiable Concentrates 31
Granules .32
Chemical Properties, Degradation Reactions and Decomposition Process ... 32
The Effect of Sunlight and Ultraviolet Radiation 34
Hydrolysis 35
The Effect of Heat 39
Oxidation 40
Reduction 40
Occurrence of Parathion Residues in Food and Feed Commodities 40
Acceptable Daily Intake 44
Tolerances 47
References 51
12
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This subsection contains a review of available data on parathion's
chemistry and presence in foods. Eight subject areas have been examined:
1. Synthesis and-production technology.
2. Physical properties of parathion.
3. Composition and formulation.
4. Chemical properties, degradation reactions and decomposition
processes.
5. Occurrence of residues in food and feed commodities.
6. Acceptable daily intake.
7. Tolerances.
Synthesis and Production Technology
The chemical processes used for parathion and methyl parathion
manufacture are almost identical. The only difference is in the alcohol
(methanol or ethanol) used in the initial reaction (with phosphorus penta-
sulfide). The equipment for producing these compounds is identical. In
most cases the same processing equipment is used for the manufacture of
both products.
The following is a list of known parathion manufacturers and
production capacity and levels.
13
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Manufacturer and
plant location
Plant
capacity!/ Estimated 1972 production
(million Ib/year) of parathion (million Ib)
Monsanto Company
Anniston, Alabama
50
10
Stauffer Chemical
Company
Mount Pleasant, Tennessee
Kerr-McGee Chemical
Corporation
Hamilton, Mississippi
Los Angeles, California
Velsicol Chemical
Corporation
Bayport, Texas
Total
30
9
3
10
102
None
1
None
14
Source: MRI estimates.
af Plant capacity is stated for methyl parathion plus (ethyl) parathion.
Stauffer and Kerr-McGee have discontinued parathion production
since 1972.
Three reactions are involved in the synthesis of parathion:
P2S5
S
ii
(C2H50)2PSH + C12
H2S
S
ii
(C2H50)2PC1 + HC1 + S
(1)
(2)
(C2H50)2PC1
(C2H50)2P>
N02 + NaCl (3)
14
-------
In the first two reactions, the intermediate diethyl phosphorothiono-
chloridate is produced. This intermediate may be produced on site or else-
where, or can be purchased from another manufacturer.
One of the most detailed descriptions of methyl parathion manufacture
is a 1953 U.S. patent. Although this patent discusses methyl parathion
manufacture, the process description is applicable to parathion synthesis.
In the patent, Schrader (1953).!' describes the reaction 3 procedure for
the manufacture of methyl parathion. According to Schrader's procedure,
this exothermic reaction is performed at 80 to 100°C. However, according
to a patent by Dvornikoff et al. (1953),—' it is preferred to operate at
a much lower temperature of from -10 to +10°C. The reaction is performed
at atmospheric pressure and requires a reaction time of 5 hr at 80 to 95°C
but about 18 hr if performed at 0°C.
The reaction is conducted in the liquid phase. One of various organic
solvents may be present. An alcoholic medium is specified by Dvornikoff
et al. (1953). However, an inert solvent such as benzene or chlorobenzene
is preferred by Schrader (1953). Monsanto employs acetone as solvent.
Copper powder may be used as a catalyst or the reaction may simply
be conducted in a copper reaction vessel, thereby shortening reaction
time appreciably. A small amount of potassium bromide can be used as an
effective co-catalyst. Aliphatic amine catalysts were cited for use in
this reaction by Toy et al. (1949).-/ At least 0.25% of such materials
as trie thy lamine, tributy lamine, N-ethyl morpholine and hexamethylene
tetramine may be used.
The reaction is carried out in a stirred, jacketed vessel. Although
the reaction is conducted at essentially atmospheric pressure, closed
vessels must be used because by-product gases are both toxic and odorous.
The yield of methyl parathion is 90% or higher. The reaction prod-
uct mixture may be pumped through a precoated filter to remove gummy im-
purities . The filtrate may then be separated into aqueous and oily
layers. The lower oily layer may then be washed with a dilute sodium
carbonate solution, then with water; it may then be steam distilled to
remove by-product trimethyl thiophosphate. After cooling and settling,
I/ Schrader, G. (to Farbenfabriken Bayer), U.S. Patent No. 2,624,745
(6 January 1953).
2/ Dvornikoff, M. N., et al. (to Monsanto Chemical Company), U.S. Patent
" No. 2,663,721 (22 December 1953).
3/ Toy, A. D. F., et al. (to Victor Chemical Works), U.S. Patent No.
2,471,464 (31 May 1949).
15
-------
the organic Layer can be dried by heating under vacuum to give the
product.
Monsanto produces parathion by a batch process in equipment dedi-
cated to methyl and ethyl parathion production. Two of the raw materials
are produced on site and the rest are received by rail. (See Table 1.)
A production schematic is shown in Figure 1.
Stauffer's method of producing parathion is believed to be similar
to Monsanto ' s .
No information is available concerning production methods at the
Kerr-McGee methyl parathion plant. The plant at Hamilton does not produce
either ^2^5 or t*ie £~nitrophenol.
Physical Properties of Parathion
Chemical Name: 0,0-Diethyl 0-£-nitrophenyl phosphorothioate
Common Name: Parathion
Trade Names; Alkron, Aileron, Bladan, Corothion, E-605, Ethyl
Parathion, Ethlon, Folidol E-605, Niran, Orthophos,
Panthion, Paramar, Parathene, Farawet, Phoskil,
Rhodiatrox, Soprathion, Stathion, Thiophos
Pesticide Class; Broad- spectrum nonsystemic insecticide; organo-
phosphate
Structural Formula: €21150 X
Tj
'
Empirical Formula;
Molecular Weight; 291.27
Analysis; C, 41.237.; H, 4.84%; 0, 27.47%; N, 4.81%; P, 10.64%;
S, 11.01%
Physical State; Pure compound is a yellow liquid. Technical mate
rial is an amber to dark brown liquid, with a
gar lie- like odor.
16
-------
Table 1. RAW MATERIALS AND BY-PRODUCTS IN THE MANUFACTURE OF PARATHION
Material
1. PS
2. C125
3. CfcHjOH
4. NaOC6H,N02
5 . Acetone
6. Soda ash
Material
1. RjS
2. HC1
3. S
4. NaCl
Raw Materials
Received Received
from by
On-site Tote bins
Louisiana Rail, tanks
Louisiana Rail, tanks
On-site
Southwest Rail, tanks
East; middle- Rail, tanks
west
Reaction By-Products
Amount produced
Form (Ib/lb AI)
Gas 0.06 calcd.
Gas 0.12 calcd.
0.11 calcd.
0.20 calcd.
Storage Remarks
Tote bins
Tank cars Vented to pro-
duction sys-
tem
Tank
Bulk For waste
disposal
Disposition Remarks
Flared S02 air pol-
lutant
Most re- Some to liquid
cycled waste
Incinerate S02 , some
H3P04?
Biol. waste Discharged to
treatment city sewer
Other Process Wastes and Losses
Material
Active ingre-
dient
Solvents
Other : Organo-
phosphates
p_-nitrophenol
Amount produced •
Form (Ib/lb AI)
Aqueous
Gas liquid
Disposition Remarks
Liquid waste < 1 ppm to
treatment city sewer
Burned
Liquid waste
treatment
Liquid waste
treatment
Source: Lawless, E. W., and T. L. Ferguson of Midwest Research Institute,
and R. von Rumker of RvR Consultants, The Pollution Potential
in Pesticide Manufacturing, for Environmental Protection Agency,
Contract No. 68-01-0142 (January 1972).
17
-------
SO2
t
Flare
H2S
SO2
Incinerator
C2H5OH-
Reactor
^ Dmlkyl
Ester
CI2.
•HCI-
Chlorinator
•Chloridothionate
NaOC6H4NO2-
Ace to ne
Parathion
Unit
NaCI-
Na2CO3-
Waste
Treatment
Plant
City
Sewer
Partial
Recovery
Parathion
Source: Lawless et al., op. cit. (1972)
Figure 1. Production schematic for parathion.
18
-------
Specific Gravity; 1.26 at 20/20°C
Density: 10.5 Ib/gal at 20°C
Melting Point; 6°C
Boiling Point; Thermally unstable and cannot be heated to normal
boiling point, which is calculated to be 375°C.
Various other boiling points are as follows:
Vapor pressure (mm Hg) Temperature (°C)
0.57 x 10"5 20
0.05 113
0.6 - 157-162
Bright et al. (1950)—' determined the following vapor pressures:
3.78 x 10"5 20
2.08 x 10~4 40
9.31 x 10'4 60
3.52 x 10'3 80
1.15 x 10'2 100
Refractive Index; n?5 = 1.5370
Surface Tension; 39.2 dynes/cm at 25°C
I/ Bright, N. F. H., J. C. Cuthill, and H. H. Woodbury, "The Vapor
Pressure of Parathion and Related Compounds," J. Sci. Food and Agr..
1:344-348 (November 1950).
19
-------
Viscosity; 15.30 cp at 25°C
Solubility; Water at 25°C—24 ppm
Miscible with common organic solvents such as acetone,
benzene, carbon tetrachloride, chloroform, ethanol,
ether, toluene and xylene; slightly soluble in heptane
and petroleum oils; slightly soluble in lipids and fats,
Flash Point (Tag Open Cup): 120°C
Volatility; 0.09 mg/m3
Analytical Methods
This subsection reviews parathion analytical methods and the
most significant of many primary information sources on the methods.
The following information sources are .described: (1) The Pesticide
Analytical Manual (PAM), vols, I, III', (2) Official Methods of Analysis
of the Association of Official Analytical Chemiata|/. (3) Analytical
Methods for Pesticides and Plant Growth Regulators^/.
The Pesticide Analytical Manual - The Pesticide Analytical Manual (PAM),
published by the Food and Drug Administration, synthesizes procedures
and methods used by FDA laboratories to examine food samples for the
presence of pesticide residues.
I/ U.S. Department of Health, Education, and Welfare, Food and Drug
Administration, Pesticide Analytical Manual. 2 vols. (1971).
2J Association of Official Analytical Chemists, Official Methods of
Analysis of the Association of Official Analytical Chemists.
llth ed., Washington, D.C. (1970).
3/ Zweig, G., and J. Sherma, Analytical Methods for Pesticides and
Plant Growth Regulators. Vol. VI; Gas Chromatographic Analysis.
Academic Press, New York (1972).
20
-------
The PAM is published in two volumes. Volume I contains procedures for
multi-residue methods (for smaples of unknown history which may contain
more than one pesticide). Volume II contains analytical methods used
for specific pesticide residues and for specific foods.
Official Methods of Analysis of the Association of Official Analytical
Chemists - The Association of Official Analytical Chemists (AOAC)
publishes an authoritative methods manual about every 5 years. The
manual is designed to provide both research and regulatory chemists with
reliable methods of analysis. The reliability of the methods must be
demonstrated by a published study showing the reproducibility of the
method by professional analysts.
When an AOAC method is adopted for the first time it is published
as "Official First Action." This designation serves notice that final
adoption is pending, and permits an opportunity for any further study
that may be deemed appropriate.
Methods that have performed successfully for at least 1 year are
raised to the status of "Official Final Action."
A few methods are adopted as "Procedures." Such methods are
generally sorting or screening methods or well-established types of
examinations, or auxiliary operations, such as sampling or preparation
of a sample, which may not have been subjected to collaborative study.
Analytical Methods for Pesticides and Plant Growth Regulators, Volume
VI. Gas Chromatographic Analysis - Chapter 6 of this text consists of
an extensive and detailed review of specific and multi-residue analytical
methods for organophosphate pesticides. This reference provides im-
portant information not available in AOAC's "Methods of Analysis" or
the PAM such as: (1) a comparison of nine procedures for extracting
phosphorus insecticides and their metabolites from field-treated crops,
(2) a review of procedures for extracting organophosphate pesticides
from water samples, (3) a review of insecticide recoveries from vege-
tables, (4) a review of various clean-up procedures, (5) a description
of various detectors, (6) extensive data comparing the relative re-
tention times of various pesticides on various column materials, and
(7) a review of the sensitivity of various gas Chromatographic systems.
21
-------
Multi-Residue Methods
Multi-residue methods for parathion are described in the AOAC
methods manual and PAM, Volume I. Zwe.ig and Sherma have compiled a
detailed review of gas chromatographic residue analyses.
AOAC Methods - One of the AOAC methods ,i/ a general method for "chlorinated
and phosphated pesticides," is an "Official First Action" and applies only
to apples and lettuce. A second AOAC multi-residue method?./ applies only
to "phosphated pesticides" (in kale, endive, carrots, lettuce, apples,
potatoes, and strawberries). This second method is also an "Official First
Action" and involved a sweep codistillation cleanup for the organophosphate
residues. (The cleanup is not adequate for electron capture detectors;
KC1 thermionic detectors must be employed.) Also described in AOAC methods
manual^/ is a single sweep oscillographic-polarographic confirmation method.
The following AOAC multi-residue method is used for chlorinated and
phosphated pesticides: A thoroughly mixed sample is extracted with
acetonitrile. Aliquots of the acetonitrile solution are diluted with
water and the pesticide residues are extracted into petroleum ether.
The residues are purified by chromatography on a Florisil column and
are eluted from the column with mixtures of petroleum and ethyl ethers.
The first eluate, (6% ethyl ether in petroleum ether) contains some
chlorinated pesticides and some phosphated pesticides. However, methyl
parathion and parathion (and diazinon) are obtained in a second eluate
(15% ethyl ether in petroleum ether). A third eluate (50% ethyl ether
in petroleum e'ther) contains malathion. The eluates are concentrated,
and the residues are determined by gas chromatography and identified by
combinations of gas, thin-layer, or paper chromatography.
PAM Procedures - The PAM multi-residue methods (PAM, 1971) apply to the
wide variety of foods tested by the FDA. However, the multi-residue
methods are not capable of detecting and measuring all pesticides.
Analytical schemes used in the detection of parathion are shown in
Figures 1 and 2. The various parts of the schemes shown in Figures 1
and 2 are outlined in detail in the PAM. (The numbers refer to the
chemical numbering system of PAM; the chapter numbers also refer to
PAM.)
Parathion is more than 80% recovered in the 15% ethyl ether in
petroleum ether fraction from the Florisil column. Over 80% recovery
is achieved from both fatty and nonfatty foods.
Relative retention times of parathion are presented below for
various column packings; the corresponding response for various
detectors is also indicated.
I/ AOAC, op_. cit., p. 475 (1970).
2/ AOAC, op_. cit., p. 484 (1970).
3/ AOAc, 0£. cit., p. 487 (1970).
22
-------
Electron Capture Detector
Column
packing
10% DC 200 on
Gas-Chrom Q
(or Anakrom Q)
15% QF-1,
10% DC 200 on
Gas-Chrom Q
Column
packing
10% DC 200 on
Gas-Chrom Q
15% QF-1,
10% DC 200 on
Gas-Chrom Q
Retention time
relati've to aldrin
(ratio)
0.98
1.88
Sulfur Detector
Retention time
relative to sulphenone
(ratio)
0.78
0.71
Response
(ng for 1/2 FSD*
at 1 x 10"9 AFS**)
15
Response
(ug for 112 FSD*
64 ohs)
1.5
1.5
* FSD = Full scale deflection.
** AFS = Amps, full scale.
23
-------
Figurr 2
GENERAL SCHEME FOR MULTIPLE RESIDUES*
Chlorinalrd (nonionic)
210
Organophosphates
230
See ScAem* 762**
Sample Preparation
141
Guideline! for
Compositing
142
Extraction and
Cleanup
Chapter 2
1
I
Gas Chromatography
(quantitative)
Chapter 3
I
Thin Layer
Chromatography
(semi - quantitative)
Chapter 4
Determinative
Methods - other
Chapter 5
Confirmatory Tests
Chapter 6
1
Chlorinated (tonic)
220
See Scheme 163
* The numbers refer to the decimal numbering system of PAM.
Chapter numbers also refer to PAM.
** Scheme 162 is presented in Figure 2.
Source: PAM, 1971.
24
-------
Figure 3
ANALYTICAL SCHEME FOR CHLORINATED (NONIONIC) AND ORGANOPHOSPHATE RESIDUES*
Clilorinalrd (Nonionic) 210
Organopliospli.-iU <- 230
1
I'roxitnalc Percentage Watrr
and Fat in Foods and Feeds 202
J-
_L
Fal'.v Foods
211 231
Non Fatly Foods
212 232
Extraction of Fat
211.13
1
Aeetonitrile
Partitioning
211.14
1
Extraction and
Partitioning
212.13
FlorisU Column
211.15
i
l
1
1
i
1
1
i
I
i
|
( 1
L 1
2nd Florisil j
Column i —
211.16 a \ ~~— *-
. »
r
Acid-Celite
Column- ^.
211.16 b
& 2nd Florisil
Column
1
Gas Chromatography
Electron Capture and Thermionic
on ys em
Gas Chromatography
Electron Capture Detector
311
J
1
Thin Layer Chromutograph-
Chlorinated 410
Orgaiiophottpliates 430
1
ICM. I.M.I. ».
|
i
*-'"" '
i
: 1
%
l._.
2nd Florisil
Column
211.16 a
1
KgO-Celite
Column
211.16 c
Alkaline
Hydrolysis
211.16 d
& MgO-Cclitc
Column
_3
]
1
l
t
* The numbers refer to the decimal numbering sy tern of PAM. The
primary analytical scheme is in bold type. Additional cleanup
and/or quantitation schemes are in italics.
Source: PAM, 1971.
25
-------
Potassium Chloride Thermionic Detector
Retention time
Column relative to p;irathion Response
packing (ratio) (mg for 1/2 FSD*)
107. DC-200 on 1.00 2
Chromosorl W-HP
(or Gas Chrom Q)
15% QF-1 + 10%
DC 200 on Chromosorb 1.00 2
W-HP (or Gas Chrom Q)
* FSD = Full scale def le< tion.
** AFS = Amps, full scale.
The PAM does not provide response data for flame photometric
detectors. However, this type of detector is now widely used for the
analysis of organophosphate residues, primarily because of the high
degree of specificity in detecting phosphorus compounds. A review of
these and other detectors is provided by Zweig and Sherma (1972)— .
Residue Analysis Principles
Both AOAC methods manual and PAM (Vol. II) describe methods for
the specific analysis of parathion residues. Zweig and Sherma?-' have
provided a review of specific residue analytical methods for parathion.
AOAC Method (Official Final Action) - According to the AOAC methods/for
specific analysis of parathion residues, parathion is extracted with
benzene or 2-propanol-benzene, and the strip solution is clarified.
I/ Zweig and Sherma, op. cit., p. 205 (1972).
21 AOAC, op. cit., p. 508 (1970).
3/ Zweig and Sherma, op. cit., p. 445 (1972).
26
-------
Parathion is brought into aqueous solution and simultaneously reduced
to its amine with zinc and hydrochloric acid. The amine is diazotized
and coupled with !I-(]-naphthyl)-ethylenediamine to form a colored
compound which is analyzed spectrophotemetrically.
The practical working range for the Beckman DU spectrophotometer
is 0 to 200 ug parathion.
The method has been employed for parathion residues in a wide
variety of fruits and vegetables.
PAM Methods - PAM (1967) lists three methods for specific residue
analysis. The first two methods have been "tested in varying degrees
and are considered reliable without further validation for the product
applications indicated." The third method has not been "thoroughly
tested through interlaboratory studies."
The First Method - This method refers to the PAM procedure for
organophosphate (PAM, 1971); this procedure is summarized in the
"Multi-Residue Methods" section of this Appendix.
The Second Method - This method refers to an AOAC procedure
(AOAC, 1965)i/; A summary of an updated AOAC method is described
in the preceding section.
According to PAM (Volume II), the AOAC method is generally applic-
able to all products excluding fats and oils.
The sensitivity is 0.2 ppm.
Cole crops develop an interfering pink color, and blank values as
high as 1 ppm and over are not uncommon with some of these crops (Rolston
and Walton, 19632-/).
Aniline and some aniline analogues interfere. Methyl anthranilate,
which is found in grapes and citrus fruits, interferes. The amount of
methyl anthranilate and hence the extent of interference differs with
the maturity and variety of the fruit. (Taschenberg and Avens, 1960-5.'.
I/ AOAC, 0£. cit.. (1965).
2j Rolston, L. H. and R. R. Walton, "Parathion Residues in Greens,"
J. Econ. Entomol.. 56:169-172 (1963).
3Y Taschenberg, E. F. and A. W. Avens, "Parathion and EPN Residue
Studies on Concord Grapes," J. Econ. Entomol., 53:441-445 (1960).
27
-------
Taschenberg-and Avens used the procedure of Averell and Norris
(1948)!/, except that the benzene solution is repeatedly washed with
10% HC1 to remove interference. Alternatively, parathion can be
determined by difference: the anthranilate is determined before the
parathion is reduced and then both compounds are measured together
after reduction. The difference in results represents the parathion.
Decomposed leafy vegetables contain decomposition products which
are not removed by the clean-up procedure and which yield false results
for parathion.Z/
The Third Method - The third method is a polarographic procedure
which can be used as a rapid scanning technique (Gogan, 1963^/.
The method has been tested on apples and several vegetables.
Parathion quantities of less than 0.1 ppm have been determined.
Methyl anthranilate does not interfere. Methyl parathion, EPN,
and PCNB give peaks sufficiently close to the parathion peak as
to interfere with determination. Recent studies by the author
indicate that the procedure can be extended to fats and oils,
except olive oil, where interferences have been encountered.
Formulation Analysis Principles
Formulation analysis procedures for parathion are described
in AOAC "Methods of Analysis" (1970). Additional information has
been provided by the Technical Service Division, Office of Pesticide
Programs of EPA.
AOAC Methods (Official Final Action) - The two AOAC methods are volumetric
(applicable to all forms of technical parathion) and colorimetric
(applicable to dusts and wettable powders).
I/ Averell, P. R. and M. V. Norris, "Estimation of Small Amounts of
o, o-diethvl o-(p-nitrophenvl)thiophosphate." Anal. Chem.. 20(8):
753-756 (August 1948).
2.1 Dow, M. L. (Food and Drug Administration), Personal communication
to PAM editors (October 1961).
3/ Gogan, R. J., "Application of Oscillographic Polarography to the
Determination of Organophosphorus Pesticides, II. A Rapid
Screening Procedure for the Determination of Parathion in Some
Fruits and Vegetables," J. Assoc. Off. Agr. Chem.. 46(2):216-222
(1963).
28
-------
The volumetric method!./ This involves a potentiometric titration
of the parathion amine (produced by reduction with zinc and hydrochloric
acid) with sodium nitrite. p_-Nitrophenol in parathion is initially
removed by extraction (aqueous sodium carbonate) and determined by
ultraviolet spectrophotometry.
The colorimetric methodl/ This involves an extraction of parathion
with alcohol followed by a hydrolysis of parathion with potassium
hydroxide to form potassium js-nitrophenate which is determined by ultra-
violet spectrophotometry.
EPA Method - In addition to the AOAC formulation methods, the Technical
Service Division of EPA employs a high-pressure liquid chromatographic
procedure for parathion analysis. The method is described as follows^/:
1. Reagents -
a. Methanol, ACS
b. Parathion standard of known purity.
2. Operating Conditions for Liquid Chromatograph - UV detector
at 254 mm. Operating conditions must be determined for the
individual liquid chromatograph to achieve optimum sensitivity
and resolution.
3. Procedure -
a. Standard preparation - Weigh 0.3 g parathion standard into
a 100 ml volumetric flask, dissolve, and make to volume
with methanol.
b. Sample preparation - Weigh a portion of sample equivalent
to 0.3 g parathion into a glass-stoppered flask, add
100 ml methanol, and shake well.
II AOAC, op_. cit.. p. 114 (1970).
2J AOAC, op_. cit.. p. 115 (1970).
3/ Bontoyan, Warren R., TSD, OPP, EPA, Personal Communication to
Dr. Alfred Meiners (September 1974).
29
-------
4. Determination - Using a high-pressure liquid syringe,
alternately inject three 5 ul portions each of standard
and sample solutions. Measure the peak area for each
peak and calculate the average for both standard and
sample. Adjustments in attenuation or amount injected
may have to be made to give convenient size peaks.
5. Calculation -
% parathion = (avg area sample)(ul std)(ug/ul std)(purity of std)(100)
(avg area std)(ul sample)(ug/ul sample)
(This method was developed by Elmer H. Hayes of the Beltsville
Chemistry Laboratory, Technical Services Division, Chemical
and Biological Investigations.)
Composition and Formulation
The most common formulations of parathion are: (a) wettable powder
concentrates (15 to 257o); (b) ready-to-use dry dust mixtures (1 to 10%);
(c) emulsifiable concentrates (2 to 8 Ib/gal); (d) granules (2 to 25%).
Wettable Powders - Parathion is often formulated as a wettable powder
containing 15 to 25% active material. Certain clays perform very well
as an absorbent carrier in wettable powder formulations. In addition to
the clay carrier, up to 5% of a wetting agent and a dispersing agent are
required in the formulation. After making the final blend, the formula-
tion must be ground to a very fine particle size to obtain maximum dis-
persion in the field spray mixture.
30
-------
Dusts - Dry dust concentrates may be prepared by impregnating certain
absorbent clays with parathion. Typical dry dust concentrates are:
20% (Ib) 25% (Ib)
Absorbent clay 79.4 74.3
Parathion (98.5%) 20.6 25.7
100.0 100.0
Dry 1 to 2.5% field strength dusts may be prepared by diluting con-
centrates to the desired strength. Secondary type diluents are used in
combination to produce the desired bulk density and flow characteristics.
Many formulators prepare field strength dusts by direct impregna-
tion. This is accomplished in the same manner as preparing a concentrate
except the mixer is first charged with the desired combination of diluents,
Typical direct impregnation formulations are:
1% (Ib) 27. (Ib)
Diluents 98.8 97.8
Parathion (98.5%) 1.2 2.2
100.0 100.0
Emulsifiable Concentrates - Parathion can be formulated into many emul-
sifiable concentrates. Table 2 has four suggested formulations.
31
-------
Granules - Large quantities of parathion granules are used to protect crop
plant roots from soil insects such as rootworms and wireworms. The amount
of active ingredient in such formulations varies from 4 to 25% depending
on crop, insect and method or time of application.
Granules from calcined or uncalcined clays are the most widely used
carriers for parathion. Calcined granules are preferred because of their
lower susceptibility to dust formation through attrition.
Chemical Properties, Degradation Reactions and Decomposition Processes
Parathion is a specific chemical compound, 0,0-diethyl 0-p_-nitro-
phenyl phosphorothioate (Chemical Abstracts nomenclature). The biologi-
cal effects of parathion are intimately associated with two other com-
pounds, paraoxon (0,0-diethyl 0-£-nitrophenyl phosphate) and a thioate
isomer of parathion (0,S-diethyl 0-p_-nitrophenyl phosphorothiolate). As
indicated below, these compounds are formed by oxidation and isomeriza-
tion of parathion.
o
(C2H50)2PO
Parathion
(C2H50)(C2H5S)PO
Thiolate isomer
Compounds of this kind are toxic primarily because they react with
acetylcholinesterase. The toxicity of parathion depends entirely upon
its oxidative conversion in vivo to paraoxon. Parathion is oxidized
enzymatically to paraoxon, but can also be oxidized to paraoxon by the
chemical action of atmospheric oxygen. The atmospheric oxidation is
32
-------
Table 2. SUGGESTED FORMULATIONS FOR PARATHION
EMULSIFIABLE CONCENTRATES
Ingredients
Parathion (98.5%)
Xylene
Emu1sifter
Parathion (98.5%)
Xylene
Emulsifier
Parathion (98.5%)
Xylene
Emulsifier
Parathion (98.5%)
Emulsifier
% by Wt
2 Ib/gal
25.69
69.31
5.00
100.00
4 Ib/gal
47.23
45.27
7.50
100.00
6 Ib/gal
8 Ib/gal
80.27
19.73
100.00
Lb/Gal
8.1221/
1.996
10.118
Source: Monsanto Company, Agricultural Division, "Parathion and Methyl
Parathion"Technical Bulletin No. AG-lb,"St. Louis, Missouri (undated),
a/ Equivalent to 2.0 Ib of 100% parathion
Specific Gravity at 25/15.6°C. 0.9485
Solution Point, °C. Cannot Freeze
b/ Equivalent to 4.0 Ib of 100% parathion
Specific Gravity at 25/15.6°C. 1.0318
Solution Point, °C. Cannot freeze
£/ Equivalent to 6.0 Ib of 100% parathion
Specific Gravity at 25/15.6°C. 1.1478
Solution Point, °C. Cannot freeze
d/ Equivalent to 8.0 Ib of 100% parathion
Specific Gravity at 25/15.6°C. 1.2142
Solution Point, °C. Cannot freeze
33
-------
accelerated by ultraviolet radiation (Cook and Pugh, 1957;-^ Frawley
et al., 1958-'). Paraoxon is much more toxic than parathion. The forma-
tion of paraoxon has been postulated as the cause of observed toxicities
much higher than expected from the observed concentrations of parathion
(Whalley et al., 1964^/) . Paraoxon reacts 10,000 times faster with
acetylcholinesterase than does parathion (Heath,
The thiolate isomer of parathion also reacts with acetylcholines-
terase 10,000 times faster than parathion. The isomerization reaction
does not proceed in vivo, but does take place in storage. The presence
of the contaminating thiolate isomer has invalidated many publications
on the biochemical and toxic properties of parathion (Heath, 1961).
The Effect of Sunlight and Ultraviolet Radiation - Parathion was one of
the first organic phosphorus compounds whose anticholinesterase activity
was shown experimentally to increase during exposure to UV light and
sunlight (Pay ton, 19531/) . Subsequent work by Cook (19556-/) and Cook and
Pugh (1957) indicated that the toxicity of parathion decreased under UV
light, but the in vitro anticholinesterase activity increased as the re-
sult of the formation of more polar products. Frawley et al. (1958)
found that the exposure of parathion to UV radiation resulted in a mix-
ture of compounds including parathion, paraoxon and oxidation and degra-
dation products. A study by Mitchell (196lZ') indicated that most organic
JL/ Cook, J. W., and N. D. Pugh, "Quantitative Study of Cholinesterase-In-
hibiting Decomposition Products of Parathion Formed by Ultraviolet
Light," J. Assoc. Offie. Agr. Chem.. 40:277-281 (1957).
2_/ Frawley, J. P., J. W. Cook, J. R. Blake, and 0. G. Fitzhugh, "Effect of
Light on Chemical and Biological Properties of Parathion," J. Agr.
Food Chem.. 6(1):28-30 (January 1958).
3/ Whalley, P. J., R. H. Adams, and B. Combes, J. Amer. Med. Assoc.. 189(5):
357 (1964).
4/ Heath, D. F., Organophosphorus Poisons» New York: Pergamon Press
(1961).
5/ Payton, J., "'Parathion1 and Ultraviolet Light," Nature. 171(4347):355-
356 (21 February 1953).
(>/ Cook, J. W., "Paper Chromatography of Some Organic Phosphate Insecticides.
V. Conversion of Organic Phosphates to in vitro Cholinesterase In-
hibitors by N-Bromosuccinimide and Ultraviolet Light," J. Assoc. Offie.
Agr. Chem.. 38:826-832 (1955).
77 Mitchell, L. C., "Separation and Detection of Eleven Organophosphate
Pesticides by Paper Chromatography," J. Assoc. Offic. Agr. Chem..
44:643-712 (1961).
34
-------
phosphorus compounds break down to form a wide variety of new compounds
on irradiation, but no attempt was made to characterize them. Studies
by Koivistoinen and Merilainen (1962)- demonstrated that both UV radia-
tion and sunlight changed parathion to several cholinesterase inhibitors.
On the basis of chromatographic behavior, the metabolites were identified
as paraoxon and the S-ethyl (thiolate) and S-phenyl isomers of parathion,
together with unknown products (Figure 2). Gar and Kapiani (1956)—' and
El-Refai and Hopkins (1966)— reported the production of similar mix-
tures by UV radiation. When methyl parathion was exposed to both UV radia-
tion and sunlight, only the methyl homologue of paraoxon was identified
(Koivistoinen and Merilainen, 1962).
Joiner et al. (1971)— have probably performed the most extensive
research to date on photodegradation products of parathion. They sub-
jected parathion to high-intensity ultraviolet radiation under artificial
and natural conditions for periods up to 35 days. They detected 12 irradia-
tion products, seven of which had not previously been observed as irradia-
tion products. These products are listed in Table 3.
In a recent study of the photochemical degradation of parathion,
0,0,8-triethylthiophosphate was identified as the major product of the
photolysis in aqueous tetrahydrofuran or ethanol. Minor products were
0,0,0-triethyIthiophosphate, paraoxon, and triethyIphosphate, which was
formed by secondary photolysis of paraoxon (Grunwell and Erickson, 1973^').
Hydrolysis - Hydrolysis is perhaps the most important degradation reaction
of organic phosphorus insecticides, because hydrolysis virtually
destroys all insecticidal activity.
_!/ Koivistoinen, P., and M. Merilainen, "Paper Chromatographic Studies on
the Effect of Ultraviolet Light on Parathion and Its Derivatives,"
Acta Agr. Scand., 12:267-276 (1962).
2/ Gar, K. A., and R. Y. Kapiani, Proclamation of the International Con-
ference of Peaceful Uses of Atomic Energy (1955), 12:185 (1956).
51 El-Refai, A., and T. L. Hopkins, "Parathion Absorption, Translocation,
and Conversion to Paraoxon in Bean Plants," J. Agr. Food Chem., 14(6)
588-592 (November-December 1966).
A/ Joiner, R. L., H. W. Chambers, and K. P. Baetcke, "Toxicity of Para-
thion and Several of Its Photoalteration Products to Boll Weevils,"
Bull. Environ. Contam. Toxicol.. 6(3):220-224 (1971).
J5/ Grunwell, J. R., and R. H. Erickson, "Photolysis of Parathion (0,0-Di-
ethyl-0-(4-nitrophenylthiophosphate). New Products," J. Agr. Food
Chem., 21(5):929-931 (September-October 1973).
35
-------
S-phenyl isomer
(C2H50)2PON02
N02 + HO
NO,
j>-nitrophenol
S-ethyl (thiolate) isomer
Adapted from Dauterman, W. C., "Biological and Nonbiological Modifications of Organophosphorus Compounds,"
Bulletin of the World Health Organization, 44(1-2-3):144 (1971).
Figure 4. Major photodegradation products of parathion.
-------
Table 3. OTHER PHOTODEC RABATION PRODUCTS OF PARATHION
£-Aminopheno1
H0« )>NH2
Diethy1 phenyl phosphate
(C2H50)2PO
Diethyl phenyl phosphorothioate
(C2H50)2PO
Ethyl bis(p_-nitrophenyl) phosphate C2H5OP (°\(.)/N02) 2
Ethyl bis(p_-nitrophenyl) phosphorothioate C2H^OPO
Diethyl phosphate
(C2H50)2POH
Monoethyl phosphate
C2H5OP(OH)2
Data from: Joiner, R. L., Piss. Abstr. Int.. 32:41698 (1971/1972).
37
-------
The extent of hydrolytic stability is, in general, related to the
electronic characteristics of the substituents attached to the phos-
phorus atom. Thus, the replacement of a phosphorus-bound oxygen atom
with a sulfur atom usually increases the resistance of the molecule to
hydrolysis. This fact probably accounts for the fact that the chemical
structures of most commercial organophosphate insecticides contain sulfur.
In parathion (and in methyl parathion) there are three potential
groups which may be hydrolyzed from the phosphorus portion of the molecule.
However, only one, the p_-nitrophenol group, is of practical significance;
the hydrolysis of the most labile group greatly increases the hydrolytic
stability of the remaining groups. For example, paraoxon has a half-life
of 9.2 days at 25°C and pH 10, diethyl phosphate, even at 100°C and pH 10
has a calculated half-life of 5 billion days (Heath, 1956;-/ Vernon,
f\ _•«••_
(C2H50)2PO @> N02 hydrolysis>
paraoxon diethyl phosphate j>-nitrophenol
further
hydrolysis
H PO + 2C-H.-OH
34 2 5
phosphoric acid ethanol
Parathion is relatively resistant to hydrolysis. The stability of
parathion in water is related to pH and temperature. Stable below pH 7,
it hydrolyzes rapidly in alkaline solution. The rate of hydrolysis also
increases appreciably with increases in temperature. Fifty percent
hydrolysis of parathion is achieved in 2.7 hr at pH 9 and 70°C, but 17 to
20 hr are required at pH 1. At pH 1 to 5, 690 days are required at 20°C
(Lawless et al., 19733-/).
I/ Heath, D. F., "The Effects of Substituents on the Rates of Hydrolysis
of Some Organophosphorus Compounds. I. Rates in Alkaline Solution,"
J. Chem. Soc.. pp. 3796-3804 (1956).
£/ Vernon, C. A., Chem. Soc. (London) Spec. Publ.. 8:17 (1957).
J3/ Lawless, E. W., T. L. Ferguson, and A. F. Meiners (Midwest Research
Institute), Methods for the Disposal of Spilled and Unused Pesticides
(Draft), for Environmental Protection Agency, Contract No. 68-01-
0098 (1973).
38
-------
In laboratory studies, the half-life of parathion in ethanol-pH 6.0
buffer solution (20:80) at 70°C was shown to be 43 hr (Ruzicka et al.,
1967- ). with Thames River water (pH 8.0, total hardness as CaC03 314 rag)
substituted for buffer solution, the half-life was 65 hr; with Irthing
River water (pH 7.5, total hardness as CaC03 42 rag) substituted, the half-
life was 68 hr. Hydrolysis under these conditions was a pseudo-first-order
reaction.
In another hydrolysis rate study, 31.27» of parathion remained after
4 weeks in neutral water (Cowart et al., 1971?-'). Studying the persistence
of parathion, Mulla (1963>2/ found that, in the laboratory at pH 8, 35°C
and a light intensity of 64 ft-candles, parathion remained undegraded
after 96 hr; in the field, however, all the insecticide was lost within
72 hr. The more rapid disappearance in the field studies was attributed
to wind action, breakdown by microbes, the presence of organic matter, and
complex edaphic factors such as absorption by soil colloids.
4/
The Effect of Heat - Metcalf and March (1953)- found that when parathion
was heated at 150°C for 24 hr, 80 to 90% decomposition resulted and degra-
dation products were formed. Five of the compounds were identified:
parathion, paraoxon, £-nitrophenol, bis(£-nitrophenyl) thionophosphate,
and—the principal product—S-ethyl parathion.
Heating most insecticidal organophosphates above 200°C results in
decomposition. According to the National Agricultural Chemicals Associa-
tion (1968),1' parathion should not be heated above 100°C. When heated
to decomposition, parathion emits highly toxic fumes of nitrogen oxides,
phosphorus, and sulfur compounds (National Agricultural Chemicals Associa-
tion, 1968).
JL/ Ruzicka, J. H., J. Thomson, and B. 8. Wheals, "The Gas Chromatographic
Determination of Organophosphorus Pesticides - Part II. A Compara-
tive Study of Hydrolysis Rates," J. Chromatoe.. 31(1):37-47 (November
1967).
2/ Cowart, R. P., F. L. Bonner, and E. A. Epps, Jr., "Rate of Hydrolysis
of Seven Organophosphate Pesticides," Bull. Environ. Contarn. Toxicol.,
6(3):231-234 (1971).
_3/ Mulla, M. S., "Persistence of Mosquito Larvicides in Water," Mosquito
News, 23(3):234-237 (September 1963).
4/ Metcalf, R. L., and R. B. March, "The Isomerization of Organic Thiophos-
phate Insecticides," J. Econ. Entomol.. 46:288-294 (April 1953).
5J National Agricultural Chemicals Association, Safety Guide for Ware-
housing Parathions. Washington, B.C. (1968).
39
-------
The hazards from fires involving organic phosphorus insecticides have
been investigated and it was concluded that: first, most of the insecti-
cide is destroyed by decomposition before it can evaporate; second, over
907o of the evaporating insecticide is destroyed by the flames; and third,
the evaporating portion is considerably diluted by the time it reaches
anyone (Smith and Ledbetter, 197li').
Oxidation - Several chemical oxidizing agents are capable of replacing
the sulfur atom in parathion with an oxygen atom. Koivistoinen and
Merilainen (1962) showed that when parathion was exposed as a thin film,
trace amounts of paraoxon were formed even in the absence of light.
2 /
A recent publication (Gunther et al., 1970=-') pointed out that para-
thion can be rapidly and conveniently oxidized to paraoxon by means of
ozone (20 to 40% conversion).
3/
Comma and Faust (1971)— noted that chlorine or potassium permanganate
would convert dilute solutions of parathion in water to paraoxon.
Reduction - Reducing agents (for example, metals in acid medium) convert
parathion to the corresponding amino compound, aminoparathion (Melnikov,
19712').
The product, 0,0-diethyl 0-4-aminophenyl thiophosphate , is nontoxic to
animals and does not have an insecticidal effect.
Occurrence of Parathion Residues in Food and Feed Commodities
The Food and Drug Administration, Department of Health, Education,
and Welfare, monitors pesticide residues in the nation's food supply
I/ Smith, W. M., Jr., and J. 0. Ledbetter,'"Hazards from Fires Involving
Organophosphorus Insecticides." Amer. Ind. Hyg. Assoc. J.. 32(7):468-
474 (July 1971).
2/ Gunther, F. A., D. E. Ott, and M. Ittig, "The Oxidation of Parathion
to Paraoxon. II. By Use of Ozone," Bull. Environ. Contarn. Toxicol.,
5(l):87-94 (1970).
^/ Comma, H. M., and S. D. Faust, "Chemical Oxidation of Organic Pesti-
cides in Aquatic Environments," Paper No. 48, 161st American Chemi-
cal Society Meeting, Los Angeles, California (29 March-12 April 1971)
b/ Melnikov, N. N., Chemistry of Pesticides, Springer-Verlag, New York,
pp. 324-329 (1971).
40
-------
through two programs. One program, commonly known as the "total diet pro-
gram," involves the examination of food ready to be eaten. This investiga-
tion measures the amount of pesticide chemicals found in a high-consumption
varied diet. The samples are collected in retail markets and prepared for
consumption before analysis. The other program involves the examination
of large numbers of samples, obtained when lots are shipped in interstate
commerce, to determine compliance with tolerances. These analyses are
complemented by observation and investigations in the growing areas to
determine the actual practices being followed in the use of pesticide
chemicals.
A majority of the samples collected in these programs are categorized
as "objective" samples. Objective samples are those collected where there
is no suspicion of excessive residues or misuse of the pesticide chemicals.
All samples of imported foods and fish are categorized as "objective" sam-
ples even though there may be reason to believe excessive residues may be
found on successive lots of these food categories.
Market-basket samples for the total diet studies are purchased from
retail stores, bimonthly, in five regions of the United States. A shopping
guide totaling 117 foods for all regions is used, but not all foods are
represented in all regions because of differences in regional dietary pat-
terns. The food items are separated into 12 classes of similar foods and
prepared for consumption by dietitians in institutional kitchens. After
preparation, the food items are composited into 12 classes of similar
foods (e.g., dairy products; meat, fish and poultry; legume vegetables;
and garden fruits) for more reliable analysis and to minimize the dilu-
tion factor. Each class in each sample is a "composite." The food items
and the proportion of each used in the study were developed in cooperation
with the Household Economics Research Division, USD A, and represents the
high-consumption level of a 16- to 19-year-old male. Each sample represents
a 2-week supply of food.
Surveillance samples are generally collected at major harvesting and
distribution centers throughout the U.S. and examined in 16 FDA district
laboratories. Some samples may be collected in the fields immediately
prior to harvest. Surveillance samples are not obtained in retail markets.
Samples of imported food are collected when offered for entry into the
United States.
The results obtained during the 5-year period, June 1964 to April
1969, are compared in Table 4 with the acceptable daily intake (ADI)
41
-------
Total organo-
phosphates
Table 4. DIETARY INTAKE OF PARATHION AND TOTAL ORGANOPHOSPHATES
Compounds
Parathlon
1964-1965
0.000001
Milligrams /kilogram body weight/day
total diet studies
1965-1966 1966-1967 1967-1968
0.000005 0.00001.
5-Year
1968-1969 average
0.00001 0.00001
0.00014
0.00025
0.00007
0.00023
0.0002
K)
Data from Duggan, R. E., 6. Q. Lipscomb, E. L. Cox, R. E. Heatwole, and R. C. King,
"Pesticide Residue Levels in Foods in the United States from 1 July 1963 to 30 June
1969." Pest. Monit. J.. 5(2):73-212 (September 1971).
-------
established by the Food and Agricultural Organization, World Health
Organization (FAO/WHO) Expert Committee (FAO/WHO, 1970l/). The
amount of parathion and total organophosphates calculated from this
high-consumption diet, approximately twice that consumed by a normal
individual, are well below the daily intake regarded as safe by the
FAO/WHO Expert Committee (Duggan et al., 1971).2J
Table 5 (Duggan et al., 1971) compares the incidence and daily
intake in milligrams of parathion found in these samples for each of
the 5 years.
Table 5. AVERAGE INCIDENT AND DAILY INTAKE OF PARATHION
1965-1966
1966-1967
1967-1968
1968-1969
Percent
positive
com-
positesa/
1.0
Daily
intake
(mg)
<0.001
Percent
positive
com-
pos ities^-'
1.4
Percent
Daily positive
intake com-
(mg) posites
0.001
0.6
Percent
Daily positive
intake com-
(mg) posites
< 0.001 3.3
Daily
intake
(mg)
< 0.001
a/ 312 composites examined.
b_/ 360 composites examined.
The results of the FDA analytical studies are tabulated for the
following food classes:
Dairy Products
Large Fruits
Small Fruits
Grains and Cereals (Human)
Leaf and Stem Vegetables
Vine and Ear Vegetables
Root Vegetables
Beans
Red Meat
Poultry
Eggs
Fish
Shellfish
Grains (Animal)
Infant and Junior Foods
Tree Nuts
Vegetable Oil Products
I/ FAO/WHO, Food and Agricultural Organization of the United Nations/World
Health Organization, 1969 Evaluations of Some Pesticide Residues in
Food, The Monographs. Geneva (1970).
2/ Duggan, R. E., G.Q. Lipscomb, E. L. Cox, R. E. Heatwole, and R. C. King,
"Pesticide Residue Levels in Foods in the United States from 1 July 1963
to 30 June 1969," Pest. Monit. J.. 5(2):73-212 (September 1971).
43
-------
The most recently available analytical data are presented in Table 6
which lists the incidence and ranges of levels for parathion detected in
the various food classes. The omission of any food class from the table
indicates that no residues were found.
The available data cover the years 1964 to 1969. Limited data are
available for the year 1970 (Corneliussen, 1972-'), and a complete update
on pesticide residue data is expected in the forthcoming September 1974
issue of the Pesticide Monitoring Journal.
Acceptable Daily Intake
The acceptable daily intake (ADI) is defined as the daily intake which,
during an entire life-time, appears to be without appreciable risk on the
basis of all known facts at the time of evaluation (Lu, 1973?-/). It is
expressed in milligrams of the chemical per kilogram of body weight (mg/
kg).
For parathion the ADI is 0.005 mg/kg. This level was set at the 1965
Joint Meeting of the FAO Committee on Pesticides in Agriculture and the
WHO Expert Committee on Pesticide Residues (FAO/WHO, 19683-/) . A joint
meeting is held annually and new evidence is considered which would war-
rant a change in the ADI of any pesticide. The level for parathion has
not been changed through 1971 (FAO/WHO,1972-').
In making the evaluation, all available research on parathion con-
cerning its biochemical effects, toxicology, and teratology is considered.
^/ Corneliussen, P. E., "Residues in Food and Feed: Pesticide Residues
in Total Diet Samples (VI)," Pest. Monit. J.. 5(4):313-329 (March 1972)
2_/ Lu, F. C., "Toxicological Evaluation of Food Additives and Pesticide
Residues and Their 'Acceptable Daily Intakes' for Man: The Role of
WHO, in Conjunction with FAO," Residue Rev., 45:81-93 (1973).
3/ FAO/WHO, Food and Agricultural Organization of the United Nations/WorId
Health Organization, 1967 Evaluations of Some Pesticide Residues in
Food, The Monographs, Geneva (1968).
4/ FAO/WHO, Food and Agricultural Organization of the United Nations/WorId
Health Organization, "Pesticide Residues in Food," Report of the 1971
Joint FAO/WHO Meeting on Pesticide Residues, World Health Organization
Tech. Rept. Series No. 502, Geneva (1972).
44
-------
Table 6. PERCENT DISTRIBUTION OF PARATHION RESIDUES
BY FISCAL YEAR IN DIFFERENT QUANTITATIVE RANGES
Percent distribution of samples
Domestic
Range ppm
No. samples
None found
Trace-0.03
0.04-0.10
0.11-0.50
0.51-1.00
1.01-1.50
1.51-2.00
Above 2.00
No. samples
None found
Trace-0.03
0.04-0.10
0.11-0.50
0.51-1.00
1.01-1.50
1.51-2.00
Above 2.00
1964-67
2.361
96.86
1.56
0.80
0.72
0.04
-
-
-
825
95.75
2.18
1.33
0.60
0.12
-
-
-
1968
1.512
94.97
2.71
1.52
0.60
0.20
-
-
-
398
95.48
3.77
0.50
0.25
-
-
-
-
1969
844
93.36
4.38
0.95
1.18
0.12
-
-
-
384
95.57
2.60
1.04
0.78
-
-
_
-
Imported
Total 1964-67 1968 1969
Large fruits
4.717 2.018 155 94
95.63 99.50 92.26 98.94
2.44 0.29 1.29 1.06
1.06 0.09 2.58
0.76 0.09 1.94
0.11 - 1.29
0.65
...
.
Small fruits
1.607 123 57 144
— ™*^^™-» wn^B* Xt^ ^HI^H
95.64 99.18 100.00 99.31
2.68 - - 0.69
1.06 ...
0.56 0.81
0.06 ...
0.65
- .
...
Total
2.267
98.99
0.40
0.26
0.22
0.09
0.04
.
-
324
99.38
0.31
.
0.31
.
0.04
—
-
Grains and cereal for human use
No. samples
None found
Trace-0.03
0.04-0.10
0.11-0.50
0.51-1.00
1.01-1.50
1.51-2.00
Above 2.00
No. samples
None found
Trace-0.03
0.04-0.10
0.11-0.50
0.51-1.00
1.01-1.50
1.51-2.00
Above 2.00
2.107
99.57
0.33
0.09
-
-
.
-
-
5.780
88.14
4.15
2.49
3.94
0.76
0.27
0.06
0.15
877
98.75
1.14
.
0.11
_
_
.
-
2.251
80.36
9.02
5.29
4.09
0.89
0.18
0.09
0.09
1§1
99.14
0.86
_
.
_
.
•
-
1.782
75.08
9.60
6.34
7.24
0.84
0.39
0.22
0.28
3.565 20 8 4
99.30 100.00 100.00 100.00
0.62 ...
0.06 ...
0.03 ...
— — — •
— • • -.
• • «• «
...
Leaf and stem vegetables
9.813 35 8 19
83.99 100.00 100.00 94.74
6.26 - - 5.26
3.83 ...
4.58 ...
0.81 ...
0.28 ...
0.10 ...
0.16 ...
32
100.00
w
—
—
—
_
.
-
62
SS^
98.39
1.61
.
m
—
^
^
_
45
-------
Table 6. (Concluded)
Percent distribution of samples
Domestic
Range ppm
No. samples
None found
Trace -0.03
0.04-0.10
0.11-0.50
0.51-1.00
1.01-1.50
1.51-2.00
Above 2.00
1964-67
4.401
98.44
0.88
0.38
0.23
0.02
-
0.02
-
1968
1.059
94.62
3.97
1.04
0.38
-
=
-
-
1969 Total
Vine and ear
848 5.308
94.69 97.08
3.18 1.87
1.42 0.68
0.71 0.34
0.02
-
0.02
-
Imported
1964-67 1968
vegetables
1.040 254
95.09 83.46
2.88 11.81
1.44 3.94
0.48 0.79
0.09
• -
.
-
1969
280
75.00
18.93
2.86
2.86
0.36
-
-
-
Total
1.574
80.64
7.18
2.10
0.95
0.13
-
-
-
Root vegetables
No. samples
None found
Trace-0.03
0.04-0.10
0.11-0.50
0.51-1.00
1.01-1.50
1.51-2.00
Above 2.00
5.425
99.26
0.55
0.14
0.01
0.01
-
-
-
1.758
97.50
1.59
0.34
0.40
0.11
-
-
0.06
1.060 8.243
97.55 98.67
1.70 0.92
0.66 0.25
0.09 0.11
0.04
» -•* -
-
0.01
165 66
100.00 100.00
-
-
-
-
-
-
-
89
95.51
2.25
2.25
-
-
-
-
-
320
98.75
0.62
0.62
-
-
-
-
-
Beans
Mo. samples
None found
Trace-0.03
0.04-0.10
0.11-0.50
0.51-1.00
1.01-1.50
1.51-2.00
Above 2.00
681
98.82
0.29
0.73
0.14
-
-
-
106
99.06
-
0.94
-
-
-
-
81 868
97.53 98.73
2.47 0.46
0.69
0.12
-
-
-
79 27
87.34 74.07
6.32 11.11
3.79 11.11
2.53 3.70
-
-
-
24
66.67
16.67
8.33
4.17
4.17
-
-
130
80.77
9.23
6.15
3.08
0.77
-
-
Data from Duggan et al., OP. ft.it. (1971).
46
-------
Tolerances
U.S. Tolerances - Section 408 of the Food, Drug and Cosmetic Act, as amended
gives procedures for establishing tolerances for pesticide chemicals on raw
agricultural commodities. Section 409 applies to food additives, including
pesticide chemicals on processed foods. Tolerances are published in the
Code of Federal Regulations, Title 40, and in the Federal Register. When
both methyl parathion and parathion are present, the tolerances apply to
their combined total. A summary of current U.S. tolerances for parathion
on raw agricultural commodities is presented in Table 7.
According to Lu (1973), U.S. tolerances which are established should
not result in the maximum ADI being reached each day. He gives the following
reasons:
1. The tolerance reflects the maximum level of residue
resulting from good agricultural practice, but this level
is often not reached.
2. The tolerance is based on the assumption that the particular
pesticide is used on all food in the class in question, and
this is rarely the case.
3. Much of the residue will be lost in storage, processing and
cooking.
The tolerances are also based upon the entire product as purchased in
the market. However, the product, as purchased, may not be entirely
consumed.
47
-------
Table 7. SUMMARY OF U.S. TOLERANCES FOR PARATHION AND/OR METHYL PARATHION
ON RAW AGRICULTURAL COMMODITIES £/
00
pptn
BBS
0.1 (N)
1.25
5
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
0.75
1
1
1
1
1
1
Almonds
Alfalfa fresh
Alfalfa hay
Apples
Apricots
Artichokes
Avocados
Barley
Beans _ ___
Beets (with or without
tops)
Beet greens
Blackberries
Blueberries (huckleberries)
Boysenberrles
Broccoli
Brussels sprouts
Cabbage
Carrots
Cauliflower
Celery
Cherries
Citrus fruits
Clover
Collards
Corn
Corn forage
Cottonseed
Cranberries
Cucumbers
Currants
Dates
Dewberries
Eggplants
1
1
0.1
1
1
1
1
1
1
1
1
1
1
1
1
1
0.2
1
1
1
1
1
1
1
1
1
1
1
1
0.1
1
1
1
(H)
(1) 00
Crop
ppm
Crop
Endive (eacarole)
Figs
Filberts
Garlic
Gooseberries
Grapes
Grass for forage
Guavas
Hops
Kale
Kohlrabi
Lettuce
Loganberries
Mangoes
Melons
Mustard greens
Mustard seed
Nectarines
Oats
Okra
Olives
Onions
Parsnips (with or
without tops)
Parsnip greens
Peaches
Pea forage
Peanuts
Pears
Peas
Pecans
Peppers
Pineapples
Plums (fresh prunes)
0.9 (1) (N)
1
1
1
1
0.2
1
1
1
1
0.5 (1) (N)
0.1 (1) (N)
0.1 (1) (N)
1
0.1
1
1
1
0.1 (1) (N)
0.1 (1) (N)
1
0.2
0.1 (1) (N)
1
1
1
1
1
0.1 (1) (N)
1
1
Potatoes
Pumpkins
Quinces
Radishes (with or with-
out tops)
Radish tops
Rapeseed
Raspberries
Rice
Rutabagas (with or with-
out tops)
Rutabaga tops
Rye
Safflower seed
Sorghum
Soybean hay
Soybeans
Spinach
Squash
Strawberries
Sugar beets
Sugarcane
Stunner squash
Sunflower seed
Sweet potatoes
Swiss chard
Tomatoes
Turnips (with or with-
out tops)
Turnip greens
Vetch
Walnuts
Wheat
Youngberrlea
Administrative guidelines - none.
Tolerances pending. - all Interim tolerances above.
(1) - Interim tolerances.
(N) - Negligible residue tolerances.
Source: Reprinted from Pesticide Chemical Hews Guide of Food Chemical News, Inc., by permission of the
publisher, first published 1 May 1974.
a/ Tolerances apply to combined methyl parathlon and parathlon residue If both are present.
-------
International Tolerances - Tolerances established by individual nations may
be based on recommendations of the FAO/WHO Expert Committee on Food Additives.
The Committee evaluates all residue data submitted by interested parties and
uses the following criteria (FAO/WHO, 1962,—') for making tolerance
recommendations:
1. Decide upon the effective level of the food additive under
consideration that would be needed in good technological
practice.
2. Examine the possible uses and list all the foods in which
the food additive might be used.
3. Calculate the daily intake level that might occur if the
food additive was used in all the foods for which it might
be a useful additive, working on the basis of the average
intake of the food materials containing the additive. This
average intake for appropriate population groups is obtained
from national food consumption surveys.
4. Obtain the necessary information from which to calculate the
average body weight of the population group concerned (usually
between 50 to 70 kg).
5. From this information, calculate the intake of the additive
in milligrams per kilograms of body weight per day.
6. Check the figure against the acceptable intakes given for the
substances in the table. If it falls within the unconditional
intake zone, the situation is satisfactory and the level
proposed may be accepted. If it falls within the conditional
intake zone, further scientific advice is required before the
level of use proposed is accepted.
I/ FAO/WHO, Food and Agricultural Organization of the United Nations/
World Health Organization, "Evaluation of the Toxicity of a Number
of Antimicrobials and Antioxidants," Sixth Report, Joint FAO/WHO
Expert Committee on Food Additives, World Health Organization Tech.
Kept. Series No. 228. Geneva (1962).
49
-------
The validity of criteria for determining tolerances was reaffirmed
at the 1966 FAO/WHO, 196?!/).
The recommendations for parathion tolerances established by the 1969
Joint Meeting of the FAO and WHO (FAO/WHO, 1970) are:
Vegetables (except carrots) 0.7 ppm
Peaches, apricots, other fresh fruits 1.0 ppm
Other fresh fruits 0.5 ppm
I/ FAO/WHO, Food and Agricultural Organization of the United Nations/
World Health Organization, "Specifications for the Identity and
Purity of Food Additives and Their Toxicological Evaluation:
Some Emulsifiers and Stabilizers and Certain Other Substances,:
10th Report, Joint FAO/WHO Expert Committee on Food Additives,
World Health Organization Tech. Kept. Series No. 373. Geneva (1967),
50
-------
References
Association of Official Analytical Chemists, Official Methods of Analysis
of the Association of Official Analytical Chemists, llth ed.,
Washington, D.C. (1970).
Averell, P. R. and M. V. Norris, "Estimation of Small Amounts of 0,0-
diethyl 0-(2-nitrophenyl)thiophosphate," Anal. Chem.. 20(8):753-756
(August 1948).
Bright, N. F. H., J. C. Cuthill, and N. H. Woodbury, "The Vapor Pressure
of Parathion and Related Compounds," J. Sci. Food and Agr.. 1:344-348
(November 1950).
Cook, J. W., "Paper Chromatography of Some Organic Phosphate Insecticides.
V. Conversion of Organic Phosphates to in vitro Cholinesterase In-
hibitors by N-Bromosuccinimide and Ultraviolet Light," J. Assoc. Offic.
Agr. Chem.. 38-826-832 (1955).
Cook, J. W., and N. D. Pugh, "Quantitative Study of Cholinesterase-
Inhibiting Decomposition Products of Parathion Formed by Ultraviolet
Light," J. Assoc. Offic. Agr. Chem.. 40:277-281 (1957).
Corneliussen, P. E., "Residues in Food and Feed: Pesticide Residues
in Total Diet Samples (VI)," Pest. Monit. J., 5(4):313-329 (March 1972).
Cowart, R. P., F. L. Bonner, and E. A. Epps, Jr., "Rate of Hydrolysis
of Seven Organophosphate Pesticides," Bull. Environ. Contam. Toxicol.,
6(3):231-234 (1971).
Dauterman, W. C., "Biological and Nonbiological Modifications of Organo-
phosphorus Compounds," Bulletin of the World Health Organization,
44(1-2-3):144 (1971).
Duggan, R. E., G. Q. Lipscomb, E. L. Cox, R. E. Heatwole, and R. C. King,
"Pesticide Residue Levels in Foods in the United States from 1 July 1963
to 30 June 1969," Pest. Monit. J.. 5(2):73-212 (September 1971).
Dvornikoff, M. N., et al. (to Monsanto Chemical Company), U.S. Patent No.
2,663,721 (22 December 1953).
El-Refai, A., and T. L. Hopkins, "Parathion Absorption, Translocation,
and Conversion to Paraoxon in Bean Plants," J. Agr. Food Chem.,
14(6):588-592 (November-December 1966).
FAO/WHO, Food and Agricultural Organization of the United States/World
Health Organization, "Evaluation of the Toxicity of a Number of Anti-
microbials and Antioxidants," Sixth Report, Joint FAO/WHO Expert
Committee on Food Additives, World Health Organization Tech. Rept.
Series No. 228. Geneva (1962).
51
-------
FAO/WHO, Food and Agricultural Organization of the United Nations/World
Health Organization, "Specifications for the Identity and Purity of
Food Additives and Their Toxicological Evaluation: Some Emulsifiers
and Stabilizers and Certain Other Substances," 10th Report, Joint
FAO/WHO Expert Committee on Food Additives, World Health Organization
Tech. Rept. Series No. 373. Geneva (1967).
FAO/WHO, Food and Agricultural Organization of the United Nations/World
Health Organization, 1967 Evaluation of Some Pesticide Residues in
Food. The Monographs. Geneva (1968).
FAO/WHO, Food and Agricultural Organization of the United Nations/World
Health Organization, 1969 Evaluations of Some Pesticide Residues in
Food. The Monographs. Geneva (1970).
FAO/WHO, Food and Agricultural Organization of the United Nations/World
Health Organization, "Pesticide Residues in Food," Report of the 1971
Joint FAO/WHO Meeting on Pesticide Residues, World Health Organization
Tech. Rept. Series No. 502. Geneva (1972).
Frawley, J. P., J. W. Cook, J. R. Blake, and 0. G. Fitzhugh, "Effect of
Light on Chemical and Biological Properties of Parathion," J. Agr.
Food Chem.. 6(1):28-30 (January 1958).
Gar, K. A., and R. Y. Kapiani, Proclamation of the International Conference
of Peaceful Uses of Atomic Energy (1955). 12:185 (1956).
Gogan, R. J., "Application of Oscillographic Polarography to the
Determination of Organophosphorus Pesticides, II. A Rapid Screening
Procedure for the Determination of Parathion in Some Fruits and
Vegetables." J. Assoc. Off. Agr. Chem.. 46(2):216-222 (1963).
Comma, H. M., and S. D. Faust, "Chemical Oxidation of Organic Pesticides
in Aquatic Environments," Paper No. 48, 161st American Chemical Society
Meeting, Los Angeles, California (29 March - 12 April 1971).
Grunwell, J. R., and R. H. Erickson, "Photolysis of Parathion (0,0-
Diethyl-0-(4-nitrophenyl)thiophosphate). New Producers," J. Agr.
Food Chem.. 21(5):929-931 (September-October 1973).
Gunther, F. A., D. E. Ott, and M. Ittig, "The Oxidation of Parathion
to Paraoxon, II. By Use of Ozone," Bull. Environ. Contain. Toxicol.,
5(l):87-94 (1970).
52
-------
Heath, D. F., "The Effects of Substituents on the Rates of Hydrolysis of
Some Organophosphorus Compounds. I. Rates in Alkaline Solution,"
J. Chem. Soc.. pp. 3796-3804 (1956).
Heath, D. F., Organophosphorus Poisons. New York: Pergamon Press (1961).
Joiner, R. L., H. W. Chambers, and K. P. Baetcke, "Toxicity of Parathion
and Several of Its PhotoaIteration Products to Boll Weevils," Bull.
Environ. Contain. Toxicol.. 6(3):220-224 (1971).
Joiner, R. L., Piss. Abstr. Int.. 32:4169B (1971/1972).
Koivistoinen, P., and M. Merilainen, "Paper Chromatographic Studies on
the Effect of Ultraviolet Light on Parathion and Its Derivatives,"
Acta Agr. Scand.. 12:267-276 (1962).
Lawless, E. W., and T. L. Ferguson (Midwest Research Institute), and
R. von Rumker (RvR Consultants), The Pollution Potential in Pesticide
Manufacturing, for Environmental Protection Agency, Contract No. 68-01-
0142 (January 1972).
Lawless, E. W., T. L. Ferguson, and A. F. Meiners (Midwest Research
Institute), Methods for the Disposal of Spilled and Unused Pesticides
(Draft), for Environmental Protection Agency, Contract No. 68-01-0098
(1973).
Lu, F. C., "lexicological Evaluation of Food Additives and Pesticide
Residues and Their 'Acceptable Daily Intakes' for Man: The Role of
WHO, in Conjunction with FAO," Residue Rev.. 45:81-93 (1973).
Melnikov, N. N., Chemistry of Pesticides. Springer-Verlag, New York,
pp. 324-329 (1971).
Metcalf, R. L., and R. B. March, "The Isomerization of Organic Thiophos-
phate Insecticides," J. Econ. Entomol.. 46:288-294 (April 1953).
Mitchell, L. C., "Separation and Detection of Eleven Organophosphate
Pesticides by Paper Chromatography," J. Assoc. Offie. Agr. Chem., 44:
643-712 (1961).
Monsanto Company, Agricultural Division, "Parathion and Methyl Parathion,"
Technical Bulletin No. AG-lb, St. Louis, Missouri (undated).
53
-------
Mulla, M. S., "Persistence of Mosquito Larvicides in Water," Mosquito
News. 23(3):234-237 (September 1963).
National Agricultural Chemicals Association, Safety Guide for Warehousing
Parathions. Washington, D.C. (1968).
Payton, J., "'Parathion1 and Ultraviolet Light," Nature. 171(4347):355-
356 (21 February 1953).
The Pesticide Chemical News Guide (1 May 1974).
Rolston, L. H., and R. R. Walton, "Parathion Residues in Greens," J. Econ.
Entomol.. 56:169-172 (1963).
Ruzicka, J. H., J. Thomson, and B. B. Wheals, "The Gas Chromatographic
Determination of Organophosphorus Pesticides - Part II. A Comparative
Study of Hydrolysis Rates," J. Chromatog.. 31(l):37-47 (November 1967).
Schrader, G. (to Farbenfabriken Bayer), U.S. Patent No. 2,624,745
(6 January 1953).
Smith, W. M., Jr., and J. 0. Ledbetter, "Hazards from Fires Involving
Organophosphorus Insecticides," Amer. Ind. Hyg. Assoc. J.. 32(7):468-
474 (July 1971).
Taschenberg, E. G. and A. W. Avens, "Parathion and EPN Residue Studies
on Concord Grapes," J. Econ. Entomol.. 53:441-445 (1960).
Toy, A. D. F., et al. (to Victor Works), U.S. Patent No. 2,471,464
(31 May 1949).
U.S. Department of Agriculture, Food and Drug Administration, Pesticide
Analytical Manual. 2 vols. (1971).
Vernon, C. A., Chem. Soc. (London) Spec. Publ.. 8:17 (1957).
Whalley, P. J., R. H. Adams, and B. Combes, J. Amer. Med. Assoc..
189(5):357 (1964).
Zweig, G., and J. Sherma, Analytical Methods for Pesticides and Plant
Growth Regulators, Vol. VI; Gas Chromatographic Analysis. Academic
Press, New York, New York (1972).
54
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SUBPART II. B. PHARMACOLOGY AND TOXICOLOGY
CONTENTS
Page
Acute, Subacute and Chronic Toxicity 57
Toxicity to Laboratory Animals 57
Acute Oral Toxicity - Rats 57
Acute Toxicity - Rats, Routes Other Than Oral 59
Subacute and Chronic Oral Toxicity - Rats 59
Toxicity of Parathion in Combination with Other Drugs 61
Acute Oral Toxicity - Mice 63
Acute Toxicity - Mice, Routes Other Than Oral 65
Subacute and Chronic Oral Toxicity - Mice 66
Acute Oral Toxicity - Guinea Pigs 67
Acute Toxicity - Guinea Pigs, Routes Other Than Oral 67
Subacute and Chronic Oral Toxicity - Guinea Pigs 67
Acute, Subacute and Chronic Toxicity - Dogs 67
Acute, Subacute and Chronic Toxicity - Cats 68
Acute, Subacute and Chronic Toxicity - Rabbits 68
Toxicity to Domestic Animals 69
Goats 69
Sheep 69
Cattle 70
Symptomology and Pathology Associated with Mammals 71
Physiological and Pharmacological Aspects of Parathion 72
Summary 73
Metabolism of Parathion 75
Absorption 75
Distribution 76
Excretion 76
Bio trans format ion .-. 77
Degradation of Parathion (and Paraoxon) 79
Tissue Residues 85
Summary 85
55
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• CONTENTS (Continued)
Page
Effects on Reproduction 85
Domestic Animals 86
Wild Avian Species 86
Teratogenic Effects 88
Mammals 88
Avian - Embryotoxicity 91
Crustaceans 94
Behavioral Effects 95
Toxicity Studies with Tissue Cultures 96
Mutagenic Effects 98
Oncogenic Effects 98
Effects on Humans 100
Acute and Subacute Toxicity 100
Symptoms of Parathion Poisoning 104
Dermal Effects 105
Inhalation Effects 110
Occupational Accidental Exposure Hazards Ill
Field Operations Ill
Manufacturing Operations 120
Accidents 121
References 123
56
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This section is concerned with information on the acute, subacute
and chronic toxicities of parathion in laboratory and domestic animals.
The metabolism of parathion is reviewed; the absorption, distribution,
excretion, biotransformation, activation and detoxification of this
compound are discussed. The effects of parathion on reproduction,
malformation of the young, and behavioral effects are also considered.
Reviews of parathion1s toxic effects on tissue cultures, and the
promotion or tendencies to bring about mutagenesis and oncogenic effects
are included, although information on these latter effects is quite
limited. The hazards posed by exposure of humans to parathion have
been reviewed in relation to acute and subacute toxicity, the symptoms
associated with parathion poisoning, the physiological and pharmacological
action, the routes of exposure (mainly dermal and inhalation), and the
hazards associated with the use of parathion in field operations and in
manufacturing plants.
Acute, Subacute and Chronic Toxicity
The information in this subsection is related to the toxicological
studies in laboratory and domestic animals.
Toxicity to Laboratory Animals -
Acute oral toxicity - rats - Tables 8 and 9 present the findings
of several studies on LD^Q values for parathion administered in rats
by oral, dermal, intraperitoneal, intravenous, intramuscular means
and by inhalation. The individual LDcn values obtained varied from
one study to another. With only one exception, females were found to
be more sensitive to oral administration of the insecticide than males.
The individual values for reported LDJQ'S in Table 8 were used to
calculate an average LD5Q value. This average oral LD^Q was 7.6 mg/kg
(range 2.04 to 30.0 mg/kg) for male rats and 3.5 mg/kg (range 1.75 to
6.0 mg/kg) for females.
If data in Table 8 are compared to data reported by Gaines (1960)—^t
there is good agreement among researchers on confidence levels for female
rats and relatively good agreement on levels for male rats. With females
the confidence limits are 3.2 to 4.0 mg/kg, and the average LDr/j is 3.5
mg/kg. The confidence limits for male rats reported by Gaines are from
10 mg/kg to 17 mg/kg; the computed average from Table 8 is 7.6 mg/kg.
One value (30 mg/kg) in Table 8 was not used in computing the average
because it was thought to lie too far outside the range of the other
values reported. If the 30 mg/kg LDcg were included in the computation,
the average would then be slightly higher than 9 mg/kg, and this value
would be very close to the lower confidence limit reported for male
rats by Gaines.
JL/ Gaines, T. G., "The Acute Toxicity of Pesticides to Rats,"
Toxicol. APP!. Pharmacol.. 2:88-99 (1960).
57
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Table 8. ACUTE ORAL TOKICITT OT PARATHION FOK IATS
Meaaureswnt
(•g/kg unless Weanlings
noted otherwise) Male Female Mixed (sale) Reference
Oral LDso 5.0 1.75 . . ./
Oral LDjo 13.0 3.60 - - b/ e/~ d/ e
Oral U>50 - 4.03 - - ~ £/
°r«l LD50 - 3.20 - I/
Oral LD50 3.6 ... y
OralLD50 - - - 1.3 h/
Oral LD50 - - 3-6 - I/
Oral LD5o 2.04 - . . T/
Oral LD5o - - 2.5 Jt/
Oral LDjo 8*6 - \f
Oral LDjo 7.0 4.0 - 1.5 ./
Oral LDjo 3.6 - ~f
Oral LDjo 7.5 ... '/
Oral U>50 5.9 2.70 - 1.75 T/
Oral LDjo 12.50 3.JO - ./
Oral LDjo 30.00* 3.00 - J/
Oral LDjo «.0 6.00 - ^/
Oral LDjo * 7.6 3.5
Range 2.04-30.0 1.75-6.0
19/20 confidence limits
(mg/kg) 10-17 3.2-4.0 - . b/
Lowest dose to kill an
adult rat
Oral 10 3.00 - c/
Dermal 10 5.00 - cV
* Hot included in average calculation.
a/ Hazleton, L. W., and E. G. Holland, "Pharmacology and Toxicology of Parathlon," Adv. Chem. Series
Ho. I. 31:31-38 (1950).
b/ Cslnes, T. B., flft, _fiit- (1960).
c/ Gainea, T. B., "Acute Toxicity of Pesticides," Toxicol. Appl. Pharmscol.. 14:515-534 (1969).
d/ Anon., "Toxic Hazards of Pesticides to Man. Report of a Study Group," WHO Tech. Rept. Ser..
114:3-51 (1956).
e_/ Technical Development Laboratories, Communicable Dlaeaae Center, Clinical Memoranda on
Economic Poisons. U.S. Department of Health, Education, and Welfare, Public Health Service,
pp. 7-12 and 17-21 (1 April 1956).
ll Delchmann. W. B., W. Pugliese. and J. Caaaldy. "Effects of Dimethyl and Diethyl Paranltro-
phenyl Thlophosphate on Experimental Animals," AMA Arch. Ind. Hyg. Occup. Med.. 5:44-51 (1952).
«,/ Edson, E. F., and D. N. Noakes, "The Comparative Toxlclty of Six Organophosphorus Insecticides
in the Rat," Toxicol. Appl. Phanaaeol.. 2:523-539 (1960).
h/ Brodeur, J., and K. P. DuBols, "Comparison of Acute Toxlcity of AntIchollnesterase Insecticides
to Weanling and Adult Male Rats," Proc. Soc. Exp. Btol. Med.. 114(2):509-511 (November 1963).
ll Edson, E. F., D. M. Sanderson, and D. N. Noakes, "Acute Toxlclty Data for Pesticides (1964),"
World Rev. Pest Con.. 4:36-41 (1965).
i/ Webb, R. E., C. C. Bloomer, and C. L. Miranda, "Effect of Casein Diets on the Toxlclty of Mala-
th ion and Parathlon and Their Oxygen Analogues." Bull. Environ. Contarn. Toxlcol.. 9(2):102-107 (1973).
k/ DuBols, K. P., and F. K. Kinoshlta, "Influence of Induction of Hepatic Mlcrosomal Enzymes by
Phenobarbltal on Toxiclty of Organic Phosphate Insecticides," Proc. Soc. Exp. Biol. Med..
129:699-702 (1968).
ll Villeneuve, D. C., and W. E. J. Phillips, "The Effect of Acute Ethanol Administration on Parathlon
Toxiclty and in vitro Parathlon Degradation on the Rat," Can. J. Physiol. Pharmscol.. 49:481-483
(1971).
m/ DuBols, K. P., "The Toxiclty of Organophosphorus Compound* to Mammals," Bulletin of the World Health
Organization. 44:233-240 (1971).
n/ Dalloz, J. P., Deiatour, and G. Lorgue, "The Organophosphorus Pesticides," Rev. Med. Vet.. Toulouse,
123(10):1356 (1972).
o/ Jacobaen, P. L., R. C. Spear, E. Wei, "Parathlon and Dlisopropylfluorophosphate (OFF) Toxlclty In
Partially Hepatectomlzed Rats," Toxlcol. Appl. Pharaacol.. 26:314-317 (1973).
£/ Alary, J-G., and J. Brodeur, "Correlation Between the Activity of Liver Enzymes and the LDjo of
Parathlon In the Rat," Can. J. Physiol. Pharmacol.. 48:829-831 (1970).
a/ Frawley, J. P., E. C. Hagan, and O. G. Fitzhugh, "A Comparative Pharmacological and Toxlcological
Study of Organic Phosphate-Antlchollnesteraee Compounds," J. Pharmscol. Exp. Thar.. 105:156-165
(1952).
r/ DuBols, K. P., J. Doull, P. R. Salerno, and J. M. Coon, "Studies on the Toxlclty and Mechanism of
~ Action of p-Nltrophenyl Diethyl Thlonophosphate (Parathion)," J. Pharmacol. Exp. Ther.. 95(1):79-91
(1949).
58
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Acute toxicity - rats, routes other than oral - The toxicity of
parathion for rats by exposures other than oral (Table 9) has not been
studied as thoroughly as by oral toxicity.
The intraperitoneal LD5g values range from 3.6 to 7.0 mg/kg for
males, and 4 mg/kg was the only value found for females. The dermal
LD,-0 for rats was about 21 mg/kg for males with much more variation for
females, 6.8 to 100 mg/kg. The LD5Q value for inhalation toxicity has
been reported as 0.0315 mg/liter (4 hr) and 0.115 mg/liter (1 hr).
Gaines states that ". . .results and use experience indicates that there
is a much closer relationship between dermal LDcQ values and the
occurrence of occupational poisoning than between oral LD50 values and
occupational poisoning."
It is interesting that the values reported for inhalation toxicity
indicate that very low levels of parathion are toxic to rats
0.115 mg/liter - 1 hr; and 0.315 mg/liter - 4 hr).
Subacute and chronic oral toxicity - rats - Only a few studies
have been reported in the open literature on subacute and chronic
toxicity of parathion in rats. Barnes and Denz (1951).!/ and Edson and
Noakes (1960) conducted relatively long-term studies on toxicity. Under
the Edson and Noakes study, rats were fed diets containing parathion
for 15 to 16 weeks, at which time survivors were sacrificed, and
macroscopic examinations were conducted. Relative organ weights and
measurement of cholinesterase activity in red cells, plasma, and whole
brain were made. In this study death due to parathion toxicity was
reported only in the animals fed at a dietary concentration of 125 ppm,
calculated to be equal to an average parathion intake-of 15.4 mg/kg/day.
Thirty percent mortality (three of 10) occurred in this group. No
mortality occurred in those groups of rats fed at dietary levels of
25 ppm (X = 2.4 mg/kg/day) or at 5 ppm (X = 0.52 mg/kg/day).
_!/ Barnes, J. M., and F. A. Denz, "The Chronic Toxicity of jx-Nitrophenyl
Diethyl Thiophosphate (E. 605): A Long-Term Feeding Experiment
with Rats." J. Hvg.. 49:430-441 (1951).
59
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Table 9. ACUTE TOXICITY OF PARATHION FOR RATS VIA ROUTES
OTHER THAN ORAL
Measurement
(rag/kg unless
noted otherwise)
IP U>50
IP LD50
IP LD50
D LD50
D LD50
D LD50
D ID50
LC50 - 1 hr (mg/je)
LC50 - 4 hr (mg/4)
Adults
Male Female Mixed
7.0 4.0
4.5
3.6
21.0 10.9
100.0
50-200
21.0 6.8
0.115
0.0315
Weanlings
(male) Reference
a/
b/
1.5 c/
d/, e/
f/
£/
y
c/
£/
IP LDso - Intraperitoneal injection.
D LDso ~ Dermal exposure.
LCso ~ Lethal concentration by inhalation.
a/ DuBois etal., .op_. _cit. (1949).
b/ Westermann, E., "Accumulation of Environmental Agents or Their Effects
~~ in the Body," Environ. Res.. 2:340-351 (1969).
£/ Kimmerle, G., and D. Lorke, "Toxicology of Insecticidal Organophos-
phates," Pflanz. Nachr. Bayer, 21:111-142 (1968).
d/ Anon., op. cit. (1956).
e/ Technical Development Laboratories, op. cit. (1956).
Edson et al., pp. cit. (1960).
f/
£/
h/
Edson et al., op. cit. (1965).
Gaines, T. B., op., cit. (1969).
60
-------
Pertinent findings from the study by Barnes and Denz (1951) are
incorporated into Table 10. No food consumption data was obtained in
their study. Dietary levels of 10 and 20 ppm did not result in any
identifiable symptoms of parathion poisoning. Subsequent examination
did not reveal any pathological lesions. A dietary level of 50 ppm
was toxic and treatment at this level resulted in 42% mortality during
the year, with most of the deaths occurring early in the test period
when the animals were young. At dietary levels of 75 and 100 ppm most
of the rats died during the first few weeks.
Chronic (dietary) toxicity of parathion fed to rats at several
levels (10,25,50, and 100 ppm in diet) was studied by Hazelton and
Holland (1950). Their tests were conducted for 104 weeks using male
rats and for 64 weeks using female rats. With the male rats 40%
mortality was observed for controls over the test period. Rats fed
parathion in the diet at 50 ppm had a mortality level of 20% and
those treated at a dietary level of 100 ppm had a mortality level of
38%. In the female rats a relatively high mortality (33%) occurred
in the controls and relatively few rats were included in each treatment
group. However, a dietary level of 10 ppm parathion did not cause
any mortalities (100% survival), and at 50 ppm the mortality rate
was only about equal to that of the untreated controls (38%). At
100 ppm, female rats exhibited evidence of toxicity and appeared
unthrifty, indicating that chronic toxicity, like acute toxicity, is
different for female and male rats.
All females in the control and 10-ppm treatment groups produced
living litters. All but one female in the 50-ppm treatment group bore
living litters.
Based on changes in cholinesterase levels, the "no-effect" level
of parathion in the rat was reported by Edson et al., (1964)-i' to be
0.02 mg/kg/day when the insecticide was fed over an 84-day period.
The smallest effect was found in the range 0.04 to 0.06 mg/kg/day.
These studies indicated that in the rat a wide margin of safety existed
between the maximum "no-effect" level over that needed to evoke a
frank toxic effect.
Toxicity of parathion in combination with other drugs - The effect
of central-depressant drugs on toxicity of parathion for rats has been
I/ Edson, E. F., et al., "Summaries of Toxicological Data: No-Effect
Levels of Three Organophosphates in the Rat, Pig, and Man," Food
Cosmet. Toxicol.. 2:311 (1964).
61
-------
Table 10. CHRONIC ORAL TOXICITY TEST IN RATS FED PARATHION^/
Concentration
of parathion
in feed (ppm)
100
Duration
of test
(days)
19
Mortality due to
poisoning (7.)
80
75
50
27
365
73
42
20
10
365
365
Comments
First death occurred in
2 hr. All survivors had
severe symptoms of poison-
ing.
Slight symptoms in 2 hr.
After second week food
consumption irregular.
First symptoms and first
death on seventh day.
Deaths occurred through
third week but not after.
Symptoms decreased in
severity and frequency
after third month.
Symptomless for entire test
period.
Symptomless for entire test
period.
7/ Adapted from the data of Barnes and Denz, OD_. cit. (1951).
62
-------
studied by Weiss and Orzel (1967).-' Following treatment with reserpine,
chlordiazepoxide, hexabarbital and phenobarbital, female rats were treated
with 2, 4, or 8 mg/kg parathion. The greatest enhancement of toxicity
was obtained at 2 and 4 mg/kg parathion. Alcohol was found to increase
toxic effects of parathion only at the 4-mg/kg dose level.
The interactions (toxicity) between polychlorinated biphenyls (PCS)
and parathion in rats was studied by Phillips et al. (1972).V The
rationale behind the study was that because PCB ingestion can modify
microsomal enzyme activity in rabbits and rats, it is possible that
organophosphate toxicity may also be altered. Adult female rats were
used in the tests. Plasma and brain cholinesterase activities were used
to measure the effects of exposure to PCB, parathion and combinations of
the two materials. The PCB was given orally (in diet) and parathion was
injected intraperitoneally.
The results of these studies showed that the feeding of PCB (Aroclor
1221) had no effect on plasma cholinesterase. It was also found that
parathion did not reduce the plasma or brain cholinesterase activity in
animals fed PCB's below that observed in animals which were not fed PCB's.
The conclusion drawn was that chronic ingestion of PCB (Aroclor 1221)
up to a level of 200 ppm in the diet did not potentiate parathion toxicity.
Potentiation of parathion toxicity did not result from feeding of Aroclor
1254 up to 20 ppm. The effect of Aroclor 1254 when fed at 200 ppm makes
interpretation of parathion toxicity effects difficult.
Acute oral toxicity - mice - A summary of the data for acute oral
toxicity of parathion to mice is given in Table 11. The average U>50
value for males was 23.0 mg/kg (range 17.5 to 30.3 mg/kg) and for male-
female groups 12.7 mg/kg (range 6.0 to 25.0 mg/kg). It appears that
the susceptibility to parathion poisoning for male rats is higher than
for male mice.
In mice, as with most other species studied, there is no appreci-
able tissue accumulation of residuals, and deaths generally occur only
in cases where parathion is administered as an acute toxic (lethal) dose.
In general, prompt and apparently complete recovery from nonlethal doses
If Weiss, L. R., and R. A. Orzel, "Enhancement of Toxicity of Anti-
cholinesterases by Central Depressant Drugs in Rats," Toxicol.
Appl. Pharmacol., 10:334-339 (1967).
2/ Phillips, W. E. J., G. Hatina, D. C. Villeneuve, and D. L. Grant,
"Effect of Parathion Administration in Rats Following Long-Term
Feeding with PCB's," Environ. Physiol. Biochem.. 2:165-169 (1972).
63
-------
Table 11. ACUTE ORAL TOXICITY OF PARATHION TO MICE
Male
Acute oral
(ing/kg)
Female
Mixed
Reference
.
-
-
18.5
-
-
-
-
-
17.5
25.6
30.3
23.0 Average
7.0-30.3 Range
8.1
6.0
25.0
-
21.0
6.4
16.9
6.7
11.6
-
-
-
12.7 Average
6.0-25.0 Range
a/
b/
c/
d/
b/
e/
e/
e/
I/
f/
£/
£/
a/
b/
£/
d/
/
t
DuBois, K. P., og. cit. (1971).
Hazelton and Holland, op. cit. (1950).
Frawley et al., 03. cit. (1952).
Vukovich, R. A., A. J. Triolo, and J. M. Coon, "The Effect of Chlor-
promazine on the Toxicity and Biotrans formation of Parathion in
Mice," J. Pharmacol. Exp. Thera., 178(2) : 395-401 (1971).
Rosival, L., F. V. Selecky, and L. Vbrovsky, "Acute Experimental
Poisoning with Organophosphorus Insecticides," Bratisl. Lek.
Listy. 38^:151-160 (1958).
Triolo, A. J., and J. M. Coon, "Toxicologic Interactions of Chlorinated
Hydrocarbon and Organophosphate Insecticides," J. Agr. Food Chem..
14(6): 549-555 (1966).
Konst, H., and P. J. Plummer, "Acute and Chronic Toxicity of Para-
thion to Warm-Blooded Animals," Can. J. Comp. Med. Vet. Sci.,
14:90-108 (1950).
64
-------
is observed with mice and other laboratory animals. Animals that survive
a single dose longer than 24 hr may generally be expected to recover com-
pletely, and there is no apparent residual toxicity (Hazelton and Holland,
1950). However, because depressed blood cholinesterase lasts throughout
the lifetime of red blood cells, this symptom remains until the red blood
cells are naturally replaced.
Acute toxicity - mice, routes other than oral - The toxicity of
parathion by intraperitoneal, intravenous and subcutaneous injection into
mice is shown in Table 12. There appears to be close agreement in the
LD50 values for male-female groups injected intraperitoneally and sub-
cutaneous ly. There were not sufficient reports found in the literature
on males and females alone to make a valid comparison of 11)50 values.
Natoff (1967)— reported mice to be more susceptible to parathion
administered intravenously than by other routes. However, in a more
recent study this same author indicated that the intraperitoneal route
was more lethal. Parathion was shown to be more toxic to female mice by
intraperitoneal injection than by intravenous injection. The estimated
median lethal dose by oral route was 85.6 uM/kg, by intraperitoneal in-
jection 50.3 uM/kg, by intravenous injection 58 uM/kg, and subcutaneously
71.3 uM/kg. These values average to about 68 uM/kg for the hepatic routes
and 65 uM/kg for the peripheral routes (Natoff, 1970?-/).
Subacute and chronic oral toxicity - mice - No information was
found concerning either the subacute or the chronic oral toxicity of
parathion to mice.
Acute oral toxicity - guinea pigs - The acute oral toxicity of
parathion for guinea pigs as reported by various workers is given in
Table 13. The LDso value for guinea pigs, male-female groups, varied
from 9.3 mg/kg to 32.0 mg/kg of body weight. The LDso values for male
guinea pigs were 16.3 mg/kg and 24.0 mg/kg of body weight.
\l Natoff, I. L., "Influence of the Route of Administration on the
Toxicity of Some Cholinesterase Inhibitors," J. Phann. Pharmacol..
19^:612-616 (1967).
2_/ Natoff, I. L., "Influence of the Route of Exposure on the Acute
Toxicity of Cholinesterase Inhibitors," Europ. J. Toxicol.,
3:363-367 (1970).
65
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Table 12. ACUTE TOXICITY OF PARATHION TO MICE--ROUTES OTHER THAN ORAL
Routed/ Male
IP 10
13.5
-
-
ID50 (mg/kg)
Female Mixed
10
-
14.7
8.2
Reference
b/
c/
d/
e/
IV
7.6
16.9
9.0 Average
4.6-14.4 Range
5.4
1.0
f/
d/
e/
e/
SC
20.8
11.0 Average
7.8-13.6 Range
d/
£/
e/
J/
a/ IP - Intraperitoneal; IV - Intravenous; SC - Subcutaneous.
b/ DuBois et al., OJL. cit. (1949).
c/ Benke, G. M., K. L. Cheever, F. E. Mirer, and S. D. Murphy, "Com-
parative Toxicity, Anticholinesterase Action and Metabolism of
Methyl Parathion in Sunfish and Mice," Toxicol. Appl. Phannacol..
28j97-109 (1974).
d/ Natoff, I. L., 0£. cit. (1967).
e/ Rosival et al., 02. cit. (1958).
f/ Vukovich et al., oj.. ^it. (1971).
66
-------
Acute toxicity - guinea pigs, routes other than oral - The dermal
LD for parathion in guinea pigs is reported as 0.60 ml/kg on intact
skifl and 0.80 ml/kg on abraded skin (Roudabush et al., 1965±'). The
LD50 for intraperitoneal injection is 12.0 mg/kg (Anon., Council of
Europe, 19642-').
Subacute and chronic oral toxicity - guinea pigs - No subacute or
chronic oral toxicity data for guinea pigs were found relative to
parathion.
Acute, subaeute and chronic toxicitv - dogs - It has been reported
(Anon., Council of Europe, 1964) that acute oral toxicity of parathion
in dogs is 3.0 to 5.0 mg/kg. The intraperitoneal LD5Q values for dogs
is 3 to 5 mg/kg of body weight (DuBois et al., 1949); 12 to 20 mg/kg
(Anon., Council of Europe, 1964). By intravenous injection, the lethal
dose is 12 to 20 mg/kg (Anon., Council of Europe, 1964).
Table 13. ACUTE ORAL TOXICITY OF PARATHION TO GUINEA PIGS
Sex
Male and female
Male and female
Male and female
Male and female
Male
Male
LD50
(mg/kg)
9.3
16.2
19.8
32.0
24.0
16.3
Reference
a/
b/
b/
c/
b/
b/
a/ Hazelton and Holland, op. cit. (1950).
b/ Konst and Plummer, op. cit. (1950).
c/ Frawley et al., op., cit. (1952).
I/ Roudabush, R. L., C. J. Terhaar, D. W. Fassett, and S. P. Dziuba,
"Comparative Acute Effects of Some Chemicals on the Skin of Rabbits
and Guinea Pigs," Toxicol. Appl. Pharmacol.. 7:559-565 (1965).
2/ Anon., Council of Europe-Netherlands Report on Parathion and Parathion-
Methyl, Ministerie von Sociale Zahen En Volksgezandheid (1964).
67
-------
The subacute toxicity of parathion for dogs was studied by Frawley
and Fuyat (1957)!' by measuring changes in plasma and RBC cholinesterase.
When parathion was incorporated in the dogs' diet at 1 ppm and fed for
24 weeks, a significant (minimal) reduction in plasma cholinesterase
occurred. At 2 and 5 ppm plasma cholinesterase reductions of 60 and 70%
were recorded. Inhibition of RBC cholinesterase occurred where diet
levels of parathion were 2 ppm or above.
Chronic (dietary) toxicity of parathion for dogs was determined by
Hazelton and Holland (1950) using 15% wettable powder given in gelatin
capsules 6 days/week for 90 days. The capsules were given either with
a meal or immediately afterward (prior administration resulted in loss of
appetite and food refusal).
At 2 mg/kg/day the dog lived 3 weeks but exhibited toxic signs con-
tinuously. At 1 and 3 mg/kg/day the animals survived for the full 90-
day test period. During the early stages the dogs were nervous and ir-
ritable but during the final month both dogs were normal in their behavior.
Neither dog showed evidence of gross pathology. Histopathological examina-
tion revealed some degenerative changes in the liver.
Acute, subacute and chronic toxicity - cats - No data were found in
the open literature on the acute, subacute and chronic oral toxicity of
parathion to cats. The subcutaneous, intraperitoneal and intravenous
LDso's are 15.0 mg/kg, 3.0 to 5.0 mg/kg and 3.0 to 5.0 mg/kg, respectively
(Anon., Council of Europe, 1964). DuBois et al. (1949) reported an
intraperitoneal 11)50 value of 12 to 20 mg/kg of body weight.
In cats, parathion has been shown to be readily absorbed through
the skin in unchanged form, although no dermal 11)50 values have been re-
ported (Fredriksson, 1964^').
Acute, subacute and chronic toxicity - rabbits - The acute oral LD50
for male rabbits is 68 mg/kg of body weight as reported by Konst and
Plummer (1950) .
\l Frawley, J. P., and H. N. Fuyat, "Effect of Low Dietary Levels of
Parathion and Systox on Blood Cholinesterase of Dogs," J. Agr. Food
Chem., 5:346 (1957).
2/ Fredriksson, T., "Studies on the Percutaneous Absorption of Para-
thion and Paraoxon. Part VI. In vivo Decomposition of Paraoxon
During the Epidermal Passage," J. Invest. Dermato1.. 42:37-40 (1964)
68
-------
The acute dermal LD5Q for mixed sexes of rabbits is 0.07 ml/kg
(Roudabush et al., 1965). Diechmann et al (1952)i/ reported the
dermal LD50 of parathion for rabbits is 870 mg/kg, which was similar
to his findings on guinea pigs. Lehman (1948), on the other hand,
reported the acute dermal LD for rabbits to be 40-50 mg/kg. In
rabbits, it has been shown tftQt parathion is absorbed dermally in an
unchanged form (Fredriksson et al., 1961-/.
No information was found concerning subacute or chronic studies
in rabbits.
Toxicity to Domestic Animals -
Goats - Of the ruminants which have been studied, the goat appears
most susceptible to parathion poisoning. Although no LD5Q values have
been reported for this animal, daily subacute oral doses as low as 8 rag/
kg were reported to have killed one experimental goat in 11 days. Other
subacute doses reported for goats range from 12 mg/kg for 5 days to
32 mg/kg for 10 days (Wilber and Morrison, 1955-2'). Unlike other ruminant
species studied, parathion is reported to cross the placenta1 blood bar-
rier and exert anticholinesterase effects on the fetus. Parathion has
been reported to appear in the milk of lactating female goats. It is
not known how long the anticholinesterase activity of milk from poisoned
goats persists (Wilber and Morrison, 1955).
Sheep - The acute oral U>50 of parathion for ewe and ram lambs is
estimated at 40 to 50 mg active ingredient per kilogram of body weight.
Lethal doses for lambs range from four doses of 24 mg/kg each to three
doses of 48 mg/kg each. The insecticide was not markedly cumulative in
its toxic effects (Mol et al., 1972.V). Sheep receiving daily subacute
doses exhibit symptoms similar to those in acutely affected animals.
Affected sheep that survived recovered completely after cessation of
treatment, and appeared to be normal with no recurring ill effects.
\J Diechmann, W. B., W. Pugliese, and J. Cassidy, "Effects of Dimethyl
and Diethyl Paranitrophenyl Thiophosphate on Experimental Animals,"
AMA Arch. Ind. Hyg. Occup. Med.. 5:44-51 (1952).
2/ Fredriksson, T., W. L. Farrior, Jr., and R. F. Witter, "Studies on
the Percutaneous Absorption of Parathion and Paraoxon. Part I.
Hydrolysis and Metabolism Within the Skin," Acta Derm. Venerol..
41:335-343 (1961).
J3/ Wilber, C. G., and R. A. Morrison, "The Physiological Action of
Parathion in Goats," Am. J. Vet. Res., 10(59):308-313 (1955).
4/ Mol, J. C. M., D. L. Harrison, and R. H. Tlefer, "Parathion:
Toxicity to Sheep and Persistence on Pasture and in Soil," N. Z.
J. Agr. Res.. 15:306-320 (1972).
69
-------
The maximum safe oral dose (MSD) for sheep has been determined to
be 10 mg/kg, whereas the minimum toxic dose (MTD) is 20 mg/kg (Radeleff
et al., 1955i/).
Data obtained from grazing studies (Mol et al., 1972) indicate that
sheep may be grazed, with no ill effects, on pastures following heavy
spraying with parathion. In this study pastures were sprayed with up to
6.0 Ib/acre (approximately seven to 27 times normal application rate).
Sheep were grazed on plots for 28-day periods beginning at 0 to 30 days
after spraying. In the most severe case (28 days grazing immediately
following spraying), sheep developed no symptoms of poisoning except
slight scouring, even when their blood cholinesterase was almost com-
pletely inactivated.
21
Cattle - Dahm et al (1950)— fed two groups of lactating cattle 1 ppm
and 5 ppm of parathion for 81 days. The parathion was given by capsule.
These levels provided 0.022 and 0.112 mg/kg/day, and they produced no
noticeable adverse effects. Two other cows were fed 5 ppm of parathion
the first week. The amount was increased each week until 40 ppm was
being consumed per week. The lowest and highest levels were equivalent
to 0.11 and 0.89 mg/kg/day. No adverse effects were observed.
The MSD and MTD for 1- to 2-week old calves have been conservatively
estimated to be 0.25 and 0.5 mg/kg, respectively, whereas the MSD for
year-old cattle is 4.0 mg/kg (Radeleff et al.. 1955). A more thorough
study carried out by Fankaskie et al. (1952)-' indicates that the above
estimates may be low. Cattle were fed a ration containing baled alfalfa
hay for a 61-day period. The average parathion concentration of all hay
fed over the 61-day period was 13.6 ppm. During this period no parathion
residues or degradation products could be detected in the urine, milk,
or jugular blood of the test animals. In an additional experiment a cow
\l Radeleff, R. D., G. T. Woodard, W. J. Nickerson, and R. C. Bushland,
"Part II. Organic Phosphorus Insecticides," The Acute Toxicity of
Chlorinated Hydrocarbon and Organic Phosphorus Insecticides to Live-
stock, U.S. Department of Agriculture, Tech. Bull. 1122, pp. 35-46 (1955),
2/ Dahm, P. A., F. C. Fountaine, J. C. Pankaskie, R. C. Smith, and F. W.
Atkeson, "The Effects of Feeding Parathion to Dairy Cows," J^
Dairy Sci.. 33(101):747-757 (1950).
J3/ Pankaskie, J. E., F. C. Fountaine, and P. A. Dahm, "The Degradation
and Detoxification of Parathion in Dairy Cows," J. Econ. Entomol.,
45:51-60 (1952).
70
-------
was fed par a th ion by direct oral administration of daily initial doses
of 1 mg/kg for 14 weeks. The dosage was increased weekly until the daily
dose reached 32 mg/kg of body weight. The authors stated that this level
was the highest intake by any survivors. During this time, no symptoms
of parathion poisoning appeared. To rule out development of tolerance
over the 14-week feeding period, another cow was fed 16 mg/kg/day for 1
week without adverse effects. As with the alfalfa feeding experiments,
no residues of parathion or £-nitrophenol were detected in urine,
jugular blood or milk. These experiments indicate that adult dairy
cattle are less susceptible to parathion poisoning than other ruminants.
Radeleff and Bush land (I960)— in a symposium on "The Nature and
Fate of Chemicals Applied to Soils, Plants and Animals" reiterated an
observation made earlier in some of their toxicological studies: with
toxic chemicals that were not of equal toxicity to adult and young animals
the dairy calf is the most susceptible of all farm animals (Radeleff and
Bushland, I960).
The minimum toxic dose of parathion (used as a dip or spray) for
1- to 2-week old calves was reported as 0.01% while that for sheep and
goats (adults) was 1.0%.
Additional evidence for the greater sensitivity of calves to para-
thion (compared to steers and sheep) was reported by Radeleff and Woodard
(1957)=/ and Radeleff (1958);!/ A lethal dose of parathion for calves
was reported to be 1.5 mg/kg while a lethal dose for steers and sheep
was 75 and 20 mg/kg, respectively. Twenty-five milligrams per kilograms
was reported to be nontoxic for steers, 10 mg/kg was nontoxic for sheep
but the nontoxic dose for calves was 0.25 mg/kg.
Symptomatology and Pathology Associated with Mammals - While the symptoms
may vary in intensity with dosage, mammals can be expected to exhibit
those symptoms typical of cholinergic poisoning. Among these symptoms
are muscle faciculation, excessive salivation, tremor, miosis, partial
paralysis, labored breathing, lachrymation, diarrhea, involuntary
I/ Radeleff, R. D., and R. C. Bushland, "The Toxicity of Pesticides for
Livestock," Symposium: The Nature and Fate of Chemicals Applied
to Soils, Plants, and Animals," Agricultural Research Service,
U.S. Department of Agriculture (27-29 April 1960).
2J Radeleff, R. D., and G. T. Woodard, "The Toxicity of Organic Phos-
phorus Insecticides to Livestock," J. Am. Vet. Med. Assoc., 130:
215-216 (1957).
3J Radeleff, R. D., "The Toxicity of Insecticides and Herbicides to
Livestock." Adv. Vet. Sci.. 4:265-276 (1958).
71
-------
urination, convulsion, depression and death (Hazelton and Holland, 1950;
Gaines, 1960; Konst and Plummer, 1950).
In acute poisonings autopsy findings usually reveal only gastroin-
testinal irritation and pulmonary hemorrhage.
In rats fed at relatively high dietary levels of parathion for long
periods of time, the symptoms reported are those of acute poisoning
(salivation, lachrymation, intestinal hyperperistalsis and muscular
tremors) occurring as recurrent episodes.
Pathologically, chronically poisoned animals show the same lesions
as those acutely poisoned--vacuolation and collapse of the acinar structure
of the submaxillary gland and pancreas along with atrophy of the thymus
and spleen (Barnes and Denz, 1951). These symptoms are most prominent
during the early exposure period and may diminish with continued feeding.
Physiological and Pharmacological Aspects of Parathion - The physiology,
pharmacology and toxicology of parathion poisoning have been described
by Hamblin and Golz (1955).—' These authors state that the only im-
portant pharmacological action of parathion is its inhibiting action on
the enzyme acetylcholinesterase.
Acetylcholine is needed for nerve impulse transmission, and this need
is met by the action of the enzyme choline acetylase. The hydrolysis of
acetylcholine to choline and acetic acid is accomplished by another enzyme,
acetylcholinesterase. There are two types of cholinesterases, true and
pseudocholinesterases. The former is found in nerve and muscle tissue
and in the erythrocytes. Pseudocholinesterase is actually a group of
enzymes which are found in the pancreas and salivary glands and other
tissues. The latter enzymes hydrolyze acetylcholine more slowly than
acetylcholinesterase.
The plasma cholinesterase in most species, including man, is pseudo-
cholinesterase. The concentration varies widely from individual to in-
dividual, and human erythrocytes contain true cholinesterase.
The absorption of parathion brings about the accumulation of acetyl-
choline, because of a failure in the disposal mechanism in parasympa-
thetic post-gang1ionic fibers, in sympathetic ganglia and in the central
nervous system as well as at the myoneural junction of muscle.
II Hamblin, D. 0., and H. H. Golz, "Parathion Poisoning, A Brief Re-
view," Ind. Med. Surg.. 24(22)-.65-72 (1955).
72
-------
Autopsy examination of animals succumbing to lethal dosages of para-
thion, in either single or multiple doses, has not revealed extensive
or wide-spread tissue damage that could be related to treatment with the
compound.
The only accumulative aspects of parathion are suggested by the
acetylcholine recovery period being contingent upon the death of the red
blood cell. Furthermore, the inhibition of the enzyme is not reversible.
Repeated doses of parathion will produce steadily decreasing levels of
enzyme activity in the blood.
In the diagnosis of parathion poisoning, the RBC cholinesterase
level is one of the more important clinical measurements. Plasma
cholinesterase is nonspecific and it has no functional relationship
with the activity of the nervous system. Exposure to anti CHE agents
is assumed when the plasma and RBC cholinesterase activity is depressed
by 25%. The excretion of p-nitrophend in the urine confirms this
assumption.
In acute poisoning, manifestations usually occur only after more
than 50% of the plasma cholinesterase is inhibited. After an acute
poisoning, it takes about 4 weeks for plasma cholinesterase to return
to normal.
Summary - Parathion is a highly toxic pesticide, as evidenced by studies
with laboratory and domestic animals, fish, other aquatic life, avian
species, wildlife and humans. The oral LD50 value for rats is about
7 rag/kg (range 2 to 30 mg/kg) for males and 4.0 rag/kg (range 2 to 6 rag/
kg) for females. The LC5Q value for inhalation toxicity has been re-
ported as 0.0315 mg/liter (4-hr exposure) to 0.115 mg/liter (1-hr ex-
posure). The LDso value for intraperitoneal injection ranges from 3.6
to 7.0 mg/kg. Dermal toxicity is much less pronounced than the other
toxicity measurements, ranging from 6.8 to 200 mg/kg; most of the re-
ported results were above 20 mg/kg.
No mortality occurred when rats were fed parathion for 15 to 16
weeks at 0.52 mg/kg/day or at 2.4 mg/kg/day. The mortality went up to
30% when the average daily dosage was increased to 15.4 mg/kg. Over a
1-year period the mortality was 42% for rats fed 50 ppm of parathion.
The mortality rose to 80% over a 19-day feeding period with a concen-
tration of parathion in the feed equal to 100 ppm.
Mice are not as susceptible to parathion poisoning as rats. The
average LDso for males was 19.8 mg/kg (range 7.0 to 30.3 mg/kg) and for
male-female groups, 12.7 mg/kg (range 6.0 to 25.0 mg/kg).
73
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The intraperitoneal and intravenous U^Q values for mice were not
as low as for rats* In general, the order of toxicity for mice was
about the same for the intraperitoneal and intravenous routes. Sub-
cutaneous injections yielded high LD5Q values (7.8 to 21.4 mg/kg).
No information was found on long-term feeding studies with mice.
Only one paper reported a dermal toxicity of 0.60 ml/kg (intact skin)
and 0.80 ml/kg (abraded skin).
The oral toxicity of parathion for guinea pigs was close to mice
(LD5Q range 9.3 mg/kg to 32.0 mg/kg). The LDr« value for intraperitoneal
injection was 12.0 mg/kg.
No information was found for the subacute and chronic oral toxicity
of parathion to guinea pigs.
The information on the toxicity of parathion in dogs was sparse.
One report on acute oral toxicity indicated that 3.0 to 5.0 mg/kg was
lethal. Two reports on the intraperitoneal LDc0 value were at variance—
12 to 20 mg/kg and 3 to 5 mg/kg.
The subcutaneous, intraperitoneal and intravenous LDcQ values are
15.0 mg/kg, 3.0 to 5.0 mg/kg and 3.0 to 5.0 mg/kg, respectively, for cats.
Another report indicated that the intraperitoneal U^Q for parathion in
cats was 12 to 20 mg/kg. No dermal toxicity data is available. No
information was found on subacute and chronic oral toxicity to cats.
One report was found for the LD50 (68 mg/kg) for oral ingestion by
rabbits. The acute dermal LD5Q appears to be about 0.07 mg/kg (abraded
skin).
There was one report on the toxicity of parathion to goats. No
LD50 values were reported. Daily doses of 8 mg/kg killed one animal
in 11 days.
The maximum safe oral dose for sheep has been determined to be 10
mg/kg and the minimum toxic dose as 20 mg/kg. One investigator reported
that the acute oral LDcn of parathion for lambs was estimated to be 45
to 50 mg/kg.
Parathion has been fed to cattle at 1 ppm and 5 ppm/day for 81 days
without any noticeable effect. One dairy cow has been fed 32 mg/kg/day
for 7 days without adverse effects. The same animal had been fed for a
number of weeks at lower gradually increasing levels.
74
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These collective data Indicate that parathion is highly toxic to
all species tested thus far by all routes. There is usually a lesser
degree of toxicity produced by dermal exposure than by other routes.
The vehicle is very important in dermal toxicity tests. Episodes of
acute toxicity are more likely to occur in nature than are chronic
poisonings. The pathology of chronic toxicity is similar to that
found in acute episodes. The young are more susceptible than
the mature organisms. There is a unique sex aspect in some species
(male rats are less susceptible than females, whereas in most other
species sex differences are not as great). The symptoms and mechan-
isms of physiological action in all species are essentially the same.
Cholinesterase depression is a sensitive clinical measurement and in
some instances too sensitive (chronic exposures). The pathological
damage appears to be minimal even in chronic exposures.
Metabolism of Parathion
The metabolism of parathion is discussed in the following seven
subsections: absorption, distribution, excretion, biotransformation,
degradation, tissue residues, and summary.
Absorption - Parathion is absorbed in animals by the oral, inhalation
or dermal routes. Nabb et al. (1966) 1' have shown that parathion
was absorbed through rabbit skin at the rate of 0.059 ug/min/cm2 based
on the inhibition of red cell acetylcholinesterase activity.
Fredriksson (1964) measured the rate of absorption of ^2p-paraoxon
through cat skin. When 50 ul of paraoxon was applied to 4.1 cm2 of
skin the absorption rate was found to be about 6 muM/min/cm . Blood
levels 3 hr later were 0.05 ug of paraoxon per milliliter. However,
approximately 90% of the paraoxon was detoxified during epidermal
passage due to a skin enxyme in cats that can split the paraoxon
molecule. In a previous study, Fredrikson (1961b) also reported the
rate of paraoxon absorption to be 0.47 to 0.95 muM/min/cm through
cat skin.
Parathion was 10 times less toxic than paraoxon when given
intravenously but was 55 times less toxic when applied to the skin
of rabbits (Nabb et al., 1966).
I/ Nabb, D. P., W. J. Stein, and W. J. Hayes, Jr., "Rate of Skin
Absorption of Parathion and Paraoxon," Arch. Environ. Health,
12:501-505 (1966).
2J Fredriksson, T., "Studies on the Percutaneous Absorption of Para-
thion and Paraoxon. Part III. Rate of Absorption of Parathion,V
Acta Derm. Venerol.. 41:353-363 (1961b).
75
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A comparative study of the acute dermal toxicity and primary irrita-
tion in rabbits and guinea pigs indicated that parathion was more toxic
to rabbits (Roudabush et al., 1965).
Distribution - The dermal and intravenous administration of
to rabbits showed very little accumulation of 35g in the blood, organs
or tissues (dermal 10 days after exposure; intravenous 1 hr after ex-
posure) (Jensen et al., 19521'). Feeding 167 mg of parathion in baled
hay to cows did not produce detectable levels of parathion or £-nitro-
phenol in milk or blood (Pankaskie et al., 1952). In the same study cows
were fed 1 to 32 mg/kg/day of parathion by capsule, and did not produce
detectable levels of parathion, £-nitrophenol °* £-aminophenol in the
milk or blood. Giachetti et al. (1966).?-/ measured the amount of paraoxon
in rat brain after treatment with 1 mg/kg of parathion by intraperitoneal
injection. At 6 hr after treatment there was 30 to 33 ng of paraoxon,
2 to 3 ng after 18 hr and only a trace at the end of 72 hr. Taylor and
Gaut (1968).3-' have written a review describing the distribution and bind-
ing of parathion and paraoxon at the enzyme level in many tissues.
Excretion - Cows fed parathion excreted aminoparathion, diethylphosphoric
acid, and phosphorothioic acid in the urine and about 17. of the dose in
the milk (Ahmed et al., 19584-/) . Cows probably also hydrolyze parathion
to £-aminophenol and excrete £-aminophenol glucuronide (Pankaskie et al.,
1952; Ahmed et al., 1958). Andersen and Karlog (1963)!/ found from in
vitro experiments with fluid that 75 to 907. of the parathion is reduced
to aminoparathion or intermediates after 10 min; conjugated £-aminophenol
was the dominant metabolite found in the urine. Cook (1957)j>/ had re-
ported earlier that the reduction of parathion to £- aminoparathion was
almost complete in 1 hr.
\J Jensen, J. A., W. F. Durham, and G. W. Pearce, "Studies on Fate of
Parathion in Rabbits, Using Radioactive Isotope Techniques," AMA
Arch. Ind. Hyg. Occup. Med.. 6:326-331 (1952).
2/ Giachetti, A., C. Grasso, and G. Bernardi, "Persistence of 0,0-Diethyl-
0-para-nitrophenyl phosphate (Paraoxon) in the Brain of the White
Rat Treated with a Single, Subtoxic Dose of Parathion," Ric. Sci.,
36(10):1077 (1966).
3/ Taylor, W. J., and Z. N. Gaut, "Poisoning with the Newer Organophos-
phorus Insecticides," Int. J. Clin. Pharmacol.. 1(3):175-183 (1968).
4/ Ahmed, M. K., J. E. Casida, and R. E. Nichols, "Bovine Metabolism of
Organophosphorus Insecticides: Significance of Rumen Fluid with
Particular Reference to Parathion," J. Agr. Food Chem.. 6:740-746
(1958).
J>/ Andersen, A. A., and 0. Karlog, "Elimination of Parathion in Cows
After Oral and Dermal Administration," Acta Vet. Scand.. 4:156-169
(1963).
6/ Cook, J. W., "In vitro Destruction of Home Organophosphates Pesticides
"~ by Bovine Rumen Fluid," J. Agr. Food Chem.. 5(11):859-863 (1957).
76
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Rats treated with 35S-parathion excreted 35S-sulfate in the urine
(Nakatsugawa et al., 1969I/). Paranitrophenol has been shown to be ex-
creted in the urine of monkeys (Lieben et al., 1952-^), and man (Wolfe
et al., 1970;!/ Roan et al., 1969^7) following exposure to parathion.
Biotransformatton - The biotransformation of parathion involves two dis-
tinct phenomena, activation and deactivation (detoxification).
Gage (1953)^ found paraoxon in a liver extract of parathion-treated
rats. Aldridge (1953)6-/ found that the serum cholinesterase enzymes of
rabbit, rat and horse have different substrate specificities and demon-
strated an enzyme which hydrolyzed parathion. Ecobichon et al. (1963)2.'
reported that human liver esterases were inhibited by compounds, includ-
ing parathion, which require activation. Gaines et al. (1966)£' found
that rats infused with 1.41 mg/kg of parathion via the intestinal vein
died. However, if 1.69 mg/kg of parathion was infused via the femoral
vein, none died within 65 min. Thus, it seemed that passage through
the liver increased parathion toxicity. Shishido and Fukami (1963)9/
I/ Nakatsugawa, T., N. M. Tolaman, and P. A. Dahm, "Degradation of Para-
" thion in the Rat," Biochem. Pharmacol.. 18(5):1103-1114 (1969).
2J Lieben, J., R. K. Waldman, and L. Krause, "Urinary Excretion of Para-
nitrophenol Following Parathion Exposure," AMA Arch. Ind. Hyg.
Occup. Med.. 6:491-495 (1952).
$/ Wolfe, H. R., W. F. Durham, and J. F. Armstrong, "Urinary Excretion
"~ on Insecticide Metabolites," Arch. Environ. Health. 21:711-716 (1970).
4/ Roan, C. C., D. P. Morgan, N. Cook, and E. H. Paschal, "Blood Cho lines-
terases, Serum Parathion Concentrates and Urine jj-Nitrophenol Con-
centrations in Exposed Individuals," Bull. Environ. Contarn. Toxicol.,
4(6):362-369 (1969).
5/ Gage, J. C., "A Cholinesterase Inhibitor Derived from 0,0-Diethyl
~ 0-£-Nitrophenyl Thiophosphate in vivo," Biochem. J.. 54:426-430 (1953),
6_/ Aldridge, W. N., "Serum Esterases, 2. An Enzyme Hydrolysing Diethyl
E-Nitrophenyl Phosphate (E600) and Its Identity With the A-Esterase
of Mammalian Sera," Biochem. J.. 53:117-124 (1953).
7/ Ecobichon, D. J., and W. Kalow, "Action of Organophosphorus Compounds
~~ Upon Esterases of Human Liver," Can. J. Biochem. Physiol.. 41:1537-
1546 (1963).
8/ Gaines, T. B., W. J. Hayes, Jr., and R. E. Linder, "Liver Metabolism
of Anticholinesterase Compounds in Live Rats: Relation to Toxicity,"
Nature, .209(5018):88-89 (1966).
9/ Shishido, T., and J. Fukami, "Studies on the Selective Toxicities of
~ Organic Phosphorus Insecticides (II) ," Botyu-Kagaku. 28(1) : 69-76
(February 1963).
77
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reported that liver and kidney slices converted parathion to paraoxon.
They also reported that the microsomal fraction and the microsomal super-
natant solutions were active in this conversion. Both fractions required
diphosphopyridine nucleotide (NAD) as a cofactor for this conversion.
Nakatsugawa and Dahm (1967)—' used ^S-parathion to demonstrate that
S was bound to liver microsomes (probably by a desulfuration reaction).
Activation by microsomes required NADPH2 and Q£. The reaction was in-
hibited by SKF-525A and other synergists.
2 /
Nevkovic et al. (1973)-' demonstrated that both NADH2- and NADPH2-
linked electron transport components were involved in the oxidative
metabolism of parathion and that the activity of NADH2- cytochrome c
reductase was significantly higher than NADPH2 - cytochrome c reductase.
o /
Orzel and Weiss (1966)—' used rat brain acetylcholinesterase in-
hibition as a measure of the conversion of parathion to paraoxon. Enzyme
inhibition was decreased by oral administration of y-aminobutyric acid,
but not by intrathecal administration. Inhibition of enzyme activity
was increased by pretreatment with chloroform and isonicotinic hydrazide,
a monoamine oxidase inhibitor. Pretreatment with SKF-525A (a microsome
inhibitor), arsenite (an oxidative enzyme inhibitor) or pyrogallol (a
transferase inhibitor) did not alter the enzyme inhibition. Hitchcock
and Murphy (1967a)-' studied parathion metabolism in liver and kidney
homogenates from rats and chickens. Kidney homogenates were half as
active as liver homogenates based on the conversion of parathion to para-
oxon. Liver required NADP and glucose-6-phosphate for maximal activity.
In 1969, Nakatsugawa et al. (1969) confirmed the initial in vivo
conversion of parathion to paraoxon in male rats using "s and
"I/ Nakatsugawa, T., and P. A. Dahm, "Microsomal Metabolism of Parathion,"
Biochetn. Pharmacol.. 16(l):25-38 (1967).
2/ Nevkovic, N., S. Vitorovic, and M. Plesnicar, "The Role of Liver
Microsomal Enzymes in the Metabolism of Parathion," Biochem.
Pharmacol., 22:2943-2946 (1973).
3/ Orzel, R. A., and L. R. Weiss, "The Effect of Various Chemicals on
Rat Brain Cholinesterase Inhibition by Parathion," Arch. Int.
Pharmacodyn. Ther.. 164(1):150-157 (1966).
^/ Hitchcock, M., and S. D. Murphy, "Activation of Parathion and Guthion
by Tissues of Mammalian, Avian, and Piscine Species," Fed. Proc.,
26(2):427 (1967a).
78
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Davison (1955)— found that the in vitro conversion of parathion was in-
hibited 527. by 10'3 M SKF-525A; 100% by iodoacetate, chloropicrin and
2,4-dinitrophenol; 90% inhibited by HgCl2, hydroxylamine and choline;
66% inhibited by £-chloromercuribenzoate and not inhibited by cyanide.
He also found that NAD and magnesium ions were required cofactors. Cyto-
chrome c was not necessary for metabolism.
o/
Fukuto and Metcalf (1969)— reviewed eight general reactions of the
mixed function oxidate system, including the desulfuration of the phos-
phorothionates. One of the reactions is primarily associated with the
conversion of parathion to paraoxon:
Mixed Function
Oxidase
+ - > (RO)3P=S - » (RO)3P=0
NADPHo „ ,_ , .
* (desulfuration)
Degradation of Parathion (and Paraoxon) - In 1958 Ahmed et al. demon-
strated that rumen fluid from cows converted parathion to aminopara-
thion, and suggested that it was excreted as a glucuronide conjugate.
Later, Williams (1970)—' measured (3-glucuronidase in rats after daily
doses of 0.25, 0.5 and 1.0 mg/kg parathion for 4, 10 or 15 days. In
females the serum p-glucuronidase was elevated in all cases. In males
the p-glucuronidase was elevated only after 15 days of treatment. There
was a decrease in serum 0-glucuronidase in both sexes which was not dose-
related .
I/ Davison, A. N., "The Conversion of Schradan (OMPA) and Parathion
into Inhibitors of Cholinesterase by Mammalian Liver," Biochem.
J,.., 61:203-209 (1955).
2_/ Fukuto, T. R., and R. L. Metcalf, "Metabolism of Insecticides in
Plants and Animals," Ann. N.Y. Acad. Sci.. 160:97-113 (1969).
3_/ Williams, C. H., "g-Glucuronidase Activity in the Serum and Liver
of Rats Treated with Parathion," Toxicol. Appl. Pharmacol., 16:533-
539 (1970).
79
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Matsumura and Ward (1966)—' found that human liver degraded para-
thion slightly faster than rat liver. Hitchcock and Murphy (1967b)£/
measured nitroreductase activity using parathion and paraoxon as sub-
strates. When NADPH and FAD were used as cofactors, the mitochondria,
microsomes and soluble fraction of rat liver contained 34, 38, and 28%
of the nitroreductase activity.
In 1967 Neal (1967a)- used 32p-labeled parathion to identify metab-
olites in the tissues of male and female rats, male mice and male guinea
pigs. The metabolites found were paraoxon, diethyl hydrogen phosphate,
diethyl hydrogen phosphorothionate and _p-nitrophenol. Oxygen and NADPH
were required for maximal activity. Phenobarbital or 3,4-benzopyrene
pretreatment increased the activity by 65 to 130%. The reaction was in-
hibited by nitrogen and pure oxygen atmospheres as well as carbon monoxide.
Continuing these studies, Neal (1967b)-' concluded that (in vitro)
inhibition of parathion metabolism indicated that the mixed function oxidase
system was a degradative pathway. Inhibition with p-chloromercuribenzoate,
cupric ion and 8-hydroxyquinoline was more effective against the con-
version of parathion to paraoxon than against its conversion to diethyl
hydrogen phosphorothionate. Conversion of parathion to diethyl hydrogen
phosphorothionate was stimulated by EDTA, barium and calcium ions. The
electron acceptors, flavin adenine dinucleotide (FAD), riboflavine,
menadione and methylene blue exhibited a concentration-dependent inhibi-
tion of the conversion of parathion to paraoxon or diethyl hydrogen phos-
phorothionate. However, the inhibition constants were different.
A summary of these reactions is indicated by the following scheme:
I/ Matsumura, F., and C. T. Ward, "Degradation of Insecticides by the
Human and the Rat Liver," Arch. Environ. Health. 13:257-261 (1966).
2/ Hitchcock, M., and S. D. Murphy, "Enzymatic Reduction of 0,0-(4-
Nitrophenyl) Phosphorothioate, 0,0-Diethyl 0-(4-Nitrophenyl) Phos-
phate, and 0-Ethyl 0-(4-Nitrophenyl).Benzene Thiophosphonate by
Tissues from Mammals, Birds, and Fishes," Biochem. Pharmaco1.t
16(9):1801-1811 (1967b).
3/ Neal, R. A., "Studies of the Enzymic Mechanism of the Metabolism of
Diethyl 4-Nitrophenyl Phosphorothionate (Parathion) by Rat Liver
Microsomes," Biochem. J.. 105:289-297.(1967a).
4/ Neal, R. A., "Studies on the Metabolism of Diethyl 4-Nitrbphenyl
Phosphorothionate (Parathion) in vitro," Biochem. J., 103:183-
191 (1967b).
80
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Parathion > Three minor metabolites
Paraoxon ^Diethyl hydrogen phosphorothlonate + £-nitrophenol
l
Diethyl hydrogen phosphate + £-nitrophenol
NADPH > Flavoprotein >-Nonheme iron protein ^Cytochrome P-450
I 1
Menadione 02
Differences in inhibition constants and inhibitions suggest that dif-
ferent enzymes or different enzymes systems may be involved in the
complete metabolism of parathion.
Studies by Nakatsugawa and Dahm (1967) showed that microsomes split
the aryl phosphate bond, and that NADPH2 and 02 are required for the
reaction. Further studies by Nakatsugawa et al. (1969) confirmed that
aryl phosphate cleavage was mostly by liver microsomal oxidases, in vivo,
using 32p_ and 35g-labeled parathion. A minor portion was also catalyzed
by nonoxidative soluble enzymes requiring reduced glutathione. They
suggested the following metabolic pathway.
Parathion - ^Diethyl phosphorothioic acid
1
Paraoxon
Desethyl paraoxon Diethyl phosphoric acid
\ *
Ethyl phosphoric acid
I
Phosphoric acid
In a review of parathion metabolism, Dahm (1970)— suggested that
paraoxon was not degraded by the same pathway as parathion. Paraoxon
was metabolized by microsomes which required NADPH2, nicotinamide,
magnesium ion and potassium chloride for maximal activities.
\] Dahm, P. A., "Some Aspects of the Metabolism of Parathion and Diazinon,"
in Biochemical Toxicology of Insecticides. P. D. O'Brien and
I. Yamamoto (Eds.), New York, Academic Press (1970).
81
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Jacobs en et al. (1973) found that the parathion W$Q in rats did
not change after partial hepatectomy and suggested that parathion tox-
icity is not due to the hepatic conversion of parathion to paraoxon. An
alternate explanation for the results is that the remaining liver was
sufficient to effect the conversion of parathion to paraoxon.
Bass et al. (1972)— reported that pretreatment of mice with DDT or
DDE protected against parathion toxicity but not that of paraoxon. In
vitro. the microsomes from mice given DDT or DDE converted more =S to =0
than those from the controls. Detoxification of paraoxon was not altered
by DDT or DDE. The increased rate of conversion of parathion to diethyl-
phosphorothioic acid could explain the decreased parathion toxicity after
DDT or DDE.
Alary and Brodeur (1970) found a close relationship between the W$Q
of parathion and paraoxon in male and female rats and the in vitro liver
oxidative and hydrolytic metabolism. Gagne and Brodeur (1972)1/ used
equitoxic doses of 32P-parathion in weanling and adult rats, and found
that parathion was more toxic to weanlings mainly because of a lower
liver enzyme activity. Brain tissue of weanlings seemed more susceptible
than that of adults but not because of an increased facilitation of para-
thion or paraoxon across the blood-brain barrier.
3/
Lichtenstein et al. (1973)- reported that soluble liver fractions
(from 105,000 and 500,000 x g) degraded parathion (207.) and paraoxon (657.)
to water-soluble metabolites which were nontoxic to insects.
Sakai and Matsumura (1971)—' identified 14 esterase bands from human
brain by thin-layer gel electrophoresis. Four of these were B-type
I/ Bass, S. W., A. J. Triolo, and J. M. Coon, "Effect of DDT on the
Toxicity and Metabolism of Parathion in Mice," Toxicol. Appl.
Pharmacol.. 22:684-693 (1972).
2/ Gagne, J., and J. Brodeur, "Metabolic Studies on the Mechanisms of
Increased Susceptibility of Weanling Rats to Parathion," Can. J.
Physiol. Pharmacol., 50:902-915 (1972).
31 Lichtenstein, E. P., T. W. Fuhremann, A. A. Hochberg, R. N. Zahlten,
and F. W. Stratman, "Metabolism of [14C] Parathion and [^C] Para-
oxon with Fractions and Subfractions of Rat Liver Cells," J. Agr.
Food Chem., 21(3):416-423 (1973).
4/ Sakai, K., and jr. Matsumura, "Degradation of Certain Organophos-
phate and Carbamate Insecticides by Human Brain Esterases,"
Toxicol. Appl. Pharmacol.. 19(4):660-666 (1971).
82
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esterases which degrade aIkoxyphosphate sites, and six were A-type
esterases which hydrolyze carboxyester sites.
Norman et al. (1973a)— reported that phenobarbital pretreatment in
rats decreased the apparent activation energy of the mixed-function oxi-
dase reactions. These results were not entirely due to an increase in
cytochrome P-450.
2/
Neal (1972)- measured the 1^ for paraoxon and diethyl phosphoro-
thioic acid in rabbit lung and liver and found lung to be much lower in
activity. The V^ax. ^or *-un8 microsomes was 20% of microsomes from liver.
The mixed function oxidase from liver was induced by both phenobarbital
and 3-methylcholanthrene, whereas only phenobarbital induced the lung mixed-
function oxidase. In these studies, lung was about 3% as active as liver.
3/
Norman et al. (1973b)— found that 3-methylcholanthrene and pheno-
barbital increased the metabolism rate of parathion by rough-surfaced,
but not by smooth-surfaced microsomes, based on microsomal protein con-
tent. Phenobarbital and 3-methylcholanthrene increased the cytochrome
P-450 content; there was no difference in the metabolic rate between
the rough and smooth microsomes of untreated, and 3-methylcholanthrene-
or phenobarbital-treated animals. However, based on the cytochrome P-450
in the entire microsome fraction, the metabolic rate was less in the 3-
methylcholanthrene- and phenobarbital-treated rats than the controls.
Cytochrome P-450 is the terminal enzyme of the mixed-function oxidase sys-
tem. The iron in the heme moiety exists in both the hi- and low-spin
state. There was no correlation between the spin state and the rate of
parathion metabolism.
47
Villeneuve et al. (1970)- reported that SKF-525A had no effect on
parathion toxicity in rats while DDT, benzpyrene and phenobarbital
\l Norman, B. J., J. A. Roth, and R. A. Neal, "Effect of Temperature on
the Mixed Function Oxidase-Catalyzed Metabolism of 0,0-Diethyl j>-
Nitrophenyl Phosphorothionate (Parathion)," Toxicol. Appl. Pharmacol.,
26:203-208 (1973a).
2/ Neal, R. A., "A Comparison of the in vitro Metabolism of Parathion in
the Lung and Liver of the Rabbit," Toxicol. Appl. Pharmacol., 23:
123-130 (1972).
3_/ Norman, B. J., W. K. Vaughn, and R. A. Neal, "Studies of the Mechanisms
of Metabolism of Diethyl £-Nitrophenyl Phosphorothionate (Parathion)
by Rabbit Liver Microsomes," Biochem. Pharmacol.. 22:1091-1101
(1973b).
4/ Villeneuve, D. C., W. E. J. Phillips, and J. Syrotiuk, "Modification
of Microsomal Enzyme Activity and Parathion Toxicity in Rats,"
Bull. Environ. Contain. Toxicol., 5(2): 125-132 (1970).
83
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decreased the toxicity by a factor of 3. Fhenobarbital and DDT de-
creased hexabarbital sleeping time, but benzpyrene and SKF-525A increased
the sleeping time.
Hollingworth et al. (1973)-' reported that glutathione-S-aryl trans-
ferase, a soluble enzyme, converted parathion to S-£-nitrophenylgluta-
thione and diethylphosphorothioic acid. This enzyme can be differentiated
from the glutathione-S-alkyl transferase that is also present in rat tis-
sues .
2/
Baeza et al. (1972)- injected rats with 10 mg/kg of parathion to
produce a 50% inhibition of red cell acetylcholinesterase. This could
be prevented by exposing the animals to 1,000 ppm of CO for 90 min prior
to treatment. When 1.06 mg/kg of paraoxon was injected intraperitoneally
no symptoms or mortalities were observed in rats. When the dose was in-
creased to 1.42 mg/kg, symptoms were observed but there were no deaths.
However, if 1,000 ppm of CO were given prior to 1.06 mg/kg of paraoxon,
80% of the animals exhibited symptoms and 40% died. If 2,500 ppm CO were
given prior to administration of 1.42 mg/kg paraoxon, 70% of the animals
died.
Parathion pretreatment decreased the normal metabolism of testo-
sterone by rat liver microsomes (Stevens, 19731/). All polar and non-
polar metabolites were decreased except for a 307. increase in one dione.
Weiss et al. (1964)£/ reported that parathion did not alter the blood
sugar levels in rabbits, dogs, or rats.
Taylor and Gaut (1968) reported that phenothiazines potentiated the
toxicity of parathion.
_!/ Hollingworth, R. M., R. L. Alstott, and R. D. Litzenberg, "Gluta-
thion S-Aryl Transferase in the Metabolism of Parathion and Its
Analogs," Life Sci.. 13:191-199 (1973).
2/ Baeza, C., A. M. Goldberg, and R. J. Rubin, "Effect of Carbon
Monoxide on Response to Parathion and Paraoxon," Toxicol. Appl.
Pharmacol., £2(2):288 (1972).
3/ Stevens, J. T., "The Effect of Parathion on the Metabolism of %-
Testosterone by Hepatic Microsomal Enzymes from the Male Mouse,"
Pharmacology. 10(4):220-225 (1973).
4/ Weiss, L. R., J. Bryant, and 0. G. Fitzhugh, "Blood Sugar Levels
Following Acute Poisoning with Parathion and 1-Naphthyl N-Methyl
Carbamate (Sevin) in Three Species," Toxicol. Appl. Pharmacol.,
6(3):363 (1964).
84
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Tissue Residues - Jensen et al. (1952) found that intravenous 35S-para-
thion did not accumulate in the blood, organs or tissues of rabbits.
Fankaskie et al. (1952) found no accumulation of parathion or free p-
aminophenol in the blood, milk or urine of cows fed 1 to 32 mg/kg/per day
parathion. Roan et al. (1969) measured parathion levels in the serum of
aerial applicator pilots. Some pilots had high serum parathion levels
and low cholinesterase activity but were asymptomatic. Giachetti et al.
(1966) gave rats 1 mg/kg of parathion IP and measured brain levels of
paraoxon. At 6 hr after injection, the brain contained 30 to 33 ng of
paraoxon. Only traces remained after 72 hr.
Summary - The following major points can be stated regarding the metabo-
lism of parathion:
1. Parathion is readily absorbed through the skin, from the stomach
and the lung.
2. Parathion is widely distributed throughout the body but does not ac-
cumulate at any site and causes no effect other than the irrevers-
ible binding of paraoxon to cholinesterase.
3. The major metabolites of parathion that are excreted are aminopara-
thion, jj-nitrophenol, diethylphosphorothioic acid, ethylphos-
phoric acid and sulfate.
4. Metabolism of parathion is in two general steps: activation
and detoxification.
5. Parathion is enzymatically hydrolyzed to paraoxon by the mixed-
function oxidase system.
6. Oxidation of parathion and/or paraoxon is inhibited by carbon
monbxide and SKF-525A.
7. Phenobarbital, 3-methylcholanthrene and benzpyrene stimulate
parathion metabolism.
8. Microsomal oxidation of parathion requires NADPHj, oxygen,
potassium chloride and magnesium ion for maximum activity.
Effects on Reproduction
The effects of parathion on reproduction are reviewed in the fol-
lowing two subsections on domestic animals and wild avian species.
85
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Domestic Animals - Some years ago, a study was made on the effect of
parathion on reproduction and milk production in goats by Wilber and
Morrison (1955). .As a test material, they utilized parathion liquid
with a purity of 98.76% or as a 257. wettable powder. They administered
oral daily doses of 16 mg/kg (25% wettable powder) for 16 days. The total
dosage given to one goat was 8,960 mg. After death the goat was found
to be carrying two fetuses which would have been born in approximately
10 days. The authors pointed out that parathion did not induce an abor-
tion in the goat. When another goat was killed near the terminal point
of chronic poisoning, she was found to be carrying two 3-month-old fetuses.
Superficially, the fetuses appeared normal in all respects. They found
that the RBC cholinesterase activity (ApH) of heart blood of the fetuses
was 0.14 and 0.17 respectively. The control value for the mother was
about 1.05. However, her value dropped to 0% of normal before necropsy.
In order to ascertain whether some anticholinesterase material crossed
the placenta and exerted an effect on the fetus, fetuses were taken from
unpoisoned goats carrying fetuses of different ages. The RBC cholinesterase
value of the nonpoisoned fetuses ran from 1.33 to 1.74. Compared with the
above data, the blood of fetuses from lactating goats poisoned with para-
thion was depressed by about 85%. They investigated the milk production
of three goats that received total doses ranging from 900 to 1,060 mg
intramuscularly. The dosage for the goats on the milk test was 10 daily
injections at a dose of 0.5 mg/kg followed by five daily injections at
1 mg/kg. These were then followed by five more daily injections at a
dose of 2 mg/kg. They found no significant increase or decrease in milk
production as compared with control periods that could be ascribed to the
parathion treatment. The production of milk by all goats decreased
sharply after initiating the final dosage, which was aimed at killing the
animals in a short time.
In reference to reproductive studies, Beck (1953)— investigated the
effect of certain insecticides on the motility and metabolism of mam-
malian spermatozoa using boar semen. From oxygen-consumption experi-
ments, the data indicated that DDT, aldrin, and malathion had a minor
inhibitory effect on respiration of boar spermatozoa, whereas parathion,
BHC, and TEPP had an intermediate effect. The insecticides had a pro-
nounced effect on the motility of the spermatozoa. The motility was
practically gone 120min after parathion treatment. Furthermore, para-
thion had only a weak inhibitory effect on glycosis of spermatozoa.
Wild Avian Species - There is a large volume of literature on the effect
of chlorinated hydrocarbons upon avian species. This interest has been
I/ Beck, S. D., "Effect of Insecticides on the Metabolism and Motility
of Mammalian Spermatozoa," J. Econ. Entomol.. 46:570-574 (1953).
86
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largely due to the propensity for chlorinated hydrocarbons to accumulate
in fatty tissue. The organic phosphorus insecticides degrade rapidly
and have fewer latent effects than the more residual chlorinated hydro-
carbons. Barnett (1950)-' fed parathion to pheasants at levels of 100
and 1,000 ppm, and he noticed a decreased gonadal activity, and there
was also a loss in total body weight. Shellenberger et al. (1966)-'
noted a similar weight loss in Japanese quail that were fed 5 ppm of
Azodrin R. Muller and Lockman (1972)2/ fed subtoxic doses of dieldrin and
parathion to yearling mallards to observe the effect on egg production,
fertility, hatchability, shell thickness, and progeny growth. Their test
groups were fed 10 ppm of parathion in the diet. The treatment was started
30 days prior to egg production and continued for 90 days thereafter.
Parathion failed to exert significant effects upon egg production, fertil-
ity, or progeny growth. Hatchability was depressed for those animals
receiving dieldrin, but parathion had no effect. The only measurable
effect of parathion was a significant reduction in mean shell thickness.
The thinner shells do not restrict successful embryonic development.
Neill et al. (1971)*' conducted a similar study using the gray partridge
as a test bird. These birds received 8 ppm of parathion. Here, again,
parathion did not have an effect upon egg production, fertility, and
hatchability. Eggs from the dieldrin treatment had a high percentage of
dead-in-the-shell embryos which could be attributed to the residue of
dieldrin that was found in the eggs. No parathion residues were detected
in the eggs. The only effect noted from parathion in these studies was
a high percentage of early and late dead embryos; the investigators
hypothesized that undentified parathion degradation products may have been
present in the eggs, resulting in an adverse effect on the metabolism, and
thereby accounting for a high percentage of dead-in-the-shell embryos.
It Barnett, D. C., "The Effect of Some Insecticide Sprays on Wildlife,"
Proc. 30th Ann. Conf. West. Assoc. State Game and Fish Commissioners.
pp. 125-134 (1950).
27 Shellenberger, T. E., 6. W. Newell, R. F. Adams, and J. Barbaccia,
"Cholinesterase Inhibition and Toxicologic Evaluation of Two
Organophosphate Pesticides in Japanese Quail," Toxicol. Appl.
Pharmacol.. 8:22-28 (1966).
3/ Muller, H. D., and D. C. Lockman, "Fecundity and Progeny Growth
Following Subacute Insecticide Ingestion by the Mallard," Poul.
Sci.. 51:239-241 (1972).
4/ Neill, D. D., H. D. Muller, and J. V. Shutze, "Pesticide Effects on
the Fecundity of the Gray Partridge," Bull. Environ. Con tarn.
Toxicol., 6(6)-.546-551 (1971).
87
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Furthermore, there was no alteration by either of the insecticides in
the growth rate.
Teratogenic Effects
Mammals - It has been reported by Kimbrough and Gaines (1968)— that
parathion can produce teratogenic effects in Sherman rats. The dosages
were 3.0 and 3.5 mg/kg given intraperitoneally on the llth day of pregnancy.
The fetuses were removed on the 20th day of pregnancy. The results are
shown in Table 14.
The average weight gain of the dams was drastically reduced; the
number of fetuses was reduced by half. The number of resorptions was
high and the weight of the fetuses from parathion-treated mothers was
30% less than the controls.
Fish (1966)2./ investigated the teratogenic potential of parathion
and methyl parathion in rats. Dosage levels were chosen which represented
about one-sixth, one-fourth, one-half, and three-fourths of the estab-
lished oral or intraperitoneal LDsQ. The doses were given intraperitoneally
in a vehicle of ethanol (20%) and propylene glycol (80%). The injections
were made on day 8, 9, 15, or 16 of gestation. In the search for anomalies,
particular attention was directed to the external appearance of the embryo.
Particular attention was given to the appearance of the brain, cervical
and thoracic cord, heart and liver. Fish found no significant differences
between control and treated animals for fetal mortality, fetal weight, or
gross anomalies. Brain cholinesterase was reduced in the embryo brain.
He did observe some large subcutaneous hematomas in the offspring of para-
thion-treated groups. The weight of the offspring from the parathion-
treated animals was uniformly less than that of the offspring of the con-
trols over the first 40 days of life. There was also a significant in-
crease in stillbirths and neonatal deaths for the animals that were ex-
posed to parathion. There has been a comment made in the Mrak Report
(1969)2/ that Fish's (1966) data were like those observed with organo-
chlorines. That is, the action of these two classes of insecticides
suggest that they do not produce specific teratogenic effects.
j./ Kimbrough, R. D., and T. B. Gaines, "Effect of Organic Phosphorus
Compounds and Alkylating Agents on the Rat Fetus," Arch. Environ.
Health, 16:805-808 (1968).
27 Fish, S. A., "Organophosphorus Cholinesterase Inhibitors and Fetal
Development," Am. J. Obstet. Gynecol.. 96(8):1148-1154 (1966).
V Mrak, E. M., "Report on the Secretary's Commission on Pesticides
and Their Relationship to Environmental Health," U.S. Dept. HEW,
p. 665 (1969).
88
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00
Table 14. THE TOXIC AND TERATOGENIC EFFECT OF PARATHION GIVEN
INTRAFERITONEALLY TO RATS ON THE 11TH DAY OF PREGNANCY*
Compound
Control
Farathion
Control
Parathion
Dose
(mg/kg)
„
3.5
3.0
Lowest dose
to kill
nonp regnant
rat
(urn/kg)
..
4
--
/
NoX
pregnant
rats
4
5
5
5
Average
weight
gain
of dams
(g)
67.78
42.27
75.24,.
41.79*'
Average
no.
fetuses
per litter
10.8
5.6
12.6
7.6
Average
no . dead
fetuses
per litter
0
0.2
0
0
Average
no.
resorptions
per no.
pregnant rats
0.5
7.0
0.8
3.8
c/
Average— Average
weight
of
fetuses
(R)
3'57b/
2.46-
3.34
2.86b-/
weight
of
placentas
(g)
0.69
0.53
0.54
0.44-'
No. and
type
of malformations
per total
None
no. fetuses
1/28 fetus edetnatous
None
None
* Data from Kimbrough and Gaines, op. cit. (1968).
a/ In some pregnant rats all fetuses were resorbed, thus reducing the total numbers
of litters.
b/ Significantly different from controls, p < 0.05.
c/ Weight of dead fetuses was included.
-------
Existing data on the transfer of parathion through the placenta
to the fetus are limited. Fischer and Plunger (1965)!/ did not find any
traces of parathion in a human fetus from a mother who had taken a fatal
dose of parathion. A study using pregnant guinea pigs also failed to
demonstrate that parathion crosses the placenta. It has been shown by
Fish (1966) that either methyl parathion or parathion given to pregnant
rats inhibits brain cholinesterase activity in the embryos. Methyl para-
oxon has been detected in the brain, liver, and muscle of the embryo
(Ackermann and Engst, 1970?./). Villeneuve et al. (1972)!/ used 1*C-
parathion in a study of placental transfer in sheep. ^C-parathion was
administered to the dam over a 5- to 15-sec time interval using a jugular
cannula. The dosage level was 0.1 rag/kg of body weight. Blood samples
were drawn from the fetus, and the mother and amniotic fluid was col-
lected at 5-min intervals initially and at longer periods of time there-
after for 48 hr. Plasma cholinesterase activity in the dam was maximally
depressed within 30 min (52%). At 48 hr the plasma cholinesterase was
still depressed by 307«. In the fetus, maximum depression occurred at 40
min and then plateaued at 20%, 4 hr after administration. After 48 hr
the activity was depressed in the fetus 9.2%. Only a small portion (2 to
57o) of the radioactivity in the fetal plasma was in the form of parathion.
The remainder of the radioactivity was in the form of unidentified metab-
olites. All the radioactivity from the parathion in the amniotic fluid
was in the form of an unidentified metabolite. The results reported in
this paper agree with other information on the metabolism of parathion
in ruminant animals where the pathways are quite different from those of
rodents or humans. It has been shown by O'Brien (1960)^' that, in the
cow, parathion is degraded to j>-aminophenol and then conjugated to form
a glucuronide. In humans and rodents, the major pathway involves the
formation of paraoxon followed by hydrolysis to £-nitrophenol, or the
direct hydrolysis of parathion to j>-nitrophenol which is then glucu-
ronidated and excreted in the urine.
_!/ Fischer, R., and C. Plunger, "Detection and Quantitative Determinq-
tion of Phosphorus Insecticides in Biological Material," Mitt Arch.
Toxicol.. 21:101-105 (1965).
2/ Ackermann, H., and R. Engst, "Presence of Organophosphate Insecticides
in the Fetus," Arch. Toxikol.. 26:17-22 (1970).
3/ Villeneuve, D. C., R. F. Willes, J. B. Lacroix, and W. E. J. Phillips,
"Placental Transfer of l^C-Parathion Administered Intravenously to
Sheep," Toxicol. Appl. Pharmacol.. 21:542-548 (1972).
kj O'Brien, R. D., Toxic Phosphorus Esters, New York: Academic Press,
pp. 227-228 (1960).
90
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Avian Embryo toxic Ity - There have been a number of reports of the toxic-
ity of parathion on avian embryos (Khera and Bedok, 1967;—' Khera and
Lyon, 1968;2/ Khera and Clegg, 1969;!/ Roger et al., 1969;*/ Oga et al.
197ll/ and Yamada, 19716/) . Khera and Bedok (1967) reported the follow-
ing toxicity when 1 mg of parathion was injected into the egg sacs of
4-day incubated chicken eggs: the shape and course of the notochord was
distorted. This distortion was associated with disproportionate and
irregularly spaced anlagen of various axial structures. Khera and Lyon
(1968) determined that chicken eggs injected on incubation days 0,4, and 7,
and duck eggs injected on days 0, 4, 7, and 10 were insuitable for toxic-
ity studies. There was a large variation among replications, lack of
dose-response relationships, and in some cases low sensitivity to the
specific lethal effect. There was a more marked mortality response at
mid-incubation for both species (10 days in chick and 13 days in duck
embryos). There were indications that duck embryos provide less vari-
able results than chick embryos. Roger et al. (1969) studied the tera-
togenic effect of bidrin in hen eggs. He included a number of other
organophosphorus compounds in his study and reported on parathion. He
observed that the injection of 1 mg of parathion/egg produced a definite
If Khera, K. S., and S. Bedok, "Effects of Thiol Phosphates on Notochordal
and Vertebral Morphogenesis in Chick and Duck Embryos," Food Cosmet.
Toxicol.. 5:359-365 (1967).
2/ Khera, K. S., and D. A. Lyon, "Chick and Duck Embryos in the Evalua-
tion of Pesticide Toxicity," Toxicol. Appl. Pharmacol.. 13:1-15
(1968).
51 Khera, K. S., and D. J. Clegg, "Perinatal Toxicity of Pesticides,"
Can. Med. Assoc. J.. 100:167-172 (1969).
4/ Roger, J-C., D. G. Upshall, and J. E. Casida, "Structure-Activity
and Metabolism Studies on Organophosphate Teratogens and Their
Alleviating Agents in Developing Hen Eggs with Special Emphasis
on Bidrin," Biochem. Pharmacol.. 18(2):373-392 (February 1969).
£/ Oga, S., C. C. Pellegatti, S. Reis, and A. C. Zanini, "Toxic and/
or Teratogenic Activity of Anticholinesterase Compounds. I.
Tetatogenicity of Parathion in Chicken Embryos," Rev. Farm. Bio-
quim. Univ. Sao Paulo, 9(2):343-355 (1971).
6/ Yamada, A., "Teratogenic Effects of Organophosphorus Insecticides in
the Chick Embryo," Osaka Shiritsu Daigaku Igaku Zasshi, 21:245-255
(1972).
91
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shortening of the spine of the embryo. Thirty percent had abnormal
feathers and 10% parrot-beak. When Oga et al. (1971) evaluated the
teratogenic effects of parathion administered to eggs at levels 59.23,
118.46, or 296.15 Jig/egg, he demonstrated dose dependency in the in-
tensity of malformations. The highest dose-inoculated group showed a
maximum incidence of teratogenic effects (44%) with treatment on the
8th day of embryogenesis. The embryos treated at the highest dose of
parathion on the 8th day showed total body malformation, overall edema,
ankylosis of the lower limbs, asymmetric implantation of the limbs, and
intestinal atony. Embryos inoculated at 59.23 ug of parathion exhibited
only limb malformations.
An effect on embryo development in hens' eggs was also reported by
Marliac (1964).I/ A concentration of 0.1 mg of parathion per egg produced
malformed embryos.
Lutz-Ostertag et al. (1969a, b),^2/ Meiniel et al. (1970) £/ and
Lutz-Ostertag et al. (1970)!/ studied the teratogenic effects of para-
thion in quail. Lutz-Ostertag et al. (1970) also investigated the
development of pheasant, duck, and chick embryos as affected by para-
thion. The teratogenic effects of parathion on the skeleton of Japanese
quail were studied by Meiniel et al. (1970). They immersed Japanese
quail eggs in a mixture of acetone and parathion which contained 20 mg
of parathion per liter of acetone. The immersion time was 30 sec. They
observed inhibition of growth of the appendicular skeleton, which is con-
sidered a serious malformation as well as considerable retardation of
the growth of the axial skeleton. The most common deformities were
lordosis of the neck and numerous flexions in the sagittal plain. Neural
\l Marliac, J. P., "Toxicity and Teratogenic Effects of 12 Pesticides in
the Chick Embryo." 48thAnn. Meeting Fed. Amer. Soc. Exp. Biol..
105 (1964).
2/ Lutz-Ostertag, Y., R. Meiniel, and H. Lutz, "Action du parathion sur
le developpement de 1'embryon de caille," C. R. Acad. Sci.,
Paris, Series D, 268:2911-2913 (1969a).
3^1 Lutz-Ostertag, Y., R. Meiniel, and H. Lutz, "Effects du parathion
sur le developpement de 1'embryon de caille et de certains de ses
organes in vivo et in vitro," Biol. Abstr.. 52(22):12, 271 (1969b).
4/ Meiniel, R., Y. Lutz-Ostertag, and H. Lutz, "Teratogenic Effects of
Parathion (Organophosphorus Insecticide) on the Skeleton of the
Embryo of the Japanese Quail (Coturnix coturnix japonica)," Arch.
Anat. Microsc. Morphol. Exp., 59(2):167-183 (1970).
5J Lutz-Ostertag, Y., R. Meiniel, and H. Lutz, "Parathion, Embryonic
Development, Sterilization and Estrogenic Effects in Birds; Com-
parison with the Effects of Aldrin," Annee Biol., 9:501-507 (1970).
92
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centers and arches were evident tn many of the cervical vertebrae. Also
the vertebral musculature was disorganized. Nonincubated eggs of pheasant,
quail, duck, and chickens were immersed in an acetone-parathion solu-
tion containing 20 g of parathion per liter (Lutz-Ostertag et al., 1970).
Other eggs received injections of 1 g of commercial parathion (10% Al/liter)
carried in 0.08 to 0.50 ml of Tyrodes solution. All of the embryos from
eggs that were immersed and survived past 9 days of incubation were
severely deformed. Deformation was exhibited by nanism, lordosis of the
neck, celosomia, light edema, achondroplasia, anury, club-shaped feather-
buds and abnormally positioned hind-legs with crisped digits were noticed.
The livers were abnormal. The most interesting features were the changes
in the urogenital tract. The gonads were partially or completely sterilized.
Parathion had acted as an antimitotic substance, markedly affecting cell
division. The Mueller's canals of the male embryos were partially re-
tained. The right Mueller's canal in female embryos was completely re-
tained. Quail embryonic testes were isolated from the embryo and cul-
tivated (5 days) in vitro in the presence of pesticides (Lutz and Lutz-
Ostertag, 1972).—' The testes appeared healthy; however, upon histologi-
cal examination there were changes in structure. The testicular tubules
were vacuolized: the gonocytes and Sertoli cells disappeared completely.
Quail embryo ovaries cultivated under the same conditions manifested
similar changes. The effect on the chick embryo was not as broad. Only
the selective disappearance of all the gonocytes was manifest. It fur-
ther has been reported that the ovary of the chick embryo undergoes more
or less .complete suppression of the corta (Lutz-Ostertag and Meiniel,
1968).-'
Dunachie and Fletcher (1969)—' used the eggs of white leghorn
chickens for teratogenic studies. They used the yolk injection method.
Parathion was far less toxic when dissolved in acetone, compared to corn
oil. Eighty-nine percent of the eggs hatched at the concentration of
50 ppm and only 19% at 500 ppm. Considering the high toxicity to mammals
of parathion, the embryonic mortality was surprisingly low. The amount
of deformities is variable but severe only at 500 ppm. Various combina-
tions of parathion and ma la thion have been evaluated. Both mortality
I/ Lutz, H., and Y. Lutz-Ostertag, "The Action of Different Pesticides
on the Development of Bird Embryos," Dru%s and Fetal Development,
Froc. International Symposium on the Effect of Prolonged Drug
Usage on Fetal Development, Beit-Berl, Kfar Saba, Israel, September
1971, pp. 127-150 (1972).
2/ Lutz-Ostertag, Y., and R. Meiniel, "In vitro Sterilizing Effect of
Parathion on Embryonic Ovaries of Chick and Quail," C. R. Acad.
Sci., Paris, Series D, 267:2178-2180 (1968).
3/ Dunachie, J. F., and W. W. Fletcher, "An Investigation of the Toxicity
of Insecticides to Birds' Eggs Using the Egg-Injection Technique,"
Ann. Appl. Blol.. 64(3):409-423 (1969).
93
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and deformities were high (38%) for parathion in a 5:50-ppm mixture with
malathion. The hatchability of 100% parathion and no malathion was 65%,
whereas a dose of 100% malathion reduced hatchability to 87%. A 50:50
mixture of these two organophosphate insecticides produced a hatchability
of 71%.
Some very interesting observations have been made by Khera and Clegg
(1969) relative to the prenatal toxicity of pesticides. These authors
point out that the use of avian eggs as a test organism has a serious
fault in that it is difficult to extrapolate to mammalian species. The
greatest difference between the avian embryos and mammalian species is
that the avian embryo is nonplacental. Since it is isolated from the
maternal organism, the avian embryo cannot benefit from the natural de-
fense mechanisms which safeguard the mammalian embryo. Furthermore, the
phylogenetic relationship between avian species and man is remote. Mam-
malian data indicate that in most cases, extremely large dose levels
(when compared to the human exposure levels) are required to induce
neonatal effects or embryotoxicity. These investigators concluded it
was unlikely that any pesticide presently in use is liable to cause
damage to the perinatal human, at normal exposure levels. They felt that
this position was supported by the lack of epidemiological data connect-
ing pesticides to perinatal toxicity in humans.
Paraoxon was one of the compounds included in a study of Flockhart
and Casida (1972)i/ in which they attempted to correlate the degree of
inhibition of esterase in the yolk sac membrane to teratogenic effects
of organophosphate insecticides.
The teratogenic effects were shown to be unrelated to hydrolysis of
diphenylacetate by homogenates of yolk sac membranes. For example, both
paraoxon and EPN gave similar degrees of esterase inhibition, but only
paraoxon treatment of hens' eggs resulted in teratogenic effects.
Crustaceans - Pesticides may get into estuarine water by drainage from
nearby treated fields, or when the pesticide is used as a control in
salt marshes and estuaries for mosquitoes. Studies have been made by
Butler et al. (1962)£/ on the effect of pesticides on adult oysters.
I/ Flockhart, I. R., and J. E. Casida, "Relationship of the Acylation
of Membrane Esterases and Proteins to the Teratogenic Action of
Organophosphorus Insecticides and Eserine in Developing Hen Eggs,"
Biochem. Pharmacol.. 21:2591-2603 (1972).
2/ Butler, P. A., A. J. Wilson, Jr., and A. J. Rick, "Effect of Pesti-
cides on Oysters," Proc. Nat. Shellfish Assoc.. 51:23-32 (1962).
94
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Thirty-one compounds were investigated by Davis (I960)- as to their ef-
fect on fertilized eggs and larvae of bivalves. It was the opinion of
these investigators that the effect of pesticides on growth is the most
sensitive index for these molluscs for establishing a level that would
(highest concentration) have no appreciable effect on the survival of
embryos, or on the survival of the fully formed veliger larvae. Davis
and Hidu (1969)—' were interested in the effects of various compounds
(52 compounds, including 17 insecticides) on the development of fertilized
eggs of the hard clam, Mercenaria mercenaria, and the American oyster,
Grassestrea virginica, and on the survival and growth of the larvae.
Parathion concentrations in the water, were 0.25, 0.50 and 1.0 ppm. They
did not measure the number of oyster eggs developing or the survival of
the larvae, but they did determine that the percent of increase in the
length of the larvae was depreciated from 1037. to 227o at the higher con-
centration. No evaluation was made for parathion for the reduction of
the number of eggs ultimately developing into normal larvae from oyster
and clam eggs.
Behavioral Effects
Al-Hachim and Fink (1968a, b, and c)^?-' have studied the behavioral
effects of DDT and parathion upon young mice whose mothers were previ-
ously treated with these compounds. They measured minimal electroshock
seizure threshold (1968a) at 70 to 90 days of age, the condition of
avoidance response (1968b) at 30 through 37 days of age, and open-field
behavior (1968c) at 60 to 66 days. In all of these studies the mothers
were given a dosage of 3 mg/kg of parathion during the first, second,
J./ Davis, H. €., "Effects of Some Pesticides on Eggs and Larvae of
Oysters (Grassestrea virginica) and Clams (Venus mercenaria),"
Commer. Fish. Rev.. 23(12):8-23 (1960).
2/ Davis, H. C., and H. Hidu, "Effects of Pesticides on Embryonic De-
velopment of Clams and Oysters and on Survival and Growth of the
Larvae." Fish. Bull.. 67(2):393-403 (1969).
3/ Al-Hachim, G. M., and G. B. Fink, "Effect of DDT or Parathion on the
Minimal Electroshock Seizure Threshold of Offspring from DDT- or
Parathion-Treated Mothers," Psychopharmacol.. Berlin, 13:408-412
(1968a).
4/ Al-Hachim, G. M., and G. B. Fink, "Effect of DDT or Parathion on Con-
dition Avoidance Response of Offspring from DDT- or Parathion-Treated
Mothers," Psychopharmacol., Berlin, 12:424-427 (1968b).
£/ Al-Hachim, G. M., and G. B. Fink, "Effect of DDT or Parathion on Open
Field Behavior of Offspring from DDT- or Parathion-Treated Mothers,"
Psychol. Rept.. 22:1193-1196 (1968c).
95
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and third trimester. There was no effect upon brain excitability, con-
ditioned avoidance response, or open-field behavior of mice whose mothers
had received the parathion. Out of the three tests, the only response
that was obtained was from DDT which produced a delayed acquisition of
controlled avoidance response. The brain excitability and the open-field
behavior of the young were normal.
It was postulated that since parathion is metabolized and excreted
by the mammals within a few days after ingestion, its effects on the
central nervous system seem to be transient, having an effect for a few
weeks after birth and disappearing when the offspring becomes older (2
months).
1 2/
Spynu (1952 and 1957)-=^=-' studied the conditioned reflexes of cats
that had been dosed with 5, 3, and 2 mg/kg of parathion in three separate
experiments (quoted by Medved et al., 19643-'). At a dosage of 5 mg/kg
orally, the conditioned reflexes of the cat were slowed within 10 to 15
min. The animal returned to normal in 3 days. After the 3 mg/kg dosage,
it required 3 hr to establish a lowering of the conditioned relfexes.
No changes could be found in animals given 2 mg/kg.
Toxicity Studies with Tissue Cultures
4/
Tissue cultures were first used by Lewis and Richards (1945)— to
determine the toxicity of DDT on chicken embryo tissues. Gabliks and
Friedman (1965)—' used HeLa cells and Chang liver cells in an attempt to
JV Spynu, E. I., "Data Concerning the Toxicology of the Insecticide Niuiph
100 and the Establishment of Tolerance Limits," Dissertation, Kiev
(1952).
2J Spynu, E. I., "The Effect of Some Organophosphorus Insecticides on the
Higher Nervous Activities and on the Cholinesterase Activity," The
Chemistry and Application of Organophosphorus Compounds, Acad. Sci.
USSR (Ed.), Moscow (1957).
3/ Medved, L. I., E. I. Spynu, and lu. S. Kagan, "The Method of Con-
ditioned Reflexes in Toxicology and Its Application for Determin-
ing the Toxicity of Small Quantities of Pesticides," Residue Rev..
6:42-74 (1964).
4/ Lewis, W. H., and A. G. Richards, Jr., "Non-Toxicity of DDT on Cells
" in Cultures," Science, 102:330-331 (1945).
5/ Gabliks, J., and L. Friedman, "Responses of Cell Cultures to In-
~~ secticides. I. Acute Toxicity to Human Cells," Proc. Soc. Exp.
Biol. Med.. 120:163-168 (1965).
96
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study insecticidal toxicity. The first evaluation of organophosphate
insecticides in tissue cultures was conducted by Gabliks et al. (1967).—
They found very little correlation between mouse liver cell cultures and
human strain Chang liver cells. Litterst et al. (1969 and 1971)-!-' used
tissue cultures to investigate the toxicity of a number of insecticides
including parathion, paraoxon, and £-nitrophenol. In the earlier study
(1969) they also used HeLa cells. They evaluated growth inhibition and
synthesis of proteins and nucleic acids in their cultures. They ob-
served that organophosphate compounds were more toxic than the chlorinated
compounds. It was found that paraoxon, an oxidation product of para-
thion, was less toxic at 40 ppm than parathion. In contrast, £-nitro-
phenol at the same concentration (40 ppm) appeared to be slightly more
toxic. If they increased the treatment levels to 250 and 500 ppm, both
paraoxon (at 250 ppm) and £-nitrophenol (at 500 ppm) caused nearly com-
plete inhibition of cell growth. The synthesis of DNA at a concentration
of 10 ppm of the insecticide indicated that only diazinon produced any
changes. Aspirin and sodium chloride were included as positive controls
in the test. The same effect observed with Diazinon®was produced by
these two chemicals. It should be pointed out that a test level of 10
ppm is relatively high as related to concentrations of insecticides
normally found in human tissues (with the exception of DDT). When the
parathion concentration was raised to 50 ppm, there was a 50% inhibition
in cell growth in 48 hr. Litterst and Lichtenstein (1971) extended the
above studies to include the cells of nonmalignant origin. They chose
normal diploid skin fibroblasts. They evaluated parathion, carbaryl,
and several metabolites such as £,£*-DDE, paraoxon, £-nitrophenol, and
1-naphthol. The response to the normal cells was the same as previously
reported with a malignant cell line, in that parathion was more toxic
than paraoxon, and £-nitrophenol was as toxic as parathion. It should
be emphasized that these results are exactly the opposite of data ob-
tained when animals are used as test organisms. In general, little dif-
ference was found between the responses of the malignant (HeLa) and the
nonmalignant (fibroblast) cells to the environmental toxicants. In
JL/ Gabliks, J., M. Bantug-Jurilla, and L. Friedman, "Responses of Cell
Cultures to Insecticides. IV. Relative Toxicity of Several
Organophosphates in Mouse Cell Cultures," Proc. Soc. Exp. Biol.
Med.. 125:1002-1005 (1967).
2/ Litterst, C. L., E. P. Lichtenstein, and K. Kajiwara, "Effects of
Insecticides on Growth of HeLa Cells," J. Agr. Food Chem., 17:
1199-1203 (1969).
:*/ Litterst, C. L., and E. P. Lichtenstein, "Effects and Interactions
of Environmental Chemicals on Human Cells in Tissue Culture,"
Arch. Environ. Health. 22:454-459 (1971).
97
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review, it is difficult to make relevant predictions concerning the
effect of -a pesticide utilizing human cells in tissue culture. Under
the conditions of the tests reported, the interaction at the level of
synthesis of macromolecules is dependent upon the cell line and the addi-
tive used, and in general, there is no significant interaction between
the two.
Mutagenic Effects
Dikshith (1973).^ studied the in vivo effects of parathion on guinea
pig chromosomes. He injected male guinea pigs with a single intratesti-
cular injection of 0.05 mg of parathion in 0.5 ml of ethanol. The animals
were killed after 24 hr. He determined the percentage of chromosomal
changes at metaphase, and these results are shown in Table 15. Chromosome
abnormalities were induced by parathion treatment in the meiotic chro-
mosomes of the male guinea pig. In some cases, the individual morphology
of the chromosomes was totally lost (chromosomal pulverization). Al-
though it was not common, parathion did induce the formation of exchange
figures. In essence, Dikshith 's (1973) work confirmed the fact that
cell division was inhibited at metaphase. It had been previously con-
jectured by Lutz-Ostertag et al. (1969a and 1969b) that parathion in-
duces embryonic abnormalities because of defective cell division.
Oncogenic Effects
No ocogenic studies per se were found concerning parathion as an
initiator of tumor development in animals. However, one study described
the effect of parathion upon the possible reduction of tumors produced in
animals by treatment with a potent carcinogen. No tumors were reported in
the two year feeding studies.
Buchet and Lauwerys (1970 and 1971)i had observed that certain
organophosphate esters inhibit tissue lipo lysis in vitro and in vivo.
Others have observed that mammary tumor incidence in rats appears to be
influenced by the quality and the quantity of the dietary fat. Rats
maintained on a diet containing 20% corn oil developed more mammary
tumors after treatment with a single dose of 7, 12 -dime thy lbenz( a) anthracene
\l Dikshith, T. S. S., "In vivo Effects of Parathion on Guinea Pig
Chromosomes," Environ. Physiol. Biochem., 3:161-168 (1973).
2J Buchet, J. P., and R. Lauwerys, "Inhibition of Rat Heart Diolein Hy-
drolase and Brain Acetylcholinesterase by Organophosphate Esters
in vitro." Bibchim. Biophys. Acta. 218:369-371 (1970).
3_/ Buchet, J. P., and R. Lauwerys, "Characterization of a Diglyceride
" Lipase in Rat Heart and Intestine," Life Sci.. 10:371-376 (1971).
98
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Table 15. PERCENTAGE OF CHROMOSOMAL CHANGES AT METAPHASE OF MALE GUINEA
PIGS AFTER PARATHION (0.05 MG/TESTICAL) TREATMENT*
Number of cells scored Number of cells observed and percent frequency
507. Clumping and
ethanol Para- Fragmentation liquification
Control^
200
200
200
200
control
200
200k/
200
200k/
thion
200
200
200
200
Cells
31
28
23
37
Percent
15.50
14.00
11.50
18.50
Cells
14
19
15
18
Percent
7.00
9.50
7.50
9.00
Other types
--
—
—
Observed
Chromatid
bridge in
one cell
200 200 200 24 12.00 10 5.00
Average 200 200 200 14.30 7.60
Source: Dikshith, op. cit. (1973); reprinted from Environmental Physiology
and Biochemistry by permission of the publisher. Year of
first publication, 1973.
&/ Chromosomal changes were not noticed in any of the cells scored.
b/ One to two cells showed features of clumping otherwise all cells
scored were normal.
99
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than rats fed a low fat diet. Lauwerys and Buchet (1972)— evaluated the
effect of parathion on mammary carcinoma produced by 7,12-dimethylbenz-
(a)anthracene (DMBA). They injected parathion twice a week into rats for
12 weeks at a level of 0.5 mg/kg followed by 1 mg/kg intraperitoneally
three times a week for 11 weeks. The triamiphos was included in the diet
of another group of rats, at a concentration of 20 ppm. Two weeks after
the beginning of the different treatments, all rats were given 0.5 ml of
DMBA solution (5 mg) orally and the treatment was repeated for 5 weeks.
Animals were autopsied at the time of death or at the end of the test
period of 23 weeks. The carcinogenic action of DMBA observed during
this study is summarized below.
Total Number of
tumor tumors per Latent period
Treatment group incidence tumor-bearing rat in days
Parathion 100 2 66
Control 90 2.6 66
Triamiphos 60 1.6 73
Control 100 2.3 66
There was no reduction of tumor incidence in the parathion treated group.
The lower tumor incidence in the triamiphos may be due to its reduction
of tissue lipolytic activity. The administration of parathion may have
allowed a return of normal lipolytic activity between successive injec-
tions .
Effects on Humans
Acute and Subacute Toxicity - There are extensive literature references
to acute and subacute poisoning of humans by parathion, largely presented
as individual or group clinical cases. In most of these instances the
actual amounts of parathion ingested, absorbed or inhaled were not known.
Hayes (1967)—' has summarized the susceptibility of man and other animals
to a number of pesticides, including parathion (Tables 16 and 17). Para-
thion is a highly toxic chemical with a fatal dose for man at a level
of 2 mg/kg for a single dose. The oral lethal dose of parathion is
_!/ Lauwerys, R., and J. P. Buchet, "Effect of Two Organophosphorus
Esters on Mammary Carcinogenesis by 7,12-Dimethylbenz(a)anthracene,"
Eur. J. Toxicol.. 5:163-167 (1972).
2/ Hayes, W. J., Jr., "Toxicity of Pesticides to Man—Risks from Present
Levels." Proc. R. Soc. Lond., 167(1007):101-127 (1967).
100
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Table 16. SPSCEPTIBILXTY OF MAN.AND OTHER ANIMALS
TO SINGLE ORAL DOSES OF PARATHION
f*
W W
0 U
4J 4) 4>
M (^ *|.j
O «W J3 M-l
j3 W *j w
4J l-l
1-4 r-l $ rH
3 CO CO
U AJ O
4J -H CO -rl
(0 0 V C
41 *r( r-4 *f-f
00 r-l r-t rH
n o g o
co B
Species ^ OT
Man
Child
Calf
Sheep 50
Steer 25
Dosage(mg/kg)
r-l O
CO 4)
O JZ O eg co ri S5
0) B rt
S co i-J
6.4
—
0-5
75
r-l
CO
CO
|V|
>>t
4J i-j
CO r-l B
4) CO rl
i-4 4J O
rH CO O M-l
f&K ITl -rl
P .S
cn 3 &
2-0 — 13
0-1 — --
1-5 — —
20 — —
References
a/,*/
S.I
d/
Q /
d/
a/ Goldblatt, M. W., "Organic Phosphorus Insecticides and the Antidotal Action
of Atropine," Fharm. J.t 164:229-233 (1950).
b/ Hayes, W. J., Jr., 1963 Clinical Handbook on Economic Poisons, PHS
~~ Publication No. 476, Washington, D.C. (1963).
£/ Kanagartatnam, K., W. H. Boon, and T. K. Koh, "Parathion Poisoning
from Contaminated Barley," Lancet. 1:538-542 (1960).
d/ Radeleff et al., op. cit. (1955).
-------
Table 17. THE SUSCEPTIBILITY OF MAN AND OTHER ANIMALS
TO REPEATED ORAL DOSES OF PARATHION
Species
Man
Dosage
(mg/kg/day)
0-1
Duration
(days)
42
Results
33% reduction of whole blood ChE;
References
Rat (F)
Dog
Pig
0-26
0-047
4-0
84
168
49
167. Inhibition of RBC ChE; 377.
inhibition of plasma ChE
807. reduction of RBC ChE; slight
inhibition of plasma ChE
607. inhibition of plasma ChE
80% inhibition of RBC ChE; no
inhibition of plasma ChE
£/ Edson et al., op. cit. (1964)
b/ Frawley and Fuyat, op. cit. (1957).
-------
estimated to be 1.43 rag/kg of body weight for a man (DuBois, 1958).-
Aa much as 0.1 mg/kg/day continuously administered for 42 days signifi-
cantly reduced plasma and RBC cholinesterase. Lethality has been re-
ported by Hayes (1963) following the ingestion by adult humans of 900,
120, and 50 mg of parathion.
2-6/
Rider and his associates (1963, 1964, 1967, 1969a, b) conducted
a number of experiments on human volunteers from the San Quentin Prison
in California to establish tolerances for various insecticides in man.
Over a 10-year period, they worked with parathion, methyl parathion,
malathion, EPN, Systox®,dichlorvos, OMPA, CARDONA, and Guthion®. Most all
of their experiments were conducted over the same time, frame, which was
oral ingestion of a capsule of various dosages of the insecticides for a
30-day period. There was one exception (1963) in which the experiments
ran for 50 days. Before the evaluations began, the prisoners were given
physical examinations, and a base was established for their plasma and
RBC cholinesterase. During the 30-day test, blood samples were taken
twice a week for esterase activity. Rider and Moeller (1963) and Rider
et al. (1969b) ran experiments using parathion on prisoners. Rider and
Moeller (1963) and Rider et al. (1969a) reported on the effect of four
dosage levels of parathion: 3.0, 4.5, 6.0 and 7.5 mg/day. They observed
only a slight depression of plasma cholinesterase for levels of 3.0, 4.5
and 6.0 mg. However, at the level of 7.5 mg/day, on day 4 the plasma
cholinesterase of one subject was down to 73% of his pretest level. On
day 9 two of the subjects had values of 64% and 687. of their control
levels, and on day 16 these two subjects had cholinesterase depressions
of 507. and 527. of their pretest level. At this point in the experiment
I/ DuBois, K. P., Postgrad. Med. J., 24:278-288 (1958).
2j Rider, J. A., and H. C. Moeller, "Tolerance of Organic Phosphates in
Man," Progress Report of Franklin Hospital Foundation, San Francisco,
California (1 October 1963).
.37 Rider, J. A., and H. C. Moeller, "Studies on the Anticholinesterase
Effects of Systox and Methyl Parathion in Humans," Fed. Proc.,
23(2):176 (1964).
4/ Rider, J. A., H. C. Moeller, and E. J. Puletti, "Continuing Studies
on Anticholinesterase Effect of Methyl Parathion, Initial Studies
with Guthion, and Dichlorvos on Humans," Fed. Proc., 26(2):427 (1967).
5J Rider, J. A., H. C. Moeller, E. J. Puletti, and J. I. Swader, "Toxic-
ity of Parathion, Systox, Octamethyl Pyrophosphoramide, and Methyl
Parathion in Man," Toxicol. Appl. Pharmacol.. 14(3):603-611 (1969a).
(J Rider, J. A., and E. J. Puletti, "Studies on the Anticholinesterase
Effects of Gardona, Methyl Parathion, and Guthion in Human Subjects,"
Fed. Proc.. 28(2):479 (1969b).
103
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the average plasma cholinesterase for the five subjects was decreased by
28% from the control value. Some depression of red blood cell cholin-
esterase was also noted at the dosage of 7.5 mg of parathion per day.
The lowest red cell cholinesterase values obtained were 63, 78, and 86%
of the pretest levels. These data are in agreement with those of Edson
et al. (1964).
Symptoms of Parathion Poisoning - The symptoms of mild exposure to para-
thion as a result of orchard spraying or other activities associated in
the fruit-growing industry have been described by Sumerford et al.
(1953>= and Arterberry et al. (1961) ."LI The modes of exposure and the
symptomatology have been discussed by Hamblin and Golz (1955). The signs
and symptoms of 246 patients admitted to a hospital in Greece with acute
parathion poisoning have been reviewed by Tsachalinas et al. (1971) ..3/
Namba (1971)!/ has presented an excellent description of the signs and
symptoms of organophosphate poisoning in patients. Reference should be
made to Hamblin and Golz's paper (1955) for the onset and progressions
of symptoms in subjects exposed to toxic amounts of parathion in spray-
ing operations. Namba (1971) has classified the signs and symptoms ob-
served in 77 patients who developed poisoning by the application of ethyl
and methyl parathion. The more prominent symptoms were weakness, nausea
or vomiting, excessive sweating, headache and excessive salivation. Namba
points out that if the exposure to organic phosphorus insecticides is suf-
ficient to produce symptoms, they usually appear in less than 12 hr.
Symptomatology that appears 24 hr after exposure is unlikely to be due to
these pesticides. A critical clinical observation is the occurrence of
tniosis, which is found in about 50% of the patients, and the latter
symptom appears in subjects even in the mild cases. Death is usually
attributed to failure of the respiratory muscles and paralysis of the
respiratory center. Cardiac involvement may occur, but is usually seen
\J Sumerford, W. T., W. J. Hayes, Jr., J. M. Johnston, K. Walker, and
J. Spillane, "Cholinesterase Response and Symptomatology from Ex-
posure to Organic Phosphorus Insecticides," AMA Arch. Ind. Hyg.
Occup. Med., 7:383-398 (1953).
2J Arterberry, J. D., W. F. Durham, J. W. Elliot, and H. R. Wolfe,
"Exposure to Parathion," Arch. Environ. Health. 3:476-485 (1961).
2/ Tsachalinas, D., G. Logaras, and A. Paradelis, "Observations on 246
Cases of Acute Poisoning with Parathion in Greece," Eur. J. Toxicol.,
4:46-49 (1971).
t*J Namba, T., "Cholinesterase Inhibition by Organophosphorus Compounds
and Its Clinical Effects," Bulletin of the World Health Organiza-
tion, 44:289-307 (1971).
104
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only at the terminal stage. Man appears to be more sensitive to the
organophosphate insecticides in that he exhibits symptoms earlier than
experimental animals, particularly central nervous system manifestations.
If an untreated organophosphate-poisoned victim is alive after 24 hr»
he is likely to recover. The account by Kanagaratnam et al. (1960)-' de-
scribes a parathion poisoning incident resulting from the use of con-
taminated barley in India. There were 53 persons involved, and the
clinical features described included collapse, fits, sweating, dyspnoea,
the effect on the pupils, the eye, blood pressure, coma, and muscular
fasciculation.
Gershon and Shaw (1961)-' felt that chronic exposure to organophos-
phate compounds produced psychiatric disorders in orchard workers. In
a small field survey, they observed in 14 men and two women schizophrenic
and depressive reactions with severe impairment of memory and difficulty
in concentration. The range of exposure for these subjects was 1-1/2 to
10 years.
No other surveys of this nature were found in the literature.
Brown (1971)-' reported on the electroencephalographic changes and
disturbance of brain function following organophosphate exposure.
Acute organophosphate poisoning disturbs central nervous system func-
tions by causing disorientation in space and time, a sense of depersonaliza-
tion, and hallucinations; with heavy exposure, convulsions occur. Acute
inhibition of brain cholinesterase would be expected to cause effects
related to the temporal lobe. EEC changes in acute organophosphate
poisoning have been reported to resemble those seen in the interictal EE6
of temporal lobe epileptics.
Dermal Effects - The information in this subsection is concerned with
observations that were made during controlled exposure to parathion.
Other data on the relationship of exposure to occupational hazards of
dermal contact are discussed in a later subsection.
4/
Fredriksson (1961a)- and Fredriksson et al. (1961) conducted a study
on the distribution of labeled parathion within the skin, and on the
_!/ Kanagartanam, K., W. H. Boon and T. K. Hoh, "Parathion Poisoning from
Contaminated Barley, "Lancet 1;538-542 (1960).
2/ Gershon, S., and F. H. Shaw, "Psychiatric Sequelae of Chronic Exposure
to Organophosphorus Insecticides," Lancet. pp. 1371-1374 (1961).
3/ Brown, H. W., "Electroencephalographic Changes and Disturbance of
Brain Function Following Human Organophosphate Exposure," Northwest
Med.. 70:845-846 (1971).
ty Fredriksson, T., "Studies on the Percutaneous Absorption of Parathion
and Paraoxon. Part II. Distribution of 32P-Labeled Parathion
Within the Skin," Acta Derm. Venerol.. 41:344-353 (1961a).
105
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hydrolysis and metabolism of this insecticide within the skin. Previous '
to their work, there had been no other studies using autoradiographic
techniques to evaluate the cutaneous distribution of parathion which had
been applied topically. Evaluations were made from skin samples taken
from man, cat, rabbit and rat (Fredriksson, 1961a). Human skin was ob-
tained at autopsy within 10 hr after death, and pieces of this skin were
nailed to a board. Six microliters of ^2P-labeled parathion was then
evenly distributed on an area of the skin of about 1.5 cm2. The para-
thion was allowed to remain in contact with the skin for 1/2, 1, 2, 4 or
24 hr. After the exposure period, the parathion was usually blotted off
the skin, and samples were frozen and examined by autoradiographic tech-
niques. It was found that parathion appeared to penetrate to some ex-
tent into hair follicles and sebaceous glands, although no certain con-
clusions could be drawn regarding the routes of absorption. There was
some increased activity below the epidermal layers. In another study
(Fredriksson et al., 1961), the possible occurrence of skin enzymes
capable of metabolizing parathion and paraoxon was investigated. Tissue
slices of liver and skin were cut and the hydrolysis of parathion was
measured by the Warburg method. It was found that parathion was not hy-
dro lyzed or transformed into paraoxon by the skin of man, cats, rats or
rabbits. Paraoxon was hydro lyzed by the skin of all species except rats,
and the enzymatic action occurred at the fastest rate in the rabbit. The
hydrolysis in rabbit skin amounted to about 207. of the paraoxon in 1 hr.
In the skin from man and cat the rate of hydrolysis was about 17..
Hayes et al. (1964)-' and Funckes et al. (1963)2-/ investigated the
excretion of £-nitrophenol and the depression of RBC cholinesterase in
human volunteers that were subjected to exposure of parathion under
s trenuous circumstances.
Hayes et al. (1964) reported on three series of tests to evaluate
the potential hazard of dermal exposure to parathion under controlled
conditions.
Series 1 involved exposure of the hand and right forearm of volun-
teers to 2% parathion dust, 2% emulsion or 47.5% emulsifiable concentrates,
After the toxicant was distributed over the hand and forearm, they were
I/ Hayes, G. R., Jr., A. J. Funckes, and W. V. Hartwell, "Dermal Ex-
posure of Human Volunteers to Parathion," Arch. Environ. Health,
8:829-833 (1964).
2/ Funckes, A. J., G. R. Hayes, Jr., and W. V. Hartwell, "Urinary Ex-
cretion of Paranitrophenol by Volunteers Following Dermal Exposure
to Parathion at Different Ambient Temperatures," J. Agr. Food Chem.,
11:455-457 (1963).
106
-------
then secured in a polyethylene bag and placed in a constant temperature
chamber. The treatments were as follows:
1. Exposure to 5 g of 2% parathion dust for 2 hr on
five successive days at 105*F.
2. Exposure to 4 liters of 2% parathion emulsion for
70 min at 81°F.
3. Exposure to 47.5% parathion emulsifiable concen-
trate for 120 min at 69°F.
4. Same as No. 3 except for 90 min at 100°F.
No significant changes in cholinesterase activity and no clinical signs
were noted.
In Series 2, a volunteer exposed his entire body to 2% parathion
dust. The dust was rubbed on the bare shoulders, back and chest, and
then he put on a rubberized suit. Seven pounds of the dust was poured
over the shoulders and down into the suit. The suit was closed and
sealed. There were two exposures for 7.5 and 7 hr with an interval of
6 weeks between exposures. The temperature was 60°F. In a later test
a male volunteer sat in a chamber, exposed totally except for his head,
and was exposed to a vapor generated by heating 2% parathion powder to
200°F. The duration of exposure was 3 hr.
In the first test plasma cholinesterase activity was depressed to
44% of baseline at 24 hr after the initiation of the test, but was within
12% of normal within 120 hr. The volunteer in the second test did not
experience symptoms of poisoning. The plasma cholinesterase was depressed
to 82% of normal.
In Series 3, filter paper pads (900 cm2) were allowed to absorb their
capacity of equal values of parathion and ether. The pads were placed
on the backs of volunteers and covered with plastic sheeting. Two
volunteers were exposed twice for 3 hr to pads containing 40 to 50 g of para-
thion at temperatures of 54°, 79°, and 104°F.
Significant depression in cholinesterase activity of red blood cells
did not occur. The cholinesterase activity was depressed 20% in plasma
Immediately after exposure at 104°F. There were no signs of poisoning.
107
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The investigators commented that some individuals can sustain high
dermal exposure to parathlon without signs of poisoning or suffering
severe depression of cholinesterase activity.
In another study (Funckes et al., 1963), data on the excretion of
£-nitrophenol and blood cholinesterase activity were measured in volun-
teers exposed to parathion dust. The exposure consisted of weekly 2-
hr applications of 27. parathion dust to two volunteers maintained at
environmental temperatures ranging from 58° to 105°F. In these studies
only the hand and forearm were exposed in a bag containing the test in-
secticide. These investigators found that there was a significant change
in £-nitrophenol excretion in urine following dermal exposures at tem-
peratures above 82°F.
More recently Maibach et al. (1971)— investigated the penetration
of parathion, malathion, and carbaryl through the skin of volunteers by
using labeled pesticides. The only variable in the experimental design
was the anatomical site of application of the dose, which was regulated
at 4 ug/cmr of skin. Applications of pesticide were made to the follow-
ing anatomical regions: forearm, palm, foot (ball), abdomen, hand
(dorsum), fossa cubitalis, scalp, jaw angle, postauricular, forehead,
ear canal, axilla, and scrotum. They found that approximately 8.6% of
parathion when applied to the forearm was absorbed, and all other absorp-
tion was referenced to the forearm data. Slightly more parathion pene-
trated the palm and the ball of the foot, whereas the abdomen and the
dorsum of the hand permitted twice as much penetration as the forearm.
The fossa cubitalis had twice the penetration of the forearm. The hairy
areas such as the scalp, the angle of the jaw, the postauricular area
and forehead had four times more penetration than the forearm, whereas
the axilla had five times as much, and penetration from the scrotum was
essentially complete.
2/
Durham et aL (1972)— measured excretion of j>-nitrophenol as an
indicator for the degree of exposure of orchard spraymen to parathion.
Both respiratory and dermal absorption were studied. From the evidence
in their study they concluded that skin contamination is potentially .
more important as a route of absorption than the respiratory route al-
though not necessarily more important in terms of poisoning. The data
\J Maibach, H. I., R. J. Feldmann, T. H. Milby, and W. F. Serat, "Regional
Variation in Percutaneous Penetration in Man," Arch. Environ. Health,
23:208-211 (1971).
2/ Durham, W. F., H. R. Wolfe, and J. W. Elliott, "Absorption and Excre-
tion of Parathion by Spraymen," Arch. Environ. Health, 24:381-
387 (1972).
108
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showed that much larger amounts ,f parathion Impinge on the skin than are
breathed in the lungs. These authors emphasize the importance (need) to
protect the skin from exposure.
It is understood that environmental factors will have an influence
on the potential occupational hazards associated with use of insecticides.
With the exception of studies with workers in pesticide plants, the bulk
of information on exposure toxicity comes from studies carried out in
outdoor work situations.
One study, however, was done in which greenhouse workers were ob-
served during a 3-month exposure to parathion in a greenhouse. Addi-
tionally, determination of cholinesterase levels of these employees were
made 5 weeks after the last application of insecticide (Culver et al.,
1958i/). In their summary of findings these authors stated that on
plant surfaces (in the greenhouse) parathion was present at initial con-
centration from 80 to 200 ppm and had an average half-concentration time
of 80 hr. It was further shown that the red blood cell cholinesterase
depression in the workers could not be definitely correlated to measured
exposures to parathion although such a correlation was inferred. The
red blood cell cholines terase depression ranged from 15 to 20% and the
size of this depression was not sufficient to elicit signs of intoxica-
tion.
7 /
Malkinson (I960)— states that "Although the largest number of cases
of toxic absorption (industrial poisoning) follows respiratory inhalation
many industrial poisons are absorbed through the skin. . ."
Although poisoning with parathion often results from entry of the
material by two or more routes (absorption through skin, respiratory
tract, conjunctive or gastrointestinal tract) many instances have been
reported where toxicity resulted primarily by absorption through the
skin (Batchelor and Walker, 1954;!/ Hamblin and Marchand, 195lft/).
JL/ Culver, D., J. Kinosian, W. Thielen, and R. Graul, "A Study of Ex-
posure to Parathion in a Greenhouse," AMA Arch. Ind. Health, 18:
235-247 (1958).
2/ Malkinson, F., "Percutaneous Absorption of Toxic Substances in In-
dustry," AMA Arch. Ind. Health, 21:87-99 (1960).
_3/ Batchelor, G. S., and K. W. Walker, ''Health Hazards Involving In-
Use of Parathion in Fruit Orchards of North Central Washington,"
Arch. Ind. Hyg.. 10:522 (1954).
4/ Hamblin, D. 0., and J. F. Marchand, "Parathion Poisoning," Am.
Practitioner and Dig. Treatment, 2:1 (1951).
109
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Inhalation Effects - Reports that assess the hazards from occupational
exposure to parathion suggest that the majority of the occupational acci-
dents are due to dermal exposure. The following information on inhala-
tion is concerned with observations under controlled conditions. Other
information on respiratory exposure is discussed under Occupational Ex-
posure Hazards. Hartwell et al. (1964)-' made a controlled study of
respiratory exposure to volunteers from parathion. The volunteers were
fitted with a breathing tube and a face mask which was attached to a
toxic-vapor-generating chamber, in which parathion was placed in open
trays as a liquid or powder and heated to various temperatures. The up-
take of parathion through the breathing apparatus was not measured. In
one series of tests on each of four consecutive days, exposure was main-
tained for 30 min to a vapor from 1 ml of fresh technical parathion
spread over 36 in2 and heated to 105° to 115°F. On the 5th day the
amount of parathion was raised to 5 ml, spread over an 80 in^ surface,
and heated to 150°F. Under these conditions, after five exposures, the
red blood cell cholinesterase was depressed by 9870 and the activity of
plasma cholinesterase was depressed by 837.. In another series, a volun-
teer breathed through a mask attached to the 6-ft x 6-ft x 8-ft plyboard
chamber for 2-1/2 hr. In this chamber, panels of cheese-cloth 3 ft x
6 ft were saturated with technical parathion and attached to the interior
walls. In addition, technical parathion was sprayed into the chamber.
The temperature of the chamber was 100°F. The subject remained well
after breathing air from this chamber. Based on £-nitrophenol excretion
as an indicator, it was calculated that the average exposure amounted
to 2.5 mg equivalents of parathion absorbed. After 2-1/2 hr the cho-
linesterase activity of the red blood cells was depressed about 24%. The
investigators felt that their study confirmed the generally accepted
respiratory exposure hazard afforded by parathion. Relating these levels
to Edson's (1957)2/ work, where the latter demonstrated that cholinesterase
activity was depressed 33% after ingested oral doses of 7.6 mg, Hartwell
et al. (1964) felt that the hazard to respiratory exposure of humans to
parathion was at least three times greater than ingestion.
J./ Hartwell, W. V., G. R. Hayes, Jr., and A. J. Funckes, "Respiratory
Exposure of Volunteers to Parathion," Arch. Environ. Health. 8:
820-825 (1964).
2/ Edson, E. F., "Effects of Prolonged Administration of Small Daily
Doses of Parathion in Rat, Pig and Man," Mineograph Bulletin,
Essex England: Chesterford Park Research Station NR Saffron
Walden, p. 22 (March 1957).
110
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Occupational and Accidental Exposure Hazards - The occupational hazards
will be broadly considered as those exposures sustained by workers in
field operations and workers in manufacturing operations.
Field operations - The occupational hazards of spraying parathion
have been investigated by a number of workers. A very early paper by
Williams and Griffiths (1951)!/ was concerned with the individual symptoms
and cholinesterase level in the blood of sprayers. Others have reported
specifically on the effects to humans in spraying operations only
(Griffiths et al., 1951;2-/ Ganelin et al., 1964;!/ Bick, 1967*/). More
complete studies involving all of the types of personnel that are con-
nected with spraying operations such as field men, warehousemen, and
residents in the area have been reported by Sumerford et al. (1953),
Hayes et al. (1957),I/ Arterberry et al. (1961).
Milby and Ottoboni (1963)- reported on an epidemic of parathion
poisoning is a 50 mile square area around Hughson, California. In this area
there were 250 peach orchards with a total area of 24,000 acres. There
were 5,000 to 8,500 peach pickers in this area between early August and
mid-September. The peaches were picked manually in hot weather. Dur-
ing this season, 94 workers were poisoned by parathion. Cholinesterase
determinations were obtained in 68 of the 94 cases and were found to be
depressed in 66 patients. One death occurred which was attributed to
parathion poisoning.
Two pounds of actual parathion were sprayed per acre (as a 25% wet-
table powder) on 20 March, 20 May, 25 June and 27 July. Picking was
started on 8 August.
I/ Williams, J. W., and J. T. Griffiths, "Parathion Poisoning in Florida
Citrus Spray Operations," J. Fla. Med. Assoc.. 37:707-709 (1951).
2/ Griffiths, J. T., C. R. Stearns, Jr., and W. L. Thompson, "Parathion
Hazards Encountered Spraying Citrus in Florida," J. Econ. Entomol.,
44:160-163 (1951).
,37 Ganelin, R. S., C. Cueto, and G. A. Mail, "Exposure to Parathion:
Effect on General Population and Asthmatics," J. Amer. Med. Assoc.,
188:807-810 (1964).
4/ Bick, M., "The Effect of Blood Cholinesterase Activity of Chronic
Exposure to Pesticides," Med. J. Aust.. 2:1066-1070 (27 May 1967).
5_/ Hayes, W. J., Jr., E. M. Dixon, G. S. Batchelor, and W. M. Upholt,
"Exposure to Organic Phosphorus Sprays and Occurrence of Selected
Symptoms," Public Health Reports. U.S. Dept. HEW, Public Health
Service, 72(9):787-794 (September 1957).
6i/ Milby, T. H., and F. Ottoboni, "Report of an Epidemic of Organic
Phosphate Poisoning in Peach Pickers, Stanislaus County,
California," State of California Department of Health, Bureau of
Occup. Health (1963).
Ill
-------
Analysis was performed for parathion residues on leaf and fruit sam-
ples. The contamination of workers' exposed skin was also determined.
The air was sampled in three orchards in the breathing zone of the workers
These sources of information led to an estimate of the total dose by all
routes of < 4,000 ug/day. The analyses performed by Milby and Ottoboni
are summarized below.
Source
Oral
Four peaches per day (residue
level of 0.5 ppm by weight)
Dermal
Palms of hands (63 in2 total and
7 ug/in2 maximum)
Backs of hands, forearms and face
(351 in2 total and 4.7 ug/in2 total)
Neck (40 in and 1.4 ug/in2 maximum)
Remainder of trunk
Respiratory
Airborne dust (35 ug/m^ and breathing
rate of 10 m3/day)
Total dose
Parathion
(KG)
500/day
440/day
1,650/day
56/day
960/day
350/day
< 4,000/day
Data from Milby and Ottoboni, pp. cit. (1963).
Quinby and Lemmon (1958)— evaluated the effects of residues left
in orchards on workers involved in picking, thinning, cultivating, and
irrigating. Williams and Griffiths (1951), in a study of orchard sprayers,
concluded that there should be a reassessment of the relationship of
blood cholinesterase to the development of symptoms. It had been con-
sidered earlier than parathion poisoning would not be evident in such
workers unless the blood cholinesterase level dropped to about 25% of
normal. However, these workers observed symptoms of parathion poison-
ing when the plasma cholinesterase levels were as high as 90% of their
control values, and the red blood cell cholinesterase was reduced to no
\J Quinby, G. E., and A. B. Lemmon, "Parathion Residues as a Cause of
Poisoning in Crop Workers," J. Amer. Med. Assoc., 166(7):740-746
(1958).
112
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to no lower than 60 to 70% of the normal control values. In the five
cases studied, four of the persons exhibited symptoms of poisoning when
the red blood cell cholinesterase was between 50 and 757. of normal.
Jegier (1964)i/examined 52 subjects for dermal and respiratory exposure
during a spraying season in the Provience of Quebec. It was found that
the maximum exposure for parathion, malathion, Sevin®, endrin and
Guthion® was less than 1% of the toxic dose. Spraying activities in-
cluded air blast spraying of apple orchards and field spraying of vegetables
and grain. A study of parathion poisoning cases reported during citrus
spray operations in Florida orchards was reported in 1950 (Griffiths et
al., 1951). Of the 48 cases reported, eight were shown to be definitely
not parathion poisoning, and 15 others were highly questionable. The
remaining 25 cases were assumed to be poison cases. However, a positive
diagnosis was lacking because of the absence of blood tests for cholin-
esterase. These investigators suggested that skin absorption was the
primary cause of parathion poisoning in these cases, and that handgun-
spray operators appeared to have far more skin exposure than speed-
sprayer operators. By checking the residues of parathion on the respirator
filter discs, they obtained additional evidence in that the hand spray
gun operators retained more parathion on their respiratory filter discs.
An extensive study of symptomatology and cholinesterase response after
exposure to organophosphorus insecticides has been reported by Sumerford
et al. (1953). This study involved a total of 258 persons, 805 samples
of red blood cells, and 802 samples of plasma which were analyzed for
cholinesterase. The workers were divided into eight groups:
• Mixing plant personnel (MPP)
. Commercial applicators (CA)
• Part-time applicators (PTA)
• Workers in orchards (WO)
• Field men, warehousemen and miscellaneous workers (FWM)
• Residents living near orchards (RNO)
• Residents far from orchards (KFO)
• Residents outside area (ROA)
I/ Jegier, Z., "Health Hazards in Insecticides Spraying of Crops," Arch,
Environ. Health. 8:670-674 (1964).
113
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This study was conducted in the apple growing area in Wenatehee,
Washington, where two types of sprays were used, parathion and tetra-
ethylpyrophosphate, and no effort was made to separate the effects of
these two organic phosphate insecticides. This study was summarized
with the following remarks:
1. The cholinesterase values for those groups known to have defi-
nite and consistent exposure (MPP, CA and PTA) were low, and the lowest
cholinesterase values were exhibited by the mixing plant personnel (MPP).
2. As one would expect, those workers who had little or no expo-
sure to insecticides maintained normal average cholinesterase values.
3. The only fatal or near fatal cases resulted from brief massive
exposures and gross carelessness rather than long-standing exposure.
4. When an illness was characterized by miosis or by any three of
a group of selected symptoms, it was possible to make a diagnosis of
poisoning if, in addition, the cholinesterase values were significantly
reduced.
They found no serious poisoning in the absence of excessive expo-
sure or severe depletion of cholinesterase values. There were occurrences
of mild illness in many of these workers when their cholinesterase values
fell within normal ranges. A follow-up study was made in the same area
by Hayes et al. (1957) during the subsequent 2-year period, with the sub-
jects again grouped in the same order as described in the work reported
above. Two hundred twenty-eight persons were involved in the follow-
up study, and these included 100 of the same subjects studied previously.
About the same number of persons were evaluated in 1953. In the latter
study only commercial applicators, residents near orchards, residents
far from orchards, and residents outside the area were compared. The
results of the follow-up study confirmed the previous demonstrated re-
lationships between blood cholinesterase levels, exposure and illness.
It was again concluded that miosis or three or more selected symptoms
are good criteria for the diagnosis of mild poisoning. No contradic-
tions in results were found in the 1952 to 1953 test when compared to
the 1951 observations. This paper also reported for the first time that
symptoms resembling mild poisoning are not significantly more common in
persons from an agricultural community than in persons living in a non-
agricultural area. A third survey (Arterberry et al., 1961) was made
114
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in this same area In Wenatchee, Washington, and again involved several
occupational groups that were studied in 1951, and in the 1952 to 1953
reports. About 115 persons were involved in the 1958 exposure study,
99 blood samples were analyzed for plasma and erythrocyte cholinesterase
activity, and 571 urine samples were taken for 2-nitrophenol content.
The latter test was added because a sensitive procedure for j>-nitrophenol
determination had been developed and was later published by Elliott et
al. (1960).^J The results of the 1958 survey were summarized by stating
that only the group with the highest potential exposure to parathion,
that is the mixing plant personnel, sustained a definite decreased in
cholinesterase activity during exposure. There was a significant excre-
tion of £-nitrophenol during the period of exposure for mixing plant
personnel, part-time ground applicators, commercial ground applicators,
aircraft application workers and workers in orchards. Furthermore, the
excretion of j>-nitrophenol by residents near the orchard was not sig-
nificant. They observed that j>-nitrophenol excretion was elevated in all
poisoning cases studied.
Bick (1967) in Australia made similar observations on the blood
cholinesterase activity in orchard workers exposed to parathion and other
organophosphorus insecticides and Sevin®. Bick collected blood samples
at the beginning of the spray season in 1962 and 5 weeks later after a
period of extensive spraying. In 1963 he again took samples before
spraying and after spraying. He selected 15 orchard workers who had a
marked decrease in plasma or red blood cell activity in 1962, and he
tested these workers at intervals of 4 to 5 weeks for an additional 13
months, and a final collection was made 6 months later in September of
1965. He reported that the mean values of RBC cholinesterase activity
for the orchard workers in 1962, before and after spraying, were sig-
nificantly less than the value obtained on a control group who lives in
a metropolitan area. After periods when no spraying activity was in-
volved, the plasma and red blood cholinesterase activity increased. It
was Bick1s opinion that the use of the protective measures which had
been recommended by responsible authorities reduced the exposure and was
reflected by the minimal effect seen on red blood cell cholinesterase.
An interesting study was conducted by Ganelin et al. (1964) to
determine if there were any deleterious effects on persons with respira-
tory disease that might be involved in exposure to organophosphorus com-
pounds. This work was done in the Phoenix, Arizona, area, where it is
I/ Elliott, J. W., K. C. Walker, A. E. Penick, and W. F. Durham, "A
Sensitive Procedure for Urinary £-Nitrophenol Determination as a
Measure of Exposure to Parathion,11 J. Agr. Food Ghent.. 8:111
(1960).
115
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known that a large number of people with respiratory and chronic diseases
live. They used 122 subjects, grouped into five specific groups.
Group 1 - Nonasthmatics, no exposure to organic phosphate insecticides,
Group 2 - Nonasthmatics, environmental exposure to organic phos-
phate insecticides.
Group 3 - Asthmatics, no exposure to organic phosphate insecticides.
Group 4 - Asthmatics, environmental exposure to organic phosphate
insecticides.
Group 5 - Nonasthmatics, with occupational exposure to insecticides,
which included the organic phosphate compounds.
The unexposed control subjects lived in Phoenix, and the environ-
mental exposure groups all lived less than 500 yards from cotton fields
treated with the insecticides. Ganelin et al. (1964) found no signifi-
cant differences between asthmatics and nonasthmatics either in the ex-
posed or unexposed groups. The £-nitrophenol excretion values were ex-
tremely low for all persons other than those in the occupational group.
Whereas there are a number of papers reported in the early 1950's
on the occupational hazards of the use of organophosphorus insecticides
in mixing and application by spraying, either from the ground or from
the air, there are very few reports concerning the immediate effect of
residual parathion in treated fields on workers or on establishment of
adequate reentry intervals. Conley reported, in a scientific meeting
in 1952, an episode where a number of workers in a vineyard which had
been sprayed 33 days before with parathion became ill about 7 hr after
work began (quoted by Quinby and Lemmon, 1958). Sixteen of the 24 de-
veloped symptoms requiring hospitalization. As far as is known, none
had previous exposure to cholinesterase inhibitors. These workers suf-
fered from weakness, diarrhea, miosis, headaches, and nausea. Symptoms
were relieved with 1/100 g of atropine. There have been conflicting
reports on the development of illness of workers in picking tobacco as
related to insecticide residues. Lieben et al. (1953) recorded suspected
parathion poisoning in tobacco pickers in Connecticut. Schaefer and
Vance (1953)— measured parathion residues on tobacco, and stated that
\J Schaefer, R. A., and G. M. Vance, "Exposure of Connecticut Tobacco
Workers to Parathion," AMA Arch. Ind. Hyg. Occup. Med.. 7:193-196
(1953).
116
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few proved illnesses from skin absorption of parathion came to the atten-
tion of the Connecticut State Department of Health although there were
thousands of workers handling tobacco leaves. Some interesting results
have been obtained by Braid and Dustan (1955)i' on the persistence of
parathion residues on immature peaches. They found that residues per-
sisted on the fruit for 14 to 20 days and on the leaves for approximately
2 days. Bobb (1954)—/ found that the ha If-life of parathion on peach
tree bark was about 2 weeks, while only 27, of the residue persisted on
the leaves after 1 week. Quinby and Lemmon (1958) investigated para-
thion poisoning in crop workers exposed to residues on pears, grapes,
apples, hops, and citrus fruit in 11 different locations. Excellent de-
tail is given in this paper on the symptoms and the types of exposure
under many different situations. In some cases mild poisoning has been
produced in workers thinning, picking, cultivating, and irrigating the
aforementioned crops that were treated with 1 Ib or more of parathion per
acre. Several of the incidences of poisoning involved exposure to foliage
or fruits sprayed not more than 2 days earlier. It is rather remarkable
that contract with pear trees, citrus trees, and grapevines caused poison-
ing as much as 12, 17 and 33 days, respectively, after application of
parathion. These investigators noted that in the group of outbreaks one
common feature was that the foliage was chest-high. The main difference
in the clinical picture between poisoning which resulted from contact
with plants or from exposure during spraying and dusting was the rela-
tive mildness, the gradual onset, and the benign nature of the symptoms.
3/
As has been reported by Ware et al {1973)- the determination of safe
reentry intervals is influenced by a number of factors including, (1)
frequency and rate of application, (2) characteristics of the foliage,
(3) height of the foliage, (4) density of the canopy, (5) the weather,
and (6) inherent characteristics relative to the particular pesticide
applied, i.e., persistence, toxicity, penetratability, etc. Other
factors involved are length of exposure time, the type of clothing worn
I/ Braid, P. E., and 6. G. Dustan, "Parathion Residues on Immature
Peaches and the Hazard in Spraying and Thinning Operations," J.
Econ. Entomol.. 48:44-46 (1955).
2/ Bobb, M. L., "Parathion Residues on Peach Bark and Foliage," J^
Econ. Entomol.. 47:190-191 (1954).
31 Ware, 6. W., D. P. Morgan, B. J. Estesen, W. P. Cahill, and D. M.
Whitacre, "Establishment of Reentry Intervals for Organophosphate-
Treated Cotton Fields Based on Human Data: I. Ethyl and Methyl
Parathion," Arch. Environ. Contain. Toxicol., 1:48-50 (1973).
117
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and presence or absence of respiratory protection. The recommended re-
entry time established must be long enough to give protection to the
worker but short enough to be tenable with profitable agriculture
practice.
In the study reported by Ware et al. (1973) on aerial application
of a mixture containing 0.5 Ib of methyl parathion, 0.5 Ib of ethyl
parathion and 2.0 Ib of toxaphene in 5 gal. of spray per acre. The crop
was mature cotton with bolls beginning to open. Ten minutes after ap-
plication two men entered the field and collected samples for 30 min;
this operation was repeated at 12, 24, 48, and 72 hr after insecticide
treatment.
Biomedical data indicated that there was no clinical evidence of
plasma or RBC cholinesterase depression or of urinary £-nitrophenol in
either subject (man) even when the field was entered immediately after
treatment.
Ware et al. (1973) reported that from the accumulation of residues
on skin and clothing that an individual can expect exposure to the fol-
lowing amounts of mixed residues during a 30-min period at the treatment
time indicated after treatment of a cotton field with methyl and ethyl
parathion.
Time after Hands and Clothing Inhalation
treatment (hr) forearms (mg) (mg) (mg/ml)
0 3.47 18.21 1.06
12 1.93 12.11 0.60
24 1.16 6.57 0.36
48 0.60 4.52 0.18
72 0.31 2.65 0.09
These authors (Ware et al., 1973) suggest that with cotton, reentry
can be safely made 12 to 24 hr after spraying with parathion.
118
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Outstanding summaries of the exposure of workers to pesticides have
been made by Wolfe et al. (1967)i/ and Hayes (1971).I/ Hayes (1971) has
brought together (based on data from Wolfe et al., 1967), the potential
exposure of workers to ethyl and methyl parathion, malathion, dichlorvos,
chlorthion, carbaryl and azinphos-methyl. Information on parathion was
shown (1) for air-blast spraying fruit orchards, (2)air-blast spraying
orchards with concentrate, (3) spraying orchards with high-pressure powered
handguns, and (4) spraying tomato plants with mist from hand-operated
knapsack sprayer. The highest exposure (respiratory) to parathion was
for spraying orchards with high-pressure powered handguns. The greatest
exposure (dermal) to parathion was air-blast spraying of fruit orchards.
Hayes (1971) expressed the thinking that, although the concentra-
tions of pesticides in working areas very often exceed threshold limit
values, the reported concentrations are not necessarily dangerous. The
threshold limit values for industrial chemicals of comparative toxicity
are usually higher than that for pesticides. A statement was made by
Hayes that about 80% of the total absorption of parathion is by the dermal
route under orchard spraying conditions. Hayes (1971) summarized factors
influencing respiratory and dermal exposure:
1. Type of formulation.
2. The concentration of the formulation.
3. The method of application.
4. The duration of application.
5. The type of work.
6. The wind and other environmental factors.
7. The attitude of the workers.
As one would expect, the variations of the exposure are wide (Wolfe
et al, 1967); dermal exposure could range as much as 200-fold and
\l Wolfe, H. R., W. F. Durham., and J. F. Armstrong, "Exposure of Workers
"~ to pesticides," Arch. Environ. Health, 14:622-633 (1967).
2/ Hayes, W. J., Jr., "Studies on Exposure During the Use of Anti-
cholinesterase pesticides, "Bulletin of the World Health Organiza-
tion. 44:277-288 (1971).
119
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the respiratory exposure in. the form of concentrate might range up to
300-fold. The type of spraying is also influential. Spraying into
trees affords much more exposure to the operator than similar spraying
on row crops. Wind speed is so important that some states have laws
specifying the highest velocity for application of certain types of
herbicides. Another environmental factor is temperature. It has been
shown (Funckes et al., 1963) that temperature affects the rate of absorp-
tion through the skin.
The potential for oral exposure from eating food items contaminated
with parathion as a result of handling with unwashed hands was evaluated
in a study by Armstrong et al. (1973).!' Two situations were considered:
(1) the effect of drift during spray operations on food items carried by
workers and (2) the contamination of foods by the hands of workers who had
been exposed to treated foliage, etc. (fruit thinners).
The results of this study indicated that the potential exposure re-
sulting from contamination of food items by unwashed hands is not high
under normal conditions of apple thinning or in the application of dilute
spray solutions. The daily intake of parathion under the conditions de-
scribed above was reported to be below 3 mg/day.
Higher intakes of insecticides by hand contamination of snack items
can be expected where sprayers carry food items such as candy bars and
where concentrated formulations are being handled.
Wolfe et al. (1967) indicated that the morbidity of persons who are
exposed from occupational standpoint is not great because (1) the
dangerous operations only occupy a few hours a day or a week; (2) the
workers usually wear protective clothing; and (3) the absorption by
workers in the field is not comparable to exposures administered to laboratory
animals.
Manufacturing operations - The number of studies conducted on the
relationship of the manufacturing and packaging of parathion as to industrial
hazards is limited.
Brown and Bush (1950)^' made a study of parathion in the atmosphere of
an industrial plant which manufactured the concentrated material.
I/ Armstrong, J. F., H. R. Wolfe, S. W. Comer, and D. C. Staiff, "Oral
Exposure of Workers to Farathion Through Contamination of Food Items,"
Bull. Environ. Contain. Toxicol.. 10:3218-3327 (December 1973).
27 Brown, H. V., and A. F. Bush, "Parathion Inhibition of Cholinesterase,"
Arch. Ind. Hyg. Occup. Med.. 1:833-636 (1950).
120
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They placed air samplers at the sites of different operations to measure
the parathion. In addition, the plasma and red blood cell cholinesterase
of the persons in the plant were determined. The evaluations for the
red blood cell cholinesterase were made over a period of 1 year at
intervals of 2, 3, and 5 months. The subjects were chemists, janitors,
utility men, engineers, supervisors, workers in mixing rooms, handymen,
and the plant superintendent. The data indicated that they felt that a
physiological effect was produced. Although the air samples showed a
maximum concentration of only 8 mg of parathion per 10 mj of air, they
felt that these concentrations may be potentially dangerous if breathed
over a long period of time. Another in-plant study was made in later
years by Hartwell and Hayes (1965).±' Using two plant sites as a test base,
these investigators compared the effectiveness of certain respiratory pro-
tection. Plant A18 ventilation system, was found to be deficient. Plant
B was a modern facility. The general ventilation was considered quite
adequate, and only nontoxic dusts were handled manually. Each formulating
plant processed phosdrin, methyl parathion, and ethyl parathion. They
both evaluated poisoning by clinical signs as well as a depression of the
cholinesterase activity of 20% or more. During the first year Plant A
sustained 17 cases of alleged poisoning, and depression in cholinesterase
activity of 20% was observed 41 times among 26 subjects. This load of
toxicity led to the installation of a system to distribute uncontaminated
compressed air to workers engaged in hazardous operations. After these
alterations no cases of poisoning occured, and depressions in cholinesterase
activity were observed only four times among 13 workers. Plant B, which
theoretically afforded better protection, had to shut down for 10 days
because of the occurence of poisoning. The fault was due to a compresser
that both supplied air to the operators and forced concentrates into the
mixing chamber. When a separate compressor was used for each operation,
no cases of poisoning were observed.
Accidents - Parathion is one of the pesticides most frequently cited
in incidents involving accidental exposure to pesticides. Preliminary data
from the EPA Pesticide Accident Surveillance System (PASS) shows that para-
thion is the third most frequently cited pesticide in 1973. Based on an
analysis of PASS data, Osmun (1974)-' stated that for 1972 and 1973, parathion
and/or methylparathion were connected with 78% of the reported episodes re-
lating to agricultural jobs, particularly those involving fields sprayed
with pesticides for which safe reentry times for workers had been set.
I/ Hartwell, W. V., and F. R. Hayes, Jr., "Respiratory Exposure to Organic
Phosphorus Insecticides," Arch. Environ. Health, 11:564-568 (1965).
21 Osmun. J. V., "PASS Information Relating to Agriculture Jobs," Internal
EPA Memo to Ed Johnson (1 April 1974).
121
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There are a number of limitations in attempting to use PASS data. First
of all, the cause-effect relationship between the pesticide(s) cited and
the effects observed have generally not been established. Secondly, only
data for 1972 through about January 1974 has generally been computerized
and readily available for retrieval. Thirdly, a large portion of the
data provided to PASS comes from California (e.g., 95 of the 257 parathion
episodes involving humans, animals, plants, and area contamination in the
computerized data base). This skewed distribution is probably a result
of the method used by California to document pesticide information. In
addition, files on the investigations made to follow up on episodes
reported in California are not part of the PASS data base. Information
in addition to that found on the pesticide episode reporting form was
available on only 12 of the 257 episodes involving parathion.
On 10 June 1974, protection standards for agricultural workers in
fields treated with parathion became effective (Quarles, 1974)1/.
These standards prohibit application of parathion when unprotected
workers are in the area being treated and require that unprotected
workers not enter fields treated with pesticides for at least 48 hr.
I/ Quarles, J., "Worker Protection Standards for Agricultural Pesticides,"
Federal Register. 39(92):16888-16891 (10 May 1974).
122
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References
Ackermann, H., and R. Engst, "Presence of Organophosphate Insecticides
in the Fetus," Arch. Toxikol.. 26:17-22 (1970).
Ahmed, M. K., J. E. Casida, and R. E. Nichols, "Bovine Metabolism of
Organophosphorus Insecticides: Significance of Rumen Fluid with
Particular Reference to Parathion," J. Agr. Food Chem.. 6:740-746
(1958).
Alary, J-G., and J. Brodeur, "Correlation Between the Activity of Liver
Enzymes and the 11)50 of Parathion in the Rat," Can. J. Physiol.
Pharmacol., 48:829-831 (1970).
Aldridge, W. N., "Serum Esterases, 2. An Enzyme Hydrolysing Diethy1
£-Nitrophenyl Phosphate (E600) and Its Identity with the A-Esterase
of Mammalian Sera," Biochem. J.. 53:117-124 (1953).
Al-Hachim, 6. M., and 6. B. Fink, "Effect of DDT or Parathion on the
Minimal Electroshock Seizure Threshold of Offspring from DDT or Para-
thion-Treated Mothers," Psychopharmacol., Berlin, 13:408-412 (1968a).
Al-Hachim, 6. M., and 6. B. Fink, "Effect of DDT or Parathion on Condi-
tion Avoidance Response of Offspring from DDT or Parathion-Treated
Mothers," Psychopharmacol.. Berlin, 12:424-427 (1968b).
Al-Hachim, 6. M., and 6. B. Fink, "Effect of DDT or Parathion on Open
Field Behavior of Offspring from DDT- or Parathion-Treated Mothers,"
Psychol. Rept.. 22:1193-1196 (1968c).
Andersen, A. A., and 0. Karlog, "Elimination of Parathion in Cows After
Oral and Dermal Administration." Acta Vet. Scand.. 4:156-169 (1963).
Anon., "Toxic Hazards of Pesticides to Man. Report of a Study Group,"
WHO Tech. Rept. Ser.. 114:3-51 (1956).
Anon., Council of Europe-Netherlands Report on Parathion and Parathion-
Methyl, Ministerie von Sociale Zahen En Volksgenzandheid (1964).
123
-------
Armstrong, J. F., H. R. Wolfe, S. W. Coiner, and D. C. Staiff, "Oral
Exposure of Workers to Parathion Through Contamination of Food
Items," Bull. Environ. Contain. Toxicol., 10:321-327 (December 1973).
Arterberry, J. D., W. F. Durham, J. W. Elliot, and H. R. Wolfe, "Expo-
sure to Parathion," Arch. Environ. Health, 3:476-485 (1961).
Baeza, C., A. M. Goldberg, and R. J. Rubin, "Effect of Carbon Monoxide
on Response to Parathion and Paraoxon," Toxicol. Appl. Pharmacol.,
22(2):288 (1972).
Barnes, J. M., and F. A. Denz, "The Chronic Toxicity of £-Nitrophenyl
Diethy1 Thiophosphate (E. 605): A Long-Term Feeding Experiment with
Rats." J. Hyg., 49:430-441 (1951).
Barnett, D. C., "The Effect of Some Insecticide Sprays on Wildlife,"
Proc. 30th Ann. Conf. West. Assoc. State Game and Fish Commissioners,
pp. 125-134 (1950).
Bass, S. W., A. J. Triolo, and J. M. Coon, "Effect of DDT on the Toxic-
ity and Metabolism of Parathion in Mice," Toxicol. Appl. Pharmacol.,
22:684-693 (1972).
Batchelor, 6. S., and K. W. Walker, "Health Hazards Involving In-Use of
Parathion in Fruit Orchards of North Central Washington," Arch. Ind.
Hyg.. 10:522 (1954).
Beck, S. D., "Effect of Insecticides on the Metabolism and Motility of
Mammalian Spermatozoa," J. Econ. Entomol., 46:570-574 (1953).
Benke, G. M., K. L. Cheever, F. E. Mirer, and S. D. Murphy,. "Comparative
Toxicity, Anticholinesterase Action and Metabolism of Methyl Parathion
in Sunfish and Mice," Toxicol. Appl. Pharmacol., 28:97-109 (1974).
Bick, M., "The Effect of Blood Cholinesterase Activity of Chronic Expo-
sure to Pesticides," Med. J. Aust.. 2:1066-1070 (27 May 1967).
Bobb, M. L., "Parathion Residues on Peach Bark and Foliage," J. Econ.
Entomol.. 47:190-191 (1954).
Braid, P. E., and G. G. Dustan, "Parathion Residues on Immature Peaches
and the Hazard in Spraying and Thinning Operations," J. Econ. Entomol.,
48:44-46 (1955).
Brodeur, J., and K. P. DuBois, "Comparison of Acute Toxicity of Anti-
cholinesterase Insecticides to Weanling and Adult Male Rats," Proc.
Soc. EXP. Biol. Med., 114(2):509-511 (November 1963).
124
-------
Brown, H. V., and A. F. Bush, "Parathlon Inhibition of Cholinesterase,"
Arch. Ind. Hyg. Occup. Med.. 1:633-636 (1950).
Brown, H. W., "Electroencephalographic Changes and Disturbance of Brain
Function Following Human Organophosphate Exposure," Northwest Med.,
70:845-846 (1971).
Buchet, J. P., and R. Lauwerys, "Inhibition of Rat Heart Diolein Hydro-
lase and Brain Acetylcholinesterase by Organophosphate Esters in
vitro," Biochim. Biophys. Acta. 218:369-371 (1970).
Buchet, J. P., and R. Lauwerys, "Characterization of a Diglyceride Lip-
ase in Rat Heart and Intestine," Life Sci., 10:371-376 (1971).
Butler, P. A., A. J. Wilson, Jr., and A. J. Rick, "Effect of Pesticides
on Oysters." Proc. Nat. Shellfish Assoc., 51:23-32 (1962).
Cook, J. W., "In vitro Destruction of Home Organophosphates Pesticides
by Bovine Rumen Fluid," J. Agr. Food Chem., 5(11):859-863 (1957).
Culver, D., J. Kinosian, W. Thielen, and R. Graul, "A Study of Exposure
to Parathion in a Greenhouse," AMA Arch. Ind. Health, 18:235-247 (1958).
Dahm, P. A., F. C. Fountaine, J. C. Pankaskie, R. C. Smith, and F. W.
Atkeson, "The Effects of Feeding Parathion to Dairy Cows," J. Dairy
Sci.. 33(101):747-757 (1950).
Dahm, P. A., "Some Aspects of the Metabolism of Para.thion and Diazinon,"
in Biochemical Toxicology of Insecticides, P. D. O'Brien and I. Yamamoto
(eds.), New York: Academic Press (1970).
Dalloz, J. P., Delatour, and G. Lorgue, "The Organophosphorus Pesticides,"
Rev. Med. Vet., Toulouse, 123(10):1356 (1972).
Davis, H. C., "Effects of Some Pesticides pn Eggs and Larvae of Oysters
(Crassostrea virginica) and Clams (Venus mercenaria)," Commer. Fish.
Rev., 23(12):8-23 (1960).
Davis, H. C., and H. Hidu, "Effects of Pesticides on-Embryonic Develop-
ment of Clams and Oysters and on Survival and Growth of the Larvae,"
Fishery Bull.. 67(2)-.393-403 (1969).
Davison, A. N., "The Conversion of Schradan (OMPA) and Parathion into
Inhibitors of Cholinesterase by Mammalian Liver," Biochem. J., 61:
203-209 (1955).
125
-------
Deichmann, W. B., W. Pugliese, and J. Cassidy, "Effects of Dimethyl and
Diethy1 Paranitrophenyl Thiophosphate on Experimental Animals," AMA
Arch. Ind. Hyg. Occup. Med.. 5:44-51 (1952).
Dikshith, T. S. S., "In vivo Effects of Parathion on Guinea Pig Chromo-
somes," Environ. Physiol. Biochem., 3:161-168 (1973).
DuBois, K. P., J. Doull, P. R. Salerno, and J. M. Coon, "Studies on the
Toxicity and Mechanism of Action of £-Nitrophenyl Diethy1 Thionophos-
phate (Parathion)," J. Pharmacol. Exp. Ther.. 95(1):79-91 (1949).
DuBois, K. P., Postgrad. Med. J.. 24:278-288 (1958).
DuBois, K. P., and F. K. Kinoshita, "Influence of Induction of Hepatic
Microsomal Enzymes by Phenobarbital on Toxicity of Organic Phosphate
Insecticides," Proc. Soc. Exp. Biol. Med., 129:699-702 (1968).
DuBois, K. P., "The Toxicity of Organophosphorus Compounds to Mammals,"
Bulletin of the World Health Organization, 44:233-240 (1971).
Dunachie, J. F., and W. W. Fletcher, "An Investigation of the Toxicity
of Insecticides to Birds' Eggs Using the Egg-Injection Technique,"
Ann. Appl. Biol.. 64(3):409-423 (1969).
Durham, W. F., H. R. Wolfe, and J. W. Elliott, "Absorption and Excretion
of Parathion by Spraymen," Arch. Environ. Health, 24:381-387 (1972).
Ecobichon, D. J., and W. Kalow, "Action of Organophosphorus Compounds
Upon Esterases of Human Liver," Can. J. Biochem. Physiol.. 41:1537-
1546 (1963).
Edson, E. F., "Effects of Prolonged Administration of Small Daily Doses
of Parathion in Rat, Pig and Man," Mimeograph Bulletin, Essex England;
Chesterford Park Research Station NR Saffron Walden, p. 22 (March 1957).
Edson, E. F., and D. N. Noakes, "The Comparative Toxicity of Six Organo-
phosphorus Insecticides in the Rat," Toxicol. Appl. Pharmacol.. 2:523-
539 (1960).
Edson, E. F., et al., "Summaries of Toxicological Data: No-Effect Levels
of Three Organophosphates in the Rat, Pig, and Man," Food Cosmet.
Toxicol., 2:311 (1964).
126
-------
Edson, E. F., D. M. Sanderson, and D. N. Noakes, "Acute Toxicity Data
for Pesticides (1964)," World Rev. Pest Con., 4:36-41 (1965).
Elliott, J. W., K. C. Walker, A. E. Penick, and W. F. Durham, "A Sensi-
tive Procedure for Urinary £-Nitrophenol Determination as a Measure
of Exposure to Parathion," J. Agr. Food Chem.. 8:111 (1960).
Fischer, R., and C. Plunger, "Detection and Quantitative Determination
of Phosphorus Insecticides in Biological Material," Mitt Arch. Toxicol..
21:101-105 (1965).
Fish, S. A., "Organophosphorus Cholinesterase Inhibitors and Fetal
Development," Am. J. Obstet. Gynecol.. 96(8):1148-1154 (1966).
Flockhart, I. R., and J. E. Casida, "Relationship of the Acylation of
Membrane Esterases and Proteins to the Teratogenic Action of Organo-
phosphorus Insecticides and Eserine in Developing Hen Eggs," Biochem.
Pharmacol.. 21:2591-2603 (1972).
Frawley, J. P., E. C. Hagan, and 0. G. Fitzhugh, "A Comparative Pharma-
cological and Toxicological Study of Organic Phosphate-Anticholines-
terase Compounds," J. Pharmacol. Exp. Ther.. 105:156-165 (1952).
Frawley, J. P., and H. N. Fuyat, "Effect of Low Dietary Levels of Para-
thion and Systox on Blood Cholinesterase of Dogs," J. Agr. Food Chem..
5:346 (1957).
Fredriksson, T., W. L. Farrior, Jr., and R. F. Witter, "Studies on the
Percutaneous Absorption of Parathion and Paraoxon. Part I. Hydrolysis
and Metabolism Within the Skin," Acta Derm. Venerol.. 41:335-343 (1961)
Fredriksson, T., "Studies on the Percutaneous Absorption of Parathion
and Paraoxon. Part II. Distribution of 32P-Labelled Parathion Within
the Skin," Acta Derm. Venerol.. 41:344-352 (1961a).
Fredriksson, T., "Studies on the Percutaneous Absorption of Parathion
and Paraoxon. Part III. Rate of Absorption of Parathion," Acta
Derm. Venerol.. 41:353-363 (1961b).
Fredriksson, T., "Studies on the Percutaneous Absorption of Parathion
and Paraoxon. Part VI. In vivo Decomposition of Paraoxon During the
Epidermal Passage," J. Invest. Dermatol.. 42:37-40 (1964).
127
-------
Fukuto, T. R., and R. L. Metcalf, "Metabolism of Insecticides in Plants
and Animals," Ann. N. Y. Acad. Sci.. 160:97-113 (1969).
Funckes, A. J., G. R. Hayes, Jr., and W. V. Hartwell, "Urinary Excretion
of Faranitrophenyl by Volunteers Following Dermal Exposure to Farathion
at Different Ambient Temperatures," J. Agr. Food Chem.. 11:455-457
(1963).
Gabliks, J., and L. Friedman, "Responses of Cell Cultures to Insecticides.
I. Acute Toxicity to Human Cells," Proc. Soc. Exp. Biol. Med.. 120:
163-168 (1965).
Gabliks, J., M. Bantug-Jurilla, and L. Friedman, "Responses of Cell
Cultures to Insecticides. IV. Relative Toxicity of Several Organo-
phosphates in Mouse Cell Cultures," Proc. Soc. Exp. Biol. Med.. 125:
1002-1005 (1967).
Gage, J. C., "A Cholinesterase Inhibitor Derived from 0,0-Diethyl 0-p_-
nitrophenyl Thiophosphate in vivo." Biochem. J.. 54:426-430 (1953).
Gagne, J., and J. Brodeur, "Metabolic Studies on the Mechanisms of In-
creased Susceptibility of Weanling Rats to Parathion," Can. J. Physiol.
Pharmacol.. 50:902-915 (1972).
Gaines, T. B., "The Acute Toxicity of Pesticides to Rats," Toxicol. Appl.
Pharmacol.. 2:88-99 (1960).
Gaines, T. B., W. J. Hayes, Jr., and R. E. Linder, "Liver Metabolism of
Anticholinesterase Compounds in Live Rats: Relation to Toxicity,"
Nature, 209(5018):88-89 (1966).
Gaines, T. B., "Acute Toxicity of Pesticides," Toxicol. Appl. Pharmaco1..
14:515-534 (1969).
Ganelin, R. S., C. Cueto, and G. A. Mail, "Exposure to Parathion: Effect
on General Population and Asthmatics," J. Amer. Med. Assoc., 188:807-
810 (1964).
Gershon, S., and F. H. Shaw, "Psychiatric Sequelae of Chronic Exposure
to Organophosphorus Insecticides," Lancet, pp. 1371-1374 (1961).
Giachetti, A., C. Grasso, and G. Bernard!, "Persistence of 0,0-Diethyl-
0-para-nitrophenyl phosphate (Paraoxon) in the Brain of the White Rat
Treated with a Single, Subtoxic Dose of Parathion," Ric. Sci.. 36(10):
1077 (1966).
128
-------
Goldblatt, M. W., "Organic Phosphorus Insecticides and the Antidotal
Action of Atropine," Pharm. J.. 164:229-233 (1950).
Griffiths, J. T., C. R. Stearns, Jr., and W. L. Thompson, "Parathion
Hazards Encountered Spraying Citrus in Florida," J. Econ. Entomol.,
44:160-163 (1951).
Hamblin, D. 0., and H. H. Golz, "Parathion Poisoning, A Brief Review,"
Ind. Med. Surg.. 24(22):65-72 (1955).
Hamblin, D. 0., and J. F. Marchand, "Parathion Poisoning," Am. Practitioner
and Dig. Treatment. 2:1 (1951).
Hartwell, W. V., G. R. Hayes, Jr., and A. J. Funckes, "Respiratory Expo-
sure of Volunteers to Parathion," Arch. Environ. Health, 8:820-825
(1964).
Hartwell, W. V., and G. R. Hayes, Jr., "Respiratory Exposure to Organic
Phosphorus Insecticides," Arch. Environ. Health. 11:564-568 (1965).
Hayes, G. R. Jr., A. J. Funckes, and W. V. Hartwell, "Dermal Exposure
of Human Volunteers to Parathion," Arch. Environ. Health. 8:829-833
(1964).
Hayes, W. J., Jr., E. M. Dixon, G. S. Batchelor, and W. M. Upholt,
"Exposure to Organic Phosphorus Sprays and Occurrence of Selected
Symptoms," Public Health Reports. U.S. Dept. HEW, Public Health Ser-
vice, 72(9):787-794 (September 1957).
Hayes, W. J., Jr., "Studies on Exposure During the Use of Anticholines-
terase Pesticides," Bulletin of the World Health Organization, 44:277-
288 (1971),
Hayes, W. J., Jr., 1963 Clinical Handbook on Economic Poisons. PHS
Publication No. 476, Washington, D.C. (1963).
Hayes, W. J., Jr., "Toxicity of Pesticides to Man—Risks from Present
Levels," Proc. R. Soc. Lond.. 167(1007):101-127 (1967).
Hazleton, L. W., and E. G. Holland, "Pharmacology and Toxicology of
Parathion," Adv. Chem. Series No. 1. 31:31-38 (1950).
Hitchcock, M., and S. D. Murphy, "Activation of Parathion and Guthion
by Tissues of Mammalian, Avian, and Piscine Species," Fed. Proc.5
26(2):427 (1967a).
129
-------
Hitchcock, M., and S. D. Murphy, "Enzymatic Reduction of 0,0-(4-Nitro-
phenyl) Phosphorothioate, 0,0-Diethyl 0-(4-Nitrophenyl) Phosphate,
and 0-Ethyl 0-(4-Nitrophenyl) Benzene Thiophosphonate by Tissues from
Mammals, Birds, and Fishes," Blochem. Pharmacol., 16(9):1801-1811
(1967b).
Hollingworth, R. M., R. L. Alstott, and R. D. Litzenberg, "Glutathion
S-Aryl Transferase in the Metabolism of Parathion and Its Analogs,"
Life Sci.. 13:191-199 (1973).
Jacobsen, P. L., R. C. Spear, E. Wei, "Parathion and Diisopropylfluoro-
phosphate (DFP) Toxicity in Partially Hepatectomized Rats," Toxicol.
Appl. Pharmacol.. 26:314-317 (1973).
Jegier, Z., "Health Hazards in Insecticides Spraying of Crops," Arch.
Environ. Health, 8:670-674 (1964).
Jensen, J. A., W. F. Durham, and G. W. Pearce, "Studies on Fate of Para-
thion in Rabbits, Using Radioactive Isotope Techniques," AMA Arch.
Ind. Hyg. Occup. Med.. 6:326-331 (1952).
Kanagartanam, K., W. H. Boon, and T. K. Hoh, "Parathion Poisoning from
Contaminated Barley," Lancet. 1:538-542 (1960).
Khera, K. S., and S. Bedok, "Effects of Thiol Phosphates on Notochordal
and Vertebral Morphogenesis in Chick and Duck Embryos," Food Cosinet.
Toxicol., 5:359-365 (1967).
Khera, K. S., and D. A. Lyon, "Chick and Duck Embryos in the Evaluation
of Pesticide Toxicity," Toxicol. Appl. Pharmacol., 13:1-15 (1968).
Khera, K. S., and D. J. Clegg, "Perinatal Toxicity of Pesticides," Can.
Med. Assoc. J., 100:167-172 (1969).
Kimbrough, R. D., and T. B. Gaines, "Effect of Organic Phosphorus Com-
pounds and Alkylating Agents on the Rat Fetus," Arch. Environ. Health.
16:805-808 (1968).
Kimmerle, G., and D. Lorke, "Toxicology of Insecticidal Organophosphates,"
Pflanz. Nachr. Bayer. 21:111-142 (1968).
Konst, H., and P. J. Plummer, "Acute and Chronic Toxicity of Parathion
to Warm-Blooded Animals," Can. J. Comp. Med. Vet. Sci.. 14:90-108 (1950)
130
-------
Lauwerys, R., and J. P. Buchet, "Effect of Two Organophosphorus Esters
on Mammary Careinogenesis by 7,12-Dimethylbenz(a)anthracene," Eur.
J. Toxicol.. 5:163-167 (1972).
Lewis, W. H., and A. G. Richards, Jr., "Non-Toxicity of DDT on Cells in
Cultures," Science. 102:330-331 (1945).
Lichtenstein, E. P., T. W. Fuhremann, A. A. Hochberg, R. N. Zahlten,
and F. W. Stratman, "Metabolism of [^C] Parathion and f^C] Paraoxon
with Fractions and Subtractions of Rat Liver Cells," J. Agr. Food
Chem.. 21(3):416-423 (1973).
Lieben, J., R. K. Waldman, and L. Krause, "Urinary Excretion of Para-
nitrophenol Following Parathion Exposure," AMA Arch. Ind. Hyg. Occup.
Med.. 6:491-495 (1952).
Litterst, C. L., E. P. Lichtenstein, and K. Kajiwara, "Effects of Insec-
ticides on Growth of HeLa Cells," J. Agr. Food Chem., 17:1199-1203
(1969).
Litterst, C. L., and E. P. Lichtenstein, "Effects and Interactions of
Environmental Chemicals on Human Cells in Tissue Culture," Arch.
Environ. Health. 22:454-459 (1971).
Lutz, H., and Y. Lutz-Ostertag, "The Action of Different Pesticides on
the Development of Bird Embryos," Drugs and Fetal Development, Proc.
International Symposium on the Effect of Prolonged Drug Usage on Fetal
Development, Beit-Berl, Kfar Saba, Israel, September 1971, pp. 127-
150 (1972).
Lutz-Ostertag, Y., and R. Meiniel, "In vitro Sterilizing Effect of
Parathion on Embryonic Ovaries of Chick and Quail," C. R. Acad. Scl..
Paris, Series D, 267:2178-2180 (1968).
Lutz-Ostertag, Y., R. Meiniel, and H. Lutz, "Action du parathion sur le
developpement de 1'embryon de caille," C. R. Acad. Set.. Paris, Series
D, 268:2911-2913 (1969a).
Lutz-Ostertag, Y., R. Meiniel, and H. Lutz, "Effects du parathion sur
le developpement de 1'embryon de caille et de certains de ses organes
in vivo et in vitro." Biol. Abstr., 52(22):12, 271 (1969b).
131
-------
Lutz-Ostertag, Y., R. Meiniel, and H. Lutz, "Parathion, Embryonic
Development, Sterilization and Estrogenic Effects in Birds; Compari-
son with the Effects of Aldrin," Annee/Biol.. 9:501-507 (1970).
Maibach, H. I., R. J. Feldmann, T. H. Milby, and W. F. Serat, "Regional
Variation in Percutaneous Penetration in Man," Arch. Environ. Health,
23:208-211 (1971).
Malkinson, F., "Percutaneous Absorption of Toxic Substances in Industry,"
AMA Arch. Ind. Health. 21:87-99 (1960).
Marliac, J. P., "Toxicity and Teratogenic Effects of 12 Pesticides in
the Chick Embryo," 48th Ann. Meeting Fed. Amer. Soc. Exp. Biol.. 105
(1964).
Matsumura, F., and C. T. Ward, "Degradation of Insecticides by the Human
and the Rat Liver," Arch. Environ. Health. 13:257-261 (1966).
Medved, L. I., E. I. Spynu, and lu. S. Kagan, "The Method of Conditioned
Reflexes in Toxicology and Its Application for Determining the Toxic-
ity of Small Quantities of Pesticides," Residue Rev.. 6:42-74 (1964).
Meiniel, R., Y. Lutz-Ostertag, and H. Lutz, "Teratogenic Effects of
Parathion (Organophosphorus Insecticide) on the Skeleton of the Embryo
of the Japanese Quail (Coturnix coturnix japonica)," Arch. Anat.
Microsc. Morphol. Exp., 59(2):167-183 (1970).
Milby, T. H., and F. Ottoboni, "Report of an Epidemic of Organic Phosphate
Poisoning in Peach Pickers, Stanislaus County, California," State of
California Department of Health, Bureau of Occup. Health (1963).
Mol, J. C. M., D. L. Harrison, and R. H. Telfer, "Parathion: Toxicity
to Sheep and Persistence on Pasture and in Soil," N. Z. J. Agr. Res..
15:306-320 (1972).
Mrak, E. M., "Report on the Secretary's Commission on Pesticides and
Their Relationship to Environmental Health," U.S. Dept. HEW, p. 665
(1969).
Muller, H. D., and D. C. Lockman, "Fecundity and Progeny Growth Following
Subacute Insecticide Ingestion by the Mallard," Foul. Sci.. 51:239-241
(1972).
Nabb, D. P., W. J. Stein, and W. J. Hayes, Jr., "Rate of Skin Absorption
of Parathion and Paraoxon," Arch. Environ. Health. 12:501-505 (1966).
132
-------
Nakatsugawa, T., and P. A. Dahm, "Microsomal Metabolism of Parathion,"
Blochem. Pharmacol.. 16(l):25-38 (1967).
Nakatsugawa, T., N. M. Tolaman, and P. A. Dahm, "Degradation of Para-
thion in the Rat," Biochem. Pharmacol.. 18(5):1103-1114 (1969).
Namba, T., "Cholinesterase Inhibition by Organophosphorus Compounds and
Its Clinical Effects," Bulletin of the World Health Organization,
44:289-307 (1971).
Natoff, I. L., "Influence of the Route of Administration on the Toxicity
of Some Cholinesterase Inhibitors," J. Phar. Pharmacol.. 19:612-616
(1967).
Natoff, I. L., "Influence of the Route of Exposure on the Acute Toxicity
of Cholinesterase Inhibitors," Europ. J. Toxicol.. 3:363-367 (1970).
Neal, R. A., "Studies of the Enzymic Mechanism of the Metabolism of
Diethyl 4-Nitrophenyl Phosphorothionate (Parathion) by Rat Liver
Microsomes," Biochem. J., 105:289-297 (1967a).
Neal, R. A., "Studies on the Metabolism of Diethyl 4-Nitrophenyl Phos-
phorothionate (Parathion) in vitro." Biochem. J.. 103:183-191 (1967b).
Neal, R. A., "A Comparison of the in vitro Metabolism of Parathion in
the Lung and Liver of the Rabbit," Toxicol. Appl. Pharmacol., 23:123-
130 (1972).
Neill, D. D., H. D. Muller, and J. V. Shutze, "Pesticide Effects on the
Fecundity of the Gray Partridge," Bull. Environ. Contam. Toxicol..
6(6):546-551 (1971).
Nevkovic, N., S. Vitorovic, and M. Plesnicar, "The Role of Liver Microsomal
Enzymes in the Metabolism of Parathion," Biochem. Pharmacol., 22:2943-
2946 (1973).
Norman, B. J., J. A. Roth, and R. A. Neal, "Effect of Temperature on the
Mixed Function Oxidase-Catalyzed Metabolism of 0,0-Diethyl £-Nitrophenyl
Phosphorothionate (Parathion)," Toxicol. Appl. Pharmacol.. 26:203-208
(1973a).
133
-------
Norman, B. J., W. K. Vaughn, and R. A. Neal, "Studies of the Mechanisms
of Metabolism of Diethyl £-Nitrophenyl Phosphorothionate (Parathion)
by Rabbit Liver Microsomes," Biochem. Pharmacol.. 22:1091-1101 (1973b).
O'Brien, R. D., Toxic Phosphorus Esters. New York: Academic Press,
pp. 227-228 (1960).
Oga, S., C. C. Pellegatti, S. Reis, and A. C. Zanini, "Toxic and/or
Teratogenic Activity of Anticholinesterase Compounds. I. Tetato-
genicity of Parathion in Chicken Embryos," Rev. Farm. Bioquim. Univ.
Sao Paulo. 9(2):343-355 (1971).
Orzel, R. A., and L. R. Weiss, "The Effect of Various Chemicals on Rat
Brain Cholinesterase Inhibition by Parathion," Arch. Int. Pharmacodyn.
Ther.. 164(1):150-157 (1966).
Osmun, J. W., "PASS Information Relating to Agricultural Jobs," Internal
EPA Memo to Ed Johnson (1 April 1974).
Pankaskie, J. E., F. C. Fountaine, and P. A. Dahm, "The Degradation and
Detoxification of Parathion in Dairy Cows," J. Econ. Entomol.. 45:
51-60 (1952).
Phillips, W. E. J., G. Hatina, D. C. Villeneuve, and D. L. Grant, "Effect
of Parathion Administration in Rats Following Long-Term Feeding with
PCB's," Environ. Physiol. Biochem.. 2:165-169 (1972).
Quarles, J., "Worker Protection Standards for Agricultural Pesticides,"
Federal Register, 39(2):16888-16891 (10 May 1974).
Quinby, G. E., and A. B. Lemmon, "Parathion Residues as a Cause of
Poisoning in Crop Workers," J. Amer. Med. Assoc., 166(7):740-746 (1958).
Radeleff, R. D., and G. T. Woodard, "The Toxicity of Organic Phosphorus
Insecticides to Livestock," J. Am. Vet. Med. Assoc.. 130:215-216 (1957),
Radeleff, R. D., G. T. Woodard, W. J. Nickerson, and R. C. Bushland,
"Part II. Organic Phosphorus Insecticides," The Acute Toxicity of
Chlorinated Hydrocarbon and Organic^Phosphorus Insecticides to Live-
stock, U.S. Dep. of Agriculture, Tech. Bull. 1122, pp. 35-46 (1955).
134
-------
Radeleff, R. D., "The Toxicity of Insecticides and Herbicides to Live-
stock," Adv. Vet. Sci.. 4:265-276 (1958).
Radeleff, R. D., and R. C. Bushland, "The Toxicity of Pesticides for Live-
stock, "Symposium: The Nature and Fate of Chemicals Applied to Soils,
Plants, and Animals," Agricultural Research Service, U.S. Dep. of Agriculture
Rider, J. A., and H. C. Moeller, "Tolerance of Organic Phosphates in
Man," Progress Report of Franklin Hospital Foundation, San Francisco,
California (1 October 1963).
Rider, J. A., and H. C. Moeller, "Studies on the Anticholinesterase
Effects of Systox and Methyl Parathion in Humans," Fed. Proc.. 23(2):
176 (1964).
Rider, J. A., H. C. Moeller, and E. J. Puletti, "Continuing Studies on
Anticholinesterase Effect of Methyl Parathion, Initial Studies with
Guthion, and Dichlorvos on Humans," Fed. Proc.. 26(2):427 (1967).
Rider, J. A., H. C. Moeller, E. J. Puletti, and J. I. Swader, "Toxicity
of Parathion, Systox, Octame thy1 Pyrophosphoramide, and Methyl Para-
thion in Man," Toxicol. Appl. Pharmacol., 14(3):603-611 (1969a).
Rider, J. A., and E. J. Puletti, "Studies on the Anticholinesterase
Effects of Gardona, Methyl Parathion, and Guthion in Human Subjects,"
Fed. Proc., 28(2):479 (1969b).
Roan, C. C., D. P. Morgan, N. Cook, and E. H. Paschal, "Blood Cholines-
terases, Serum Parathion Concentrates and Urine £-Nitrophenol Concen-
trations in Exposed Individuals," Bull. Environ. Contarn. Toxicol.,
4(6):362-369 (1969).
Roger, J-C., D. G. Upshall, and J. E. Casida, "Structure-Activity and
Metabolism Studies on Organophosphate Teratogens and Their Alleviating
Agents in Developing Hen Eggs with Special Emphasis on Bidrin,"
Biochem. Pharmacol., 18(2):373-392 (February 1969).
Rosival, L., F. V. Selecky, and L. Vbrovsky, "Acute Experimental Poison-
ing with Organophosphorus Insecticides," Bratisl. Lek. Listy, 38:151-160
(1958).
135
-------
Roudabush, R. L., C. J. Terhaar, D. W. Fassett, and S. P. Dziuba, "Com-
parative Acute Effects of Some Chemicals on the Skin of Rabbits and
Guinea Pigs," Toxicol. Appl. Pharmacol., 7:559-565 (1965).
Sakai, K., and F. Matsumura, "Degradation of Certain Organophosphate
and Carbamate Insecticides by Human Brain Esterases," Toxicol. Appl.
Pharmacol.. 19(4):660-666 (1971).
Schaefer, R. A., and G. M. Vance, "Exposure of Connecticut Tobacco
Workers to Parathion," AMA Arch. Ind. Hyg. Occup. Med.. 7:193-196
(1953).
Shellenberger, T. E., G. W. Newell, R. F. Adams, and J. Barbaccia,
"Cholinesterase Inhibition and Toxicologic Evaluation of Two Organo-
phosphate Pesticides in Japanese Quail," Toxicol. Appl. Pharmacol.,
8:22-28 (1966).
Shishido, T., and J. Fukami, "Studies on the Selective Toxicites of
Organic Phosphorus Insecticides (II)," Botyu-Kagaku. 28(l):69-76
(February 1963).
Spynu, E. I., "Data Concerning the Toxicology of the Insecticide Niuiph
100 and the Establishment of Tolerance Limits," Dissertation, Kiev
(1952).
Spynu, E. I., "The Effect of Some Organophosphorus Insecticides on the
Higher Nervous Activities and on the Cholinesterase Activity," The
Chemistry and Application of Organophosphorus Compounds, Acad. Sci.
USSR (ed.), Moscow (1957).
Stevens, J. T., "The Effect of Parathion on the Metabolism of 3H-Testos-
terone by Hepatic Microsomal Enzymes from the Male Mouse," Pharmacology,
10(4):220-225 (1973).
Sumerford, W. T., W. J. Hayes, Jr., J. M. Johnston, K. Walker, and
J. Spillane, "Cholinesterase Response and Symptomatology from Ex-
posure to Organic Phosphorus Insecticides," AMA Arch. Ind. Hyg. Occup.
Med., 7:383-398 (1953).
Taylor, W. J., and Z. N. Gaut, "Poisoning with the Newer Organophosphorus
Insecticides," Int. J. Clin. Pharmacol.. 1(3):175-183 (1968).
Technical Development Laboratories, Communicable Disease Center, Clini-
cal Memoranda on Economic Poisons. U.S. Dept. HEW, Public Health
Service, pp. 7-12 and 17-21 (1 April 1956).
136
-------
Triolo, A. J., and J. M. Coon, "Toxicologic Interactions of Chlorinated
Hydrocarbon and Organophosphate Insecticides," J. Agr. Food Chetn.,
14(6):549-555 (1966).
Tsachalinas, D., G. Logaras, and A. Paradelis, "Observations on 246
Cases of Acute Poisoning with Parathion in Greece," Eur. J. Toxicol..
4:46-49 (1971).
Villeneuve, D. C., W. E. J. Phillips, and J. Syrotiuk, "Modification of
Microsomal Enzyme Activity and Parathion Toxicity in Rats," Bull.
Environ. Contain. Toxicol., 5(2): 125-132 (1970).
Villeneuve, D. C., and W. E. J. Phillips, "The Effect of Acute Ethanol
Administration on Parathion Toxicity and in vitro Parathion Degrada-
tion on the Rat," Can. J. Physiol. Pharmacol.. 49:481-483 (1971).
Villeneuve, D. C., R. F. Willes, J. B. Lacroix, and W. E. J. Phillips,
"Placental Transfer of ^C-Parathion Administered Intravenously to
Sheep," Toxicol. Appl. Pharmacol.. 21:542-548 (1972).
Vukovich, R. A., A. J. Triolo, and J. M. Coon, "The Effect of Chlorpro-
mazine on the Toxicity and Biotransformation of Parathion in Mice,"
J. Pharmacol. Exp. Thera., 178(2):395-401 (1971).
Ware, G. W., D. P. Morgan, B. J. Estesen, W. P. Cahill, and D. M.
Whitacre, "Establishment of Reentry Intervals for Organophosphate-
Treated Cotton Fields Based on Human Data: I. Ethyl and Methyl
Parathion," Arch. Environ. Con tarn, Toxico 1.. l:48.-59 (1973).
Webb, R. E., C. C. Bloomer, and C. L. Miranda, "Effect of Casein Diets
on the Toxicity of Malathion and Parathion and Their Oxygen Analogues,"
Bull. Environ. Contain. Toxicol., 9(2): 102-107 (1973).
Weiss, L. R., J. Bryant, and 0. G. Fitzhugh, "Blood Sugar Levels Follow-
ing Acute Poisoning with Parathion and 1-Naphthyl N-Methyl Carbamate
(Sevin) in Three Species," Toxicol. Appl.' Pharmacol.. 6(3):363 (1964).
Weiss, L. R., and R. A. Orzel, "Enhancement of Toxicity of Anticholines-
terases by Central Depressant Drugs in Rats," Toxicol. Appl. Pharmacol.,
10:334-339 (1967).
Westerman, E., "Accumulation of Environmental Agents or Their Effects in
the Body," Environ. Res., 2:340-351 (1969).
137
-------
Wilber, C. 6., and R. A. Morrison, "The Physiological Action of Parathion
in Goats," Am. J. Vet. Res., 10(59):308-313 (1955).
Williams, C. H., "B-Glucuronidase Activity in the Senna and Liver of
Rats Treated with Parathion," Toxicol. Appl. Pharmacol.. 16:533-539
(1970).
Williams, J. W., and J. T. Griffiths, "Parathion Poisoning in Florida
Citrus Spray Operations," J. Fla. Med. Assoc., 37:707-709 (1951).
Wolfe, H. R., W. F. Durham, and J. F. Armstrong, "Exposure of Workers
to Pesticides," Arch. Environ. Health. 14:622-633 (1967).
Wolfe, H. R., W. F. Durham, and J. F. Armstrong, "Urinary Excretion on
Insecticide Metabolites," Arch. Environ. Health, 21:711-716 (1970).
Yamada, A., "Teratogenic Effects of Organophosphorus Insecticides in
the Chick Embryo," Osaka Shiritsu Daigaku Igaku Zasshi. 21:245-255
(1972).
138
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SUBPART II. C. FATE AND SIGNIFICANCE IN THE ENVIRONMENT
CONTENTS
Page
Effects on Aquatic Organisms 141
Fish 141
Laboratory Studies 141
Field Studie 146
Lower Aquatic Organisms 150
Laboratory Studies 150
Field Studies 151
Effects on Wildlife 157
Laboratory Studies 157
Field Studies 161
Effects on Beneficial Insects 163
Bees 163
Parasites and Predators 165
Interactions with Lower Terrestrial Organising. 168
Reviews 168
Field Studies 169
Laboratory Studies 170
139
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Page
Residues in Soil 172
Laboratory Studies 172
Field and Combined Field-Laboratory Studies 179
Short-Term Studies 179
Long-Term Field Studies 183
Monitoring Studies 185
Summary 188
Residues in Water 189
Laboratory and Field Studies 189
Monitoring Studies 193
Residues in Air 193
Residues in Nontarget Plants 195
Bioaccumulation, Biomagnification 196
Environmental Transport Mechanisms 197
References 199
140
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Effects on Aquatic Organisms
Fish -
Laboratory studies - Acute toxicity data for parathion's effect on
fish is summarized in Table 18. It is obvious that toxicity of parathion
varies considerably depending upon the species (see Table 19 for scientific
names of fish) and upon the method used. The toxicities of parathion to
the natural population of fish ranges from a low of 0.047 ppm (48 hr LC50)
in bluegill to a high of 6.25 ppm (48 hr TLm) in carp. Exposure times
used in the studies cited in Table 18 ranged from 2 hr to 1 week. Some
of the differences in toxicity are undoubtedly due to differences in the
maturity of the fish used and in their physical condition.
The effects of maturity on the toxicity of parathion for bluegill
can be inferred from the TLm data in Table 20. There is a difference in
the susceptibility of young (small) bluegill compared to older (large)
bluegill; the larger fish are less susceptible to parathion poisoning.
While the difference in TLm is not great (about two times), the con-
tamination of a water system by parathion at a level below the TLm f°r
adult fish could still have a lethal effect on the immature members of
the population.
Pickering et al. (1962)^' have made a comparison of the toxicity
of organophosphate insecticides for bluegill and white rats (Table 21).
It would be more valid to compare fish toxicity, which is associated
with continuous contact with the pesticide through the gills, with
inhalation data for rats, which are derived through continuous expos-
ure to the respiratory tract. Kimmerle and Lorke (1968)2' reported an
inhalation LCso for male rats to be 0.0315 mg/liter with a 4 hr
exposure time.
The reduction in fish-brain acetylcholinesterase (AChE) activity
may be used to monitor waters for the presence of organophosphate contami-
nants although cautious interpretations should be made (Gibson et al. 1969)-'
Nevertheless, Coppage and Matthews (1974)^' state: "...AChE measure-
ments are probably the best general index of organophosphate poisoning
of fish in the environment."
.!/ Pickering, Q. H., C. Henderson, and A. E. Lemke, "The Toxicity of
Organic Phosphorus Insecticides to Different Species of Warmwater
Fishes." Trans. Am. Fish. Soc.. 91(2):1750184 (1962).
2j Kimmerle, G., and D. Lorke, "Toxicology of Insecticidal Organophos-
phates," Pflanz. Nachr. Bayer. 21:111-142 (1968).
3/ Gibson, J. R., J. L. Ludke, and D. E. Ferguson, "Sources of Error
in the Use of Fish-Brain Acetylcholinesterase Activity as a Monitor
for Pollution," Bull. Environ. Contain. Toxicol.. 4:17-23 (1969).
4/ Coppage, D. L., and E. Matthews, "Short-Term Effects of Organophos-
phate Pesticides on Cholinesterases of Estuarine Fishes and Pink
Shrimp." Bull. Environ. Contam. Toxicol.. 11:483-488 (1974).
141
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Table 18 . ACUTE TOUCHY OF PARATHION TO FISH
Fl»h toted
Fathead minnow
Fathead minnow
Bluegill
Blueglll
Bluegill
Carp
Carp
Rainbow trout
Rainbow trout
Brook trout
Puopklnseed sunflih
Pumpklnseed sunflsh
Green (unflah
Largemouth ban
Mummlchog
Tllapla
Tllapla
Striped mullet
Golden shiner
Bullhead
Mosquito fish
Rice fish
Goldfish
Gupples
Toxlclty
calculated
(oral)
TL50
TLj,
LC50*
"so
n»
401 Mortality
801 Mortality
SOI Mortality
"•50
TI»
U»50
"50
TI*
EC50*
"50
TL.
LC50
"50
IP-0 Mortality
501 Mortality
Toxlclty
measured
(PP»)
1.4-1.6
2.5
0.095
0.047
0.141
3.2-6.25
.00
.00
.30
.80
0.155-0.42
110 mg/kg
0.155
0.19
0.15
0.375
0.60
0.125
0.931
40 mg/kg
0.19
2.9
2.7
0.06
References
a/, b/
c/
I/
e/
I/
I/. &/
i/
£/
a/, d/
I/ "
it
•/
I/
a/
I/
«/
d/
«/
I/
i/
* Because death was used as the end point, \JC$Q, ECjg> *nd TLq, values are comparable.
a/ Pickering et al.. op. clt. (1962).
b/ Henderson, C., and Q. H. Pickering, "Toxlclty of Organic Phosphorus Insecticides to Fish,1'
~ Trans, Am. Fiih.Soc.. 87:39-51 (1958).
£/ Anon., National Water Quality Laboratory (EPA), unpublished data (24 May 1974).
d/ Gibson, J. R., "Comparative Biochemistry of Parathlon Metabolism In Three Species of Fishes,"
Piss. Abstr. Int.. 32i(4): 2365-B (1971).
e/ Federal Water Pollution" Control Administration, "Water Quality Criteria," Report of the National
Technical Advisory Committee, p. 37 (1968).
i/ Sreenlvasan, A., and G. K. Swamlnathan, "Toxicity of Six Organophosphorus Insecticides to Fish,"
~ Curr. Set.. India, 36:397-398 (August 1967).
g/ Nishiuchl, Y., and Y. Hashimoto, "Toxicity of Pesticides to Some Freshwater Organisms," Rev.
Plant Protec. Res.. 2:137-139 (1969).
h/ Mulla, M. S., J. St. Amant, and L. D. Anderson, "Evaluation of Organic Pesticides for Possible
~ Use as Fish Toxicants," Prog. Fish-Cult.. 29(l):36-42 (1967).
if Lewallen, L. L., and W. H. Wilder, "Toxicity of Certain Organophosphorus and Carbamate
Insecticides to Rainbow Trout," Mosquito News. 22(4):369-372 (1962).
i/ Wood, E. M., "The Pathology of Pesticide Toxicity in Fish," Unpublished, USDI, Columbia, Missouri.
k/ Benke, G. M., K. L. Cheever, F. E. Mirer, and S. D. Murphy, "Comparative Toxicity, Anticholln-
esterase Action and Metabolism of Methyl Parathlon in Sunfish and Mice," Toxtcol. Appl. Pharmacol..
28:97-109 (1974).
I/ Lowe", J. I., P. D. Wilson, and R. B. Davlson, "Laboratory Bioassays," Progress Report for Fiscal Year
1969. Bureau of Commercial Fisheries Center for Estuarlne and Menhaden Research, Pesticides
Field Station, Gulf Breeze, Florida, U.S. Dept. Interior, Circular 335, pp. 20-28 (1970).
m/ Lahav, M., and S. Sarlg, "Sensitivity of Pond Fish to Cotnlon (Azinphosmethyl) and Parathlon,"
Bamldgeh. 21(3):67-74 (1970).
n/ Murphy, S. D., R. R. Lauwerys, and K. L. Cheever, "Comparative Antlchollnesterase Action of
Organophosphorus Insecticides in Vertebrates," Toxlcol. Appl. Pharmacol.. 12:22-35 (1968).
142
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Table 19. COMMON AND SCIENTIFIC NAMES OF FISH USED IN CONTROLLED
TOXICITY TESTS WITH PARATHION
Common name Scientific name
Fathead minnow Pimephales promelas
Bluegill Lepomis macrochirus
Carp Cyprlnus carpio
Rainbow trout Salmo gairdneri
Brook trout Salvelinus fontinalis
Green sunfish Lepomis cyanellus
Pumpkinseed sunfish Lepomis gibbosus
Largemouth bass Micropterus salmoldes
Mummichog Fundulus heteroclitus
Tilapia Tilapia aurea
Striped mullet Mugil cephalus
Golden shiner Notemigonus crysoleucas
Black bullhead Ictalurus melas
Mosquito fish Gambusta affinis
Rice fish Oryzias latipes
Goldfish Carassius auratus
Guppy Lebistes reticulatus
Spot Leiostomus xanthurus
Pinfish Lagodon rhomboldes
Table 20. COMPARATIVE TOXICITY OF PARATHION'AND MALATHION
INSECTICIDES TO CENTRARCHIDS
Insecticide
96 hr
Bluegills
small
TL^ (ppm, AI)
Bluegills
large
Green
sunfish
Largemouth
bass
Parathion 0.065 0.14 0.42 0.19
Malathion 0.11 0.24 0.12 0.05
Data from: Pickering et al., op. cit. (1962).
143
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Table 21. TOXICITY OF THREE ORGANOPHOSPHATE INSECTICIDES
TO BLUEGILL AND WHITE RATS
Bluegill White rats
96 hr TL,n Oral LD$Q
Insecticide (mg/1) (me/Kg)
Parathion 0.095 13.0
Methyl Parathion 1.90 28.0
Malathion 0.090 1,375.0
Data from: Pickering et al.. op. cit. (1962).
The relationship between AChE inhibition to death of estuarine
animals was studied by Coppage and Matthew (1974). In this study the
effect of parathion on spot and pinfish AChE activity at concentrations
of LC4Q to LCgg were determined. When spot were exposed to parathion
at 10 ppb for 24 hr, AChE activity (brain) was reduced 88% and when
pinfish were used as the test animal the activity was reduced 90%.
These studies appeared to Indicate that AChE activity reduced to
80% of normal was critical in short-term organophosphate poisonings.
The lethal threshold probably varies among species.
The relationship of brain AChE inhibition to death after exposure
to parathion concentrations that killed from 40 60% of sheepshead
minnows in 2, 24, 48, and 72 hr was studied by Coppage (1972).-' The
AChE activity was measured at 2 hr for the 2-hr lethal dose, at 6 and
24 hr for the 24-hr lethal dose, at 24 and 48 hr for the 48-hr lethal
dose and at 24, 48 and 72 hr for the 72-hr lethal dose.
The 48- and 72-hr exposures caused AChE to fall below 17.7% of
normal for 24 hr preceding death. The 24-hr exposure caused AChE to
fall to and remain below 17.7% for 18 hr prior to death. Death in all
lethal exposures occurred at AChE levels ranging from 0 to 15.4% of
normal.
I/ Coppage, D.L., "Organophosphate Pesticides: Specific Level of Brain
AChE Inhibition Related to Death in Sheepshead Minnows," Trans.
Am. Fish Soc.. 101:534-536 (1972).
144
-------
Problems that may arise by using in vitro reduction of AChE as a
measure of insecticide toxicity were demonstrated by Coppage (1971).*'
He reported that by comparing the percentage of the inhibition of
AChE with the 48-hr LDso of parathion and other organophosphates, good
correlation between the in vitro inhibition and toxicity could not be
established. This author stated that only in vivo inhibition can be a
meaningful indicator of toxicity and that this required bioassays in
order to determine the exact relationship of AChE inhibition to concen-
tration of insecticide, length of exposure and death.
The responses of mosquito fish which had developed a resistance to
organochlorine compounds were compared to those of naturally sensitive
fish when both groups were exposed to parathion (Chambers and Tarbrough,
1974).-' It was shown that organochlorine-resistant populations of
mosquito fish can tolerate more parathion in the spring than in the fall
(about 1.6-fold greater).
The poisoning effects of parathion in fish usually appear first as
erractic movements followed by the fish swimming on its side. As the
poisoning progresses, the fish will come to the surface and gulp for
air. In most studies the cessation of gill movement is taken to be
the time of death.
Parathion poisoning produced lesions in the liver, kidney and
gills. However, the liver changes were nonspecific, generalized
degenerative changes. Characteristic liver changes in moribund fish
were swelling of parenchymal cells and congestion of the sinusoids.
The kidney lesions were apparently glomerular damage with the appearance
of proteinaceous material both in Bowman's space and in the connecting
tubules. Pathology of the gill consisted primarily of thickening of
the epithelial layer surrounding the capillaries of the individual
lamellae.-'
Parathion poisoning in the frog is reported to produce anemia and
leucopenia. Increases in concentration resulted in a progressive
neutropenia and a lymphocystosis. Clotting time was increased.
I/ Coppage, D. L., "Characterization of Fish Brain Acetylcholinesterase
with an Automated pH Stat for Inhibition Studies," Bull. Environ.
Contain. Toxicol.. 6:304-310 (1971).
2J Chambers, J. E., and J. D. Yarbrough, "Parathion and Methyl Para-
thion Toxicity to Insecticide-Resistant and Susceptible Mosquito
Fish (Gambusia affinis)? Bull. Environ. Contain. Toxicol., 4:315-
320 (1974).
3/ Wood, E. M. "The Pathology Of Pesticide Toxicity in Fish," Unpublished,
U.S. Department of Interior, Columbia, Missouri.
145
-------
Generally toxicosis was shown by a drooping posture and a de-
creased muscle tone; occasionally spastic paralysis occurred.
When parathion exposure was increased to 15 ppm, a generalized
edema resulted. Tremors, salivation or hemorrhage was not observed
(Kaplan, and Glaczenski, 1965).!.'
Sanders (1970)1/ reported TL^Q values in mg/liter for 1-week-
old frog tadpoles (Pseudacris triseriata) for 24, 48, and 96 hr to
be 1.6 (0.4-3.0), 1.4 (0.91-2.8) and 1.0 (0.3-2.0), respectively.
o /
Field studies - Dolphin and Peterson (I960)— investigated the
fish toxicity of parathion with a view to its possible use for the
control of the Clear Lake gnat (Chaoborus astictopus) in Clear Lake,
Lake County, California. Parathion was added to Clear Lake water at
different concentrations in 5-gal aquaria to which five test fish each
were added. The 24-hr LC50 of parathion to Clear Lake bluegill (Lepomis
machochirus) was found to be 0.013 ppm. The approximate LC^Q of para-
thion to the Clear Lake gnat, the target insect, was 0.018 ppm. Thus,
parathion was toxic to fish at dosages required for insect control.
In the summer and fall of 1959, two farm ponds were treated with
parathion by injecting a 1:10 acetone-pond water formulation contain-
ing the required amount of technical grade parathion from a Hudson pack
sprayer into the wake of a small boat which was being rowed back and
forth along the length of the pond.
I/ Kaplan, H. M., and S. S. Glaczenski, "Hematological Effects of
Organophosphate Insecticides in the Frog (Rana pipiens),"
Life Sci.. 4(7):1213-1219 (1965).
2/ Sanders, H. 0., "Pesticide Toxicities to Tadpoles of the Western
Chorus Frog Pseudacris triseriata and Fowler's Toad Bufo
woodhousii fowlert, Copeia. No. 2, pp. 246-251 (1970).
37 Dolphin, R. E., and R. N. Peterson, "Developments in the Research
and Control Program of the Clear Lake Gnat Chaoborus astictopus,
D.&S.," Proc. and Papers of Twenty-Eighth Ann. Conf., California
Mosquito Control Assoc., pp. 90-94 (1960).
146
-------
One pond was treated with parathion at a dilution rate of 1:60
million (0.017 ppm). Four days after treatment, 100% mortality of
Clear Lake gnats was achieved. There was heavy fish mortality 2 weeks
after treatment, including 388 green sunfish, 11 bluegill, and 12 brown
bullhead.
A second farm pond was treated in the same manner with parathion
at the rate of 1:100 million (0.01 ppm). In this case, Clear Lake gnat
mortality 4 days after treatment was 45%. Two weeks after treatment,
four dead bluegill were observed. Thus, the results of the pond tests
were in good agreement with the aquarium tests.
Nicholson et al. (1962)i/ and Grzenda et al. (1962)2/ described
the results of insecticide contamination of a 2.7-acre pond draining a
40-acre watershed where peaches were the principal crop. Parathion was
used for pest control in the watershed from 11 April to 1 August 1960.
Before insecticide use started in 1960, parathion residues of 1.7 ppm
were present in a surface soil sample, indicating carry-over of para-
thion residues in the soil from the preceding season. Surface soil
samples taken during and after the parathion spray season in 1960 con-
tained from 0.23 to 1.39 ppm of parathion. Prior to insecticide use
in 1960, pond bottom mud samples contained 1.9 ppm of parathion, while
two water samples contained 0.02 ppb. Most of the parathion present in
the pond immediately before the 1960 spray season apparently entered the
pond adsorbed on soil during a period of accelerated soil erosion in
March of 1960.
The parathion content of the pond water increased as the spraying
season progressed, while the parathion content of pond mud decreased,
presumably due to decomposition of existing residues and slower soil
erosion. Populations of fish, zooplankton, aquatic insects and Oligochaeta
were unaffected by the parathion residues in the pond water and mud.
However, there was a significant reduction in the numbers of immature
aquatic insects. Bluegills that normally feed primarily on immature
chironomids fed almost entirely on planktonic Crustacea when the insect
crop became severely reduced.
I/' Nicholson, H. P., H. J. Webb, G. J. Lauer, R. E. O'Brien, A. R.
Grzenda, and D. W. Shanklin, "Insecticide Contamination in a Farm
Pond. Part I - Origin and Duration," Trans. Am. Fish.Soc., 91(2):
213-221 (1962).
2_/ Grzenda, A. R., G. J. Lauer, and H. P. Nicholson, "Insecticide Con-
tamination in a Farm Pond Part II - Biological Effects," Trans.
Am. Fish.Soc.. 91(2):213-221 (1962).
147
-------
The amounts of parathion found In the pond water (0.01 to 1.22 ppb)
were well below known levels of acute toxicity to fish. The study demon-
strates that bluegill populations can survive chronic exposure to para-
thion in the range of 0.01 to 1.22 ppb for at least 6 months without
detectable adverse effects. The fish in this field study may actually
have been exposed more or less continuously to low levels of parathion
for at least 17 months.
Mulla et al. (1963)17 investigated the toxicity of parathion and
other insecticides to some aquatic wildlife species including the mosquito
fish (Gambusia affinis) and the aquatic larval stages of the bullfrog
(Rana catesbelana), the Western toad (Bufo boreas) and Hammond's spade-
foot toad (Scaphiopus hammondi). The toxicants were applied to 1/16-acre
field ponds at a volume of 8 gal/acre as aqueous sprays prepared from
emulsion concentrates. At the rate of 0.1 Ib Al/acre, parathion pro-
duced 18% mortality of mosquito fish 1 day after treatment. At the rate
of 0.4 Ib Al/acre, mosquito fish mortality was 96% when the fish were
exposed 1 day after treatment, 32% when exposed after 2 days, and 8% when
exposed after 3 days. The same application rates of parathion were non-
toxic to the tadpoles when these were exposed to the contaminated water
for 24 hr.
2 /
Miller et al. (1966)— studied the water translocation of parathion
and its subsequent occurrence in fish and mussels in a simulated cran-
berry bog in the greenhouse. 35S-labeled parathion was applied at the
rate of 1 Ib Al/acre to the model bog. The bog was flooded 24 hr after
application, and the water was left on for 4 hr, simulating a frost
protection flooding. Estuarine fish (Fundulus heteroclitus) and fresh-
water mussels (Elliptic complanatus) were then exposed to the contam-
inated water in aquaria. Specimens were analyzed periodically.
The majority of the parathion originally present disappeared from
the water within 144 hr. During this time, three labeled parathion
degradation products were encountered. Of 60 fish present in the aquarium,
only 12 were alive after the first 24 hr. The parathion concentration
in the aquarium declined from 0.07 to 0.02 ppm during this period.
After 48 hr, three of the remaining fish showed symptoms of poisoning.
II Mulla, M. S., L. W. Isaak, and H. Axelrod, "Field Studies on the
Effects of Insecticides on Some Aquatic Wildlife Species," J._
Econ. Entomol., 56(2):184-188 (1963).
2_/ Miller, C. W.,B. M. Zuckerman, and A. J. Charig, "Water Transloca-
tion of Diazinon- C and Parathion-35S Off a Model Cranberry Bog
and Subsequent Occurrence in Fish and Mussels," Trans. Am. Fish.
Soc., 95:345-349 (1966).
148
-------
On analysis, these specimens showed an accumulation of parathion to 2.1
ppm, while the surrounding aquarium water at this time analyzed 0.01
ppm parathion. Mussels also accumulated parathion, but to a lesser
degree than the fish.
Holland et al. (1967)i/ employed a fish brain acetylcholinesterase
test to monitor pollution by organophosphorus pesticides along the
Atlantic and Gulf coasts. Seven laboratories cooperated by sending
fish from their areas periodically for AChE assay. A total of 93 sam-
ples of spot (Leiostomus xanthurus) and sheepshead minnows (Cyprinodon
variegatus) from 43 stations were analyzed. Low AChE activity was
found in 17 samples (18.3%), but 13 of these were from only two areas.
Fish that showed low AChE activity (73 to 88% of normal) from South
Carolina came from the vicinity of the Ashley River near Charleston.
This river receives wastes from plants producing a variety of organo-
phosphate chemicals. Fish from the Galveston area with low enzyme
activity (75 to 847. of normal) generally came from stations along the
eastern edge of Trinity Bay. The authors did not ascertain which organo-
phosphate insecticides may have been responsible for the observed fish
brain AChE depression.
The Environmental Protection Agency's Gulf Breeze Environmental
Research Laboratory recently analyzed samples of whole fish and of fish
organs collected by the Texas Parks and Wildlife Department at different
points in Texas for residues of parathion and other pesticides. Para-
thion residues found ranged from 21 to 170 ppb, wet weight. The para-
thion residue levels were generally much lower than residues of organo-
chlorine pesticides found in the same specimens.
The Water Quality Criteria Data Book. Vol 3 (Battelle Columbus,
._ » j _ _ —rV^™^«i«—i ___...
1971) — a summary review of the effects of commercial chemical products
on aquatic organisms, includes references to two further reports on
parathion fish toxicity. When parathion was applied for the control of
mosquito larvae to a lake in Salt Lake County, Utah, at the rate of
0.35 Ib Al/acre, there were no fish losses, and no adverse effects were
observed on mammals, birds, reptiles, and amphibians. Invertebrates
were not affected uniformly. Crustaceans and larvae of the insect
family Ephydridae were not harmed, but spiders and aquatic insects
other than Ephydridae were harmed in various degrees. Aquatic beetles
were affected more seriously than other insects, except mosquito larvae.
I/ Holland, H. T., D. L. Coppage, and P. A. Butler, "Use of Fish Brain
Acetylcholinesterase to Monitor Pollution by Organophosphorus
Pesticides," Bull. Environ. Contain. Toxicol.. 2(3):156-162 (1967).
2_/ Battelle's Columbus Laboratories, "Effects of Chemicals on Aquatic Life,"
'Water Quality Criteria Data Book, Vol. 3:B167-B186, Environmental
Protection Agency (1971).
149
-------
Mulla and Isaak (1961)!' treated ponds in the BakersfieId, California,
area with parathion from a 50% emulsifiable concentrate. At 0.1 Ib AI/
acre, 22% mortality of mosquito fish (Gambusia affinis) occurred in 24 hr.
At 0.4 Ib parathion Al/acre, there was 92% mortality of the fish in 24 hr.
In these field tests, the fish were exposed in cages placed in the ponds.
The Federal Water Pollution Control Administration's "Water Quality
Criteria," (1968) includes parathion in "Pesticide Group A," defined as
chemicals that are acutely toxic to shrimp at concentrations of 5 ug/liter
and less. On the assumption that 1/100 of this level represents a
reasonable safety factor, it is recommended that environmental levels
of these substances not be permitted to rise above 50 ng/liter of water.
This level is so low that the pesticides in this category (including
parathion) could not be applied directly in or near the marine habitat
without danger of causing damage. The 48-hr TI^ of parathion to shrimp
is listed at 1.0 ug/liter. Shrimp vere selected as the test organism
because they are among the most sensitive marine organisms in regard to
their reaction to chemicals.
Lower Aquatic Organisms - For purposes of this review, "lower aquatic
organisms" are defined to include primary producers (phytoplankton,
attached algae, moss, and vascular plants); consumers (protozoa,
rotifers, and Crustacea); benthic invertebrates (annelids, insects,
Crustacea, and mollusca); decomposers (fungi and bacteria).
Laboratory studies - The aquatic species other than fish and frogs
which have been studied under controlled conditions are few in number.
Lowe et al. (1970) studied the effect of parathion on shrimp (Penaeus
duorarum), and oysters (Crassostrea virginica). They found that a
48-hr ECejQ was obtained with juvenile shrimp at a parathion concentra-
tion of 0.0002 ppm, and that oyster shell growth was decreased 22 percent at
1.0 ppm in a 96-hr test. Naqvi and Ferguson (1970)1' found that the
LD50 (24 hr) for freshwater shrimp (Palaemonetes kadiakensis) was 0.0082
ppm.
If Mulla, M. S., and L. W. Isaak, "Field Studies on the Toxicity of
Insecticides to the Mosquito Fish, Gambusia affinis," J. Econ.
Entomol., 54(6)-.1237-1242 (1961).
2_f Naqvi, S. M., and D. E. Ferguson, "Levels of Insecticides Resistance
in Freshwater Shrimp, Palaemonetes kadiakensis," Trans. Am. Fish.
Soc., 99:697 (1970).
150
-------
These data also indicate that parathion contamination of streams
and other aquatic habitats at levels well below that having a direct
toxic effect on fish can still have an indirect effect by destroying
organisms in the food chain.
Lowe et al. (1971)i^ performed a study in which oysters were grown
from juvenile to sexual maturity in seawater polluted with 1 ppb para-
thion. A significant difference between the weights of treated and of
the untreated controls was not found.
Field studies - The Federal Water Pollution Control Administration's
"Water Quality Criteria" (1968) lists the 48-hr Tl^ values of parathion
to the stonefly (Pteronarcys californica) and to Daphnia pulex as 11 and
0.4 ug/liter, respectively. Parathion ranks intermediate among the insecti-
cides included in this listing in regard to its toxicity to these two
aquatic organisms.
Further data on the toxicity of parathion to Daphnia pulex and to
other zooplankton organisms, and to benthic invertebrates are summarized
in Tables 22 and 231 The immobilization values (EC^Q) of parathion to
the zooplankton species range from 0.37 to 0.8 ppb. The LC50 values of
parathion to several species of stoneflies, caddisflies and mayflies,
and to one species each of amphipods and freshwater shrimp varied con-
siderably, depending upon the species and the experimental conditions
such as temperature and length of exposure. Parathion was considerably
more toxic to most of these species than, for instance, malathion. How-
ever, it was less toxic than malathion to the amphipod (Gammarus lacustris).
2 /
Ware and Roan (1971)— reviewed the literature on the interaction
of pesticides with aquatic microorganism and plankton. The data cited
from several original research papers in a brief section dealing with
organophosphate insecticides again confirm that parathion, along with
other organic phosphates, is subject to adsorption and degradation by
such organisms as yeasts (Torulopsis utilis), bacteria (Pseudomonas
fluorescens. Thiobacillus thiooxidans, Bacillus subtilis), and green
algae (Chlorella pyrenoldosa).
I/ Lowe, J. I., P. D. Wilson, and A. J. Wilson, "Chronic Exposure of
Oysters to DDT, Toxaphene and Parathion," Proc. Nat. Shellfish
Assoc., 61:71-79 (1971).
2/ Ware, G. W., and C. C. Roan, "Interaction of Pesticides with
Aquatic Microorganisms and Plankton," Residue Reviews, 33:15-45
(1971).
151
-------
Table 22. EC5Q (IMMOBILIZATION) VALUES (ppb) OF THREE
ORGANOPHOSPHATE INSECTICIDES TO ZOOPLANKTON
Temperature Time Methyl
Species (°F) (hr) Malathlon Parathion parathlon Reference
Daphnla pulex 21°C 48 2 a/
48 0.76 LC50 W
60 48 1.8 0.6 c/
60 48 1.8 d/
Daphnia magna 68 24 0.9 0.8 c/
68 48 4.8 d/
68 50 0.9 0.8 c/
20°C 50 0.9 0.8 I/
Daphnla
carlnata 78 64 0.2 0.5 fj
Simocephalus 60 48 3.5 0.37 £/
serrulatus 70 48 6.2 0.47 c/
Source: Li, M., and R. A. Fleck, "The Effects of Agricultural Pesticides in
the Aquatic Environment, Irrigated Croplands, San Joaquin Valley,"
Pesticide Study Series - 6, Environmental Protection Agency,
Office of Water Programs, Applied Technology Division, Rural Waste
Branch TS-00-72-05, 268 pp. (1972).
a/ Cope, 0. B., "Contamination of the Freshwater Ecosystem by Pesticides,"
J. Appl. Ecol., 3 (Suppl):33-44 (A special issue on Pesticides in the
Environment and Their Effects on Wildlife) (1966). (In: Li and Fleck,
1972.)
b_/ Priester, L. E., "The Accumulation in Metabolism of DDT, Parathion and
Endrin by Aquatic Food-Chain Organisms," Ph.D. Thesis, Clemson Univer-
sity (1965). (In: Li and Fleck, 1972.)
c/ Sanders, H. 0., and 0. B. Cope, "Toxicities of Several Pesticides to Two
~~ Species of Cladocerans," Trans. Am. Fish.Soc.. 95(2):165-169 (1966).
d/ Federal Water Pollution Control Administration, Water Quality Criteria,
~ Report of the National Technical Advisory Committee, p. 37 (1968).
e/ Anderson, B.C., "The Toxicity of Organic Insecticides to Daphnia." In:
"~ Transactions of the Second Seminar on Biological Problems in Water
Pollution, Cincinnati, Ohio, U.S. Public Health Service, pp. 94-95(1959).
(In: Li and Fleck, 1972.)
f/ Matida, Y., and N. Kawasaki, "Study on the Toxicity of Agricultural Control
"~ Chemicals in Relation to Freshwater Fisheries Management," No. 2 Toxicity
of Agricultural Insecticides to Daphnia carinata, King, Bull. Freshwater
Fish Res. Lab., Tokyo 8:1-6 (1958). (In: Li and Fleck, 1972.)
152
-------
Table 23. LC5Q VALUES (ppb) OF THREE ORGANOPHOSPHATE
INSECTICIDES TO BENTHIC INVERTEBRATES
Species
Stone files
Pteronarcys caltfornlca
Acroneurla paciftca
Pteronarcella badla
^^^•••M^^^^^^^^^^B ^H^^H^^B
Claassenla sabulosa
Caddlsflles
Arctopsyche grandls
Hydropsyche callfornlca
Temperature
CO
15.5
15.5
21.0
48-50'F
11-12
11-12
11-12
15.5
12.8
12.8
12.8
12.8
12.8
12.8
11-12
11-12
11-12
12.8
12.8
12.8
12.8
12.8
12.8
15.5
15.5
48-50'F
15.5
15.5
15.5
15.5
51-54°F
51-54eF
Time (hr)
(* - days)
24
48
48
48
48
72
96
96
5*
10*
15*
20*
25*
30*
48
72
96
5*
10*
15*
20*
25*
30*
24
48
48
96
24
48
96
96
96
Malathlon
35
20
21
180
72.5
50.0
10
45.0
24.0
15.5
8.8
12
16.0
7.0
7.7
5.1
3.3
3.2
2.4
0.78
10
60
6
1.1
13
6.0
2.8
32
22.5
Parathion
28
11
11
75
32.0
32.0
5.4
36.0
2.7
2.2
2.2
2.2
2.2
6
2.9
2.8
0.93
0.46
0.45
0.44
0.44
0.44
8.0
5.6
4.2
8.8
3.5
1.5
7
0.43
Methyl
parathlon Reference
«/
a/
b/
1l
d/
d/
d/,
a/
7/
f/
f/
f/
f/
I/
d/
d/
d/,
f/
11
£/
f/
f/
I/
a/
I/
b/
a/
a/
a/
e/
e/
e/
e/
153
-------
Table 23. (Continued)
Temperature
CC)
Time (ht)
(* - days)
Halathion
Parathion
Methyl
parathion
Reference
Mayflies
Ephemerella grandis
Baetla so.
Amphipods
GanmaruB lacustris
48-50°F
21
70° F
70'F
60*F
70»F
59°F
96
48
24
48
48
48
96
100
6
3.8
1.8
1.8
1.0
1.62
12
6.0
6
3.5
12.8
e/
b/
c/
It
e/
Freshwater shrimp
Palaemonetes radlakensis
Crayfish
Procambarus clarkl
21-27
21-27
16-32
16-32
16-32
24
24
24
48
72
6.6
11.8
2.5
23.3
50
40
40
h/
W
i/
I/
i/
Source: Li and Fleck, op. cit. (1972).
a/ Sanders, H. 0. and 0. B. Cope, "The Relative Toxicities of Several Pesticides to Naiads of
Three Species of Stoneflies," Limnology and Oceanography. 13(1):112-117 (1968)
b/ Cope, 0. B., op. clt., (1966).
£/ FWPCA, op. cit., (1968).
A/ Jensen, L. D. and A. R. Gaufin, "Effects of Ten Organic Insecticides on Two Species of Stonefly
Naiads," Trans, Am. Fish Soc.. 93:27-34 (1964a).
e/ Gaufin, A. R., L. D. Jensen A. V. Nebeker, T. Nelson, and R. W. Teel, "The Toxicity of Ten
Organic Insecticides to Various Aquatic Invertebrates," Water Sewage Works. 12:276-79 (1965).
(In: Li and Fleck, 1972.)
if Jensen, L. D. and A. R. Gaufin, "Long-Term Effects of Organic Insecticides on Two Species of
Stonefly Naiads," Trans. Am. Fish Soc.. 93:357-63 (1964b). (In: Li and Fleck, 1972.)
£/ Sanders, H. 0., "Toxicity of Pesticides to the Crustacean Cannnarus lacustris." Technical Papers
No. 25 pp. 18, United States Department of the Interior Fish and Wildlife Service (1969).
h/ Nagvl, S. M., and D. E. Ferguson, "Levels of Insecticide Resistance in Freshwater Shrimp,
Palaemonetes kadiakensis." Trans. Am. Fish Soc.. 99:696-99 (1970). (In: LI and Fleck,
1972.)
if Muncy, R. J., and A. D. Oliver, Jr., "Toxicity of Ten Insecticides to the Red Crawfish,
Procambarus clarkl (Girard)," Trans. Am. Fish Soc.. 92:428-31 (1963). (In: Li and Fleck,
1972.)
154
-------
The observations by Nicholson et al. (1962) and Grzenda et al.
(1962) on the effects of parathion contamination in a farm pond drain-
ing a 40-acre watershed grown to peaches treated with parathion have
been described in greater detail elsewhere in this subsection (p.139).
Based on their careful, comprehensive studies under field conditions
representative of a real-life situation, these authors reported that
"the fish, zooplankton, aquatic insect , and Oligochaeta populations
appeared to be unaffected by parathion residues in pond water and mud.
However, there was a significant reduction in immature aquatic insect
numbers associated with insecticide use. The data indicate this was
caused indirectly by mortality in the adult populations resulting from
exposure to parathion residues in the watershed. Zooplankton were not
utilized as food by bluegills when Immature chironomids were relatively
abundant. However, when the insect standing crop became severely re-
duced, the fish fed almost entirely on planktonic Crustacea. "
The studies by Mulla et al. (1963) also described in greater de-
tail above (see p.110) included observation on the effects of parathion
on tadpoles of three species of amphibia, i.e., the bullfrog (Rana
catesbeiana), the Western toad (Bufo boreas), and Hammond's spadefoot
toad (Scaphiopus hammondi). Parathion applied to 1/16-acre field ponds
at rates of 0.1 and 0.4 Ib Al/acre did not produce mortality when the
tadpoles were exposed to the contaminated water for periods of 24 hr.
A number of further studies, in addition to those summarized in
Tables 22 and 23 , deal with interactions between parathion and aquatic
organisms in isolated systems under laboratory conditions.
Zuckerman et al. (1970)1' found that the alga Chlorella pyrenoidosa
proteose degraded parathion in axenic cultures incubated for 7 days at
20°C.
JL/ Zuckerman, B. M., K. Deubert, M. Mackiewicz, and H. Gunner, "Studies
on the Biodegradation of Parathion," Plant Soil 33(2):273-81 (1970)
155
-------
Moore (1970)-' and Poorman (1973)-^ investigated the effects of
parathion on growth and survival of Euglena gracilis, a species which
they describe as a "photosynthetic microorganism," along with Kortus
et al. (1971)-' ("aquatic alga"), while Gregory et al. (1969)4-/ con-
sider E^ gracilis to be a flagellate.
In Moore's tests, parathion inhibited the growth rate of E. gracilis
only at the highest rate tested, 1.2 ppm. In the presence of 0.01 M
glucose, 10 ppm of parathion did not affect the respiration rate of
E^ gracilis over a period of 80 min.
Poorman found that parathion at 50 and 100 ppm depressed the growth
rate of E^ gracilis only to a small extent during a 24-hr exposure.
When the organism was exposed to parathion for 7 days, there was con-
siderable growth stimulation as compared to untreated controls. These
results indicate that parathion is not likely to adversely affect £._
gracilis under field conditions.
Gregory et al. (1969) found that Euglena gracilis ("a flagellate"),
two species of algae, and two species of ciliates, maintained on cul-
ture media at 26eC in an environmental chamber under continuous illumi-
nation, concentrated parathion 50 to 116 times when exposed to 1 ppm
w/v of the insecticide for 7 days. The supernatant liquids in the cul-
tures contained only small amounts of parathion. The authors attribute
this to three possible reasons, i.e., adsorption by the living organism,
sorption by nonliving materials, and/or codistillation with water.
32
Kortus et al. (1971) studied the uptake of P-labeled parathion
by Euglena gracilis maintained under light at 28°C. Parathion uptake
was determined at frequent intervals between 1 and 180 min. The maxi-
mum uptake of parathion (69%) occurred immediately after addition of
the pesticide. The activity decreased precipitously during the follow-
ing 15 min and continued to drop at a slower pace after that time.
I/ Moore, R. B., "Effects of Pesticides on Growth and Survival of
Euglena gracilis Z.," Bull. Environ. Contarn. Toxicol., 5(3):226-230
(1970).
2/ Poorman, A. E., "Effects of Pesticides on Euglena gracilis I.
Growth Studies," Bui L Environ. Contam. Toxicol., 10(1)-.25-28 (1973).
3_/ Kortus, J., P. Macuch, J. Mayer, K. Durcek, and V. Krcmery, "Uptake
of 32-P-Parathion and 32-P Imidan," J. Hyg. Epidemiol. Microbiol.
Immunol.. (Prague) 15(1):101-103 (1971).
4/ Gregory, W. W., Jr., J. K. Reed, and L. E. Priester, Jr., "Accumula-
tion of Parathion and DDT by Some Algae and Protozoa," J. Protozool.,
16(1):69-71 (1969).
156
-------
The data reviewed In this section indicate that parathion is
extremely toxi<5 to aquatic insects, highly toxic to the lower aquatic
fauna, and relatively nontoxic to the lower aquatic flora. A number
of aquatic microorganisms degrade parathion. Many of these organisms
also preferentially sorb and thus accumulate parathion from aqueous
media. This sorption process may be independent of life processes;
sorption rates of live and dead organisms showed little differences.
Effects on Wildlife
Laboratory Studies - Most birds on which controlled experimentation
has been done are those which are either important as game animals
or are considered nuisances. (Keith and Mulla, 1966;— Tucker and
Haegele, 1971;!/ Schafer et al., 1973;!/ Rudd and Genelly, 1956;£/
Heath et al., 1972-/). The use of pesticides in the field noticeably
affects songbirds.
The results of the controlled experiments appear to indicate that
while the LDcg values for toxicity of parathion range from 1 mg/kg to
about 24 mg/kg depending on species, with two exceptions, the LD^Q values
were in the range of 1 mg/kg to 5.95 mg/kg (Table 24). The common and
scientific names of the avian species are shown in Table 25. With game
birds the results recorded in the table indicate that when the species
(mallard, pheasant, partridge (Chukar), quail (Japanese)) are ranked from
most sensitive to least sensitive, the mallard duck is most sensitive
(LD5Q 1 to 2.13 mg/kg) to parathion, and the Chukar partridge is least
sensitive (U>5o 24.0 mg/kg) to parathion intoxication.
I/ Keith, J. 0., and M. S. Mulla, "Relative toxicity of Five Organophosphorous
Mosquito Larvicides to Ducks," J. Wildlife Manae.. 30(3):553-563
(1966).
2_/ Tucker, R. K., and M. A. Haegele, "Comparative Acute Oral Toxicity
of Pesticides to Six Species of Birds," Toxicol. Appl. Phannacol.,
20:57-65 (1971).
3/ Schafer, E. W. , R. B. Brunton, N. F. Lockyer, and I. W. DeGrazio,
"Comparative Toxicity of 17 Pesticides to the Quelea, House Sparrow,
and Red-Winged Blackbird," Toxicol. Appl. Phannacol.. 26:154-157
(1973).
4/ Rudd, R. L., and R. E. Genelly, Pesticides; Their Use and Toxicity
in Relation to Wildlife. State of California Department of Fish
and Game, Game Bull. No. 7, pp. 108-113 (1956).
5/ Heath, R. G., J. W. Spann, E. F. Hill, and J. F. Kreitzer, "Comparative
Dietary Toxicities of Pesticides to Birds," Bureau of Sport Fish-
eries and Wildlife, Special Scientific Report, Wildlife No. 152
(February 1972).
157
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Table 24. ACUTE TOXICITY OF PARATHION TO AVIAN SPECIES
LD50 (rag/kg)
Oral Dermal Reference
Mallard ducks 1.9, 2.13
Pheasant 12.4
Chukar partridge 24.0
Japanese quail 5.95
Pigeon 2.52
House sparrow 1.3, 3.36 1.8
Quelea 1.8 1.8
Red-winged blackbird 2.4
Starling 5.6
£/ Keith and Mulla, op. cit. (1966).
b_/ Tucker and Haegele, op. cit. (1971).
£/ Schafer et al., op. cit. (1973).
-------
The information on dermal toxicity for wild birds Is limited; only
one paper was found (Schafer et al., 1973). These investigators studied
the oral and dermal toxicity of 17 chemicals on Quelea, the house
sparrow, and on the red-winged blackbird. The acute oral and dermal
LD50 values for Quelea exposed to parathion were 1.8 mg/kg and 1.8 tng/kg,
respectively. The acute oral and dermal LD5o values for the house spar-
row were 1.3 mg/kg and 1.8 mg/kg, respectively.
While oral toxicity values are important and laboratory measure-
ments of lethality are basic in predicting the immediate impact of a
pesticide on the environment, measurements of dermal toxicity would
appear to be equally if not more important, in that wildlife mortality
has been reported by some to occur chiefly through contact with foliage
(Rudd and Genelly, 1956). However, based on the limited amount of data
shown in Table 24, there is little difference between the oral and dermal
LDcQ values.
The toxic effect of feeding parathion to four species of birds was
studied by Heath et al. (1972). These birds were at least 9 days old
before administration of the diets carrying the chemical. Data from
this study are summarized in Table 26.
Table 26. AVIAN DIETARY TOXICITY (8 Days)
LC50 in feed (ppm) (95% conf. limits)
Methyl Parathion Parathion
Bobwhite quail 90 (73-111) 194 (150-245)
Japanese quail 46 (38-55) 44 (36-53)
Pheasant 116 (101-134) 365 (316-420)
Mallard 682 (541-892) 275 (183-373)
Data of Heath et al., op. cit. (1972)
The Japanese quail were more susceptible than bobwhlte quail,
pheasant or mallard ducks to parathion poisoning. It is interesting
to note that it required nearly five times as much parathion to kill
the bobwhite species as it did to kill the Japanese quail.
159
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One of the difficulties in fully assessing the hazard potential
for wild birds from laboratory studies is emphasized by the statement
of Heath et al. (1972): "our particular interest, however, was in
dietary toxicity because ingestion is undoubtedly the predominant route
of exposure in wild species." This statement is in opposition to that
of Rudd and Genelly (1956): "Wildlife mortality occurs chiefly through
contact with foliage." Regardless of the most probable route of entry
for parathion in wild birds, the age of the birds at the time of expo-
sure has a decided influence on the outcome of the ocposure.
Ducks from 36 hr of age to 6 months of age have been used to deter-
mine the relative toxicity of parathion for birds in these different
age groups. The results of this study by Hudson et al. (1972)!/ are
shown in Table 27.
Table 27. EFFECT OF AGE ON PARATHION
TOXICITY IN MALLARD DUCKS*/
Approximate
age of ducks (mg/kg)
36 hr 1.65
7 days 1.44
30 days 1.65
6 months 2.34
a/ Data from Hudson et al., op. cit. (1972).
The lethality does not appear to change between 36-hr ducklings
(LD5Q 1.65 mg/kg) and 1-month-old birds. However, as the ducks mature,
they become less susceptible to parathion intoxication (11)50 2'3^ m8/k8~~
6 months). This is in agreement with the findings of Brodeur and DuBois
(1963),— who concluded that young rats were almost always more suscepti-
ble to anticholinesterase insecticides than older animals.
I/ Hudson, R. H., R. K. Tucker, and M. A. Haegele, "Effect of Age on
Sensitivity: Acute Oral Toxicity of 14 Pesticides to Mallard
Ducks of Several Ages," Toxicol. Appl. Pharmacol.. 22:556-561
(1972).
2/ Brodeur, J., and K. P. DuBois, "Comparison of Acute Toxicity of
Anticholinesterase Insecticides to Weanling and Adult Male Rats,"
Proc. Soc. Exp. Biol. Med.. 114(2):509-511 (November 1963).
160
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Although bradycardia is generally reported In parathion poisoning
in mammals, tachycardia is found to be a more consistent response to
parathion poisoning with avian species such as quail and ducks. After
tachycardia commenced, the respiratory rate increased and remained high
until death occurred. In both mallards and quail a small but consistent
rise occurs in the hematocrit (see Table 28). It was observed that
parathion poisoning did not significantly alter the blood pressure in
the two avian species (McFarland and Lacy, 1968).!/
Table 28. EFFECTS OF INTRAVENOUS INJECTIONS OF
PARATHION ON HEMATOCRIT OF DUCKS AND QUAIl£'
Mallard ducks (36)^ Japanese quail (46)
Hematocrit Males Females Males Females
Before parathion exposure 48.2 47.3 47.6 45.1
After parathion exposure 51.8 50.5 50.8 47.6
a/ Data from McFarland and Lacy, op. cit. (1968).
b/ Number of birds.
The birds mentioned in Table were given intravenous injections as
follows: mallards, 0.61 to 1.70 mg/kg; quail 3.9 to 5.7 mg/kg.
Field Studies - Robel et al. (1972)—' reported on the effects of para-
thion and other insecticides on populations of wild rodents in Kansas,
based on observations made from 1965 to 1969. The study was conducted
on two sites in Ellis County, Kansas, in a newly created irrigation
district that had not been intensively cultivated prior to 1965. No
insecticidal residues were found in samples of water, soil, plants,
or animals collected from the study sites prior to initiation of the
study in 1965. Parathion was applied to one field (the second field
I/ McFarland, L. Z., and P. B. Lacy, "Acute Anticholinesterase Toxicity
in Ducks and Japanese Quail," Toxicol. Appl. Pharmacol., 12:105-
114 (1968).
2/ Robel, R. J., C. D. Stalling, M. E. Westfahl, and A. M. Kadoum,
"Effects of Insecticides on Populations of Rodents in Kansas -
1965-69," Pest. Monit. J.» 6(2):115-121 (September 1972).
161
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served as an untreated control) at recommended and commonly used rates of
application of 0.38, 1.4, 0.79, and 1.01 Ib Al/acre in 1965, 1966, 1967, and
1968, respectively. Live rodents were trapped in the treated and con-
trol field from 1965 through 1969. A total of 4,661 rodents were cap-
tured, of which 162 were analyzed for residues.
No parathion residues were found in any of these specimens. The
species composition of the trapped rodents was similar for the treated
and the untreated study area, as were the population levels of Peromyscus
maniculatus. which comprised about 74% of the total rodent population
in the two areas. Average minimal longevity for P^ maniculatus and
monthly survival between June and September did not differ significantly
between the treated and untreated area. Thus, none of the parameters
observed in this study indicated any effects on the wild rodent popula-
tion from the use of parathion at field rates over a 4-year period.
Bejer-Petersen et al. (1972)I/ studied the effects of spray treat-
ments of parathion and other insecticides in forests on birds living
in nest boxes. Parathion spraying (rate not given in abstract) was
carried out in 1965 and in 1967 at a time when nestlings of Parus
major and P. ater were most numerous. The loss rate of Parus nestlings
was adversely affected by the parathion treatment. The breeding success
of Ficedula hypoleuca. the third species in these tests, was 50%, com-
pared to 64 to 100% in control areas. Parathion residues in these birds
ranged from traces to 11 ppm. In several of the broods of each species,
reduced brain cholinesterase activity was observed. The sprayings had
no effect on bird populations in the years following the treatment.
7 /
Bucknell (1970)i/ reported deaths of a number of species of birds
following the application of parathion in granulated form. The bird
species most frequently affected were magpies, gulls, hawks, blackbirds,
thrushes, and finches.
The summary on parathion by Pimentel (1971)P_' includes the follow-
ing three reports on wildlife toxicity.
I/ Bejer-Petersen, B., R. R. Hermansen, and M. Weihe, "On the Effects
of Insecticide Sprayings in Forests on Birds Living in Nest Boxes,"
Dan. Ornithol. Foren. lidsskr.. 66(1,2):30-50 (1972).
2_/ Bucknell, E. S., "Side-Effects of Granulated Insecticides in
Canterbury," Proc. N. Z. Weed Pest Contr. Conf. No. 23, pp. 124-126 (1970).
3/ Pimentel, D., "Ecological Effects of Pesticides on Nontarget Species,"
Executive Office of the President, Office of Science and Technology,
U.S. Government Printing Office, Washington, D.C. (1971).
162
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Buttlker (1961)I/ reported on a large-scale spray program carried
out on a citrus estate In the Union of South Africa. Parathion was
applied at 7.5 Ib Al/acre for the control of citrus insects. In the
treated grove, nearly 800 birds were found dead.
Mulla (1966)2/ reported that mallard ducks appeared to be un-
affected when duck ponds were treated with parathion at the rate of
0.85 Ib Al/acre.
In a USDI (1966)-' study, parathion was applied at rates of 0.5
and 3.0 Ib Al/acre. Pheasants were not affected by the lower rate,
but there was about 10% mortality at the 3.0-lb rate.
Our search of the literature and of other information sources
failed to yield additional data on the toxicity of parathion to wild-
life under field conditions. The data on the oral acute toxicity of
parathion to wildlife summarized by Tucker and Crabtree (1970)4' in-
dicate that parathion is highly toxic to all species studied. This is
also evident from the data on the toxicity of parathion to wildlife
summarized by Pimentel (1971).
Parathion labels carry the warning "Poisonous to fish and wild-
life. This product is toxic to fish and wildlife. Birds and other
wildlife in treated areas may be killed."
Effects on Beneficial Insects
Bees - Several investigators have reported on the toxicity of parathion
to bees (Apis mellifera) by direct topical application, or by exposing
bees to sugar solutions containing parathion, to parathion deposits on
inert surfaces, or to vapors from parathion residues. By all of these
routes of application, parathion is highly toxic to bees.
I/ Buttiker, W., "Ecological Effects of Insect Control on Bird Popula-
tions, "int. Union Conserva. Nature Natur. Resources, Tech. Meeting,
..Warsaw 1960, Proc . ,. 8:48-60 (1961). Quoted from: Pimenta Pimentel
2/ Mulla, M. S., "Vector Control Technology and Its Relationship to the
Environment and Wildlife," J. Appl. Ecol.. 3( Supplement on
Pesticides in the Environment and Their Effects on Wildlife): 2 1-28
(1966). Quoted from: Pimentel (1971).
3_/ USDI, "Wildlife Research; Problems, Programs and Progress. Pesticide-
Wildlife Relations," Fish and Wildlife Serv., Bureau Sport Fish Wildlife
Clrc. 43, 117 pp. (1966). Quoted from: Pimentel (1971).
4/ Tucker, R. K., and D. 6. Crabtree, "Handbook of Toxicity of Pesticide
to Wildlife," U.S. Department of the Interior, Fish and Wildlife
Service, Denver Wildlife Research Center, Resource Publication No.
84, p. 82 (1970).
163
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The Handbook of Toxicology (WADC, 1959)!/ states: "Parathion is
perhaps the most generally potent insecticide presently in commerce."
This is clearly supported by tabular listings of the effects of lethal
dosages of parathion on a considerable number of insects.
Stephen (1972)I/ recently studied the effects of chronic sublethal
doses of parathion on the behavior of the leafcutter bee (Megachile
rotundata). Bees emerging from diapause were treated topically with
sublethal doses of parathion (1 ug/g) at 2-or 3-hr intervals over a
24-hr period. The authors concluded that the rhythmic responses to
parathion appeared to be light-cued, while the response to dieldrin,
another pesticide tested in the same manner, was temperature-dependent.
In a companion study on the effect of parathion on the ability of the
leafcutter bee to synchronize its activity rhythm to the environment,
there was no evidence of the clock being affected. Web spinning be-
havior of the spider, Araneus diadamatus, was not affected by a single
application of parathion, but the amount of silk available was reduced.
Barker (1970)—' investigated whether the classical antidotes
against parathion poisoning in mammals, atropine sulfate and N-methyl-
pyridinium-2-aldoxime (PAM), would work on honeybees. When parathion
was applied to the thorax of bees, the 24-hr 1^5 Q was 0.08 to 0.16 ug/
bee. Treated bees showed no reduction in mortality when atropine sul-
fate with or without salts of PAM was fed, applied topically, or in-
jected. Thus, these parathion antidotes were ineffective on bees, at
least under the conditions of this experiment.
4 5/
Johansen (1972a,b)—*—investigated the toxicity of field-weathered
residues of parathion and other insecticides to different species of bees,
I/ WADC, "Insecticides," The Handbook of Toxicology, Vol. Ill, Wright-
Patterson Air Force Base, Ohio Air Force Systems Command, WDAC
Tech. Report 55-16 (1959).
21 Stephen, W. P., "The Effects of Chronic Sublethal Doses of Pesti-
cides on Behavior and Longevity in Arthropods," Oregon State
Univ. Environ. Health Sci. Cent. Annu. Progr. Rep., pp. 161-167 (1972)
3/ Barker, R. J., "Cholinesterase Reactivators Tested as Antidotes for
Use on Poisoned Honeybees," J. Econ. Entomol., 63(6) -.1831-1833
(December 1970).
4_/ Johansen, C. A., "Spray Additives for Insecticidal Selectivity to
Injurious vs Beneficial Insects," Environ. Entomol., l(l):51-54
(February 1972a).
5/ Johansen, C. A., "Toxicity of Field-Weathered Insecticide Residues
to Four Kinds of Bees," Environ. Entomol., l(3):393-394 (June 1972b).
164
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Parathion from a 4-lb/gal emulsifiable liquid was applied to alfalfa
at the rate of 0.5 Ib Al/acre. Three kinds of bees were exposed to
the parathion residues 10 hr after application. Bee mortality was
determined after 24 hr and ranged from 41 to 667.. When bees were ex-
posed to 3-hr old residues of parathion on alfalfa treated at 0.5 Ib
Al/acre, mortalities ranged from 91 to 100%. On 8-hr old residues,
mortalities ranged from 61 to 93%.
The entomological literature contains many other records of the
toxic!ty of parathion to bees. Within the limits of time and resources
available for this review, it was not possible, and was hot considered
of prime importance to collect and review the entire literature on the
toxicity of parathion to bees. The high toxicity of this insecticide
to bees has been well established and is universally recognized. Para-
thion labels state: "This product is highly toxic to bees exposed to
direct treatment or residues on crops." Many extension service recom-
mendations concerning parathion carry specific warnings applicable to
local conditions, crops, etc.
Parasites and Predators - The importance of naturally occurring parasites
and predators of insect and mite pests in suppressing these pests and
reducing or preventing economic damage from their activities has been
increasingly recognized in recent years. A number of investigators have
studied the effects of parathion on such parasites and predators, mostly
under laboratory conditions.
Hamilton and Kieckhefer (1969)^' investigated the toxicity of para-
thion to predators of the English grain aphid (Macrosiphum avenae).
Adult and larval forms of the three most numerous and ubiquitous preda-
tors of cereal aphids in South Dakota, Hippodamia convergens (the con-
vergent lady beetle), Nabis americoferus. and Chrysopa carnea were
field-collected for laboratory mortality tests. By topical applica-
tion to adults, the LDgg °f parathion to the aphid was 1.8 ug/g, while
it was 21 ug/g to N^ americoferus and 40 ug/g to H^ convergens. LC5Q
values of parathion to the same insects were determined by exposing the
insects to 4 and 24-hr-old deposits of appropriate concentrations. Again,
the LC5Q values of parathion to the predators were much higher than
to the aphid.
I/ Hamilton, E. W., and R. W. Kieckhefer, "Toxicity of Malathion and
Parathion to Predators of the English Grain Aphid," J. Econ.
Entomol.. 62(5):1190-1192 (October 1969).
165
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Craft and Jeppson (1970)i/ studied the toxicity of parathion and
other insecticides to Typhlodromus occidentalis, an important natural
enemy of plant feeding mites in the Western United States. Strains of
this phytoseiid mite from Washington, Utah, and California were studied
at the University of California insectary. All predator strains were
uniformly tolerant to field use rates of parathion. The results' clearly
indicate that strains of this predator from four different locations
have developed a high degree of tolerance to parathion.
. A /
Moffitt et al. (1972)-' studied the toxicity of parathion and several
other frequently used orchard pesticides to the convergent lady beetle
(Hippodamia convergens), one of the more common and important predators
of aphids in deciduous fruit orchards in Washington. When adult beetles
were sprayed directly with parathion at 0.125 and 0.25 Ib AI/100 gaL
or exposed to residues from parathion sprays of these concentrations,
none survived. In orchard tests, percent survival of H^ convergens
adults exposed to residues of parathion applied at 0.125 and 0.25 Ib
AI/100 gal.was zero when the beetles were exposed for 2 days to 2-day-
old residues. When exposed'for 2 days to residues 9 days old, 83% of
the beetles survived in one test, none in another. Only 2% survived
exposure to 12-day-old deposits for 5 days.
The U>5o of parathion to adult beetles (topical application) was
0.062 ug/beetle.
These data indicate that parathion applications at the above rates
would not be compatible with survival of adult beetles under field
conditions.
•a /
Lingappa et al. (1972)—' studied the effects of parathion on three
developmental stages of Lysiphlebus testaceipes, a parasite of the
greenbug (Schizaphis graminum). Field-collected parasites were used
to experimentally parasitize greenbugs. One, four, and eight days after
parasitization, the greenbugs were transferred to sorghum plants about
I/ Croft, B. A., and L. R. Jeppson, "Comparative Studies on Four
Strains of Typhlodromus occidentalis. II. Laboratory Toxicity
of Ten Compounds Common to Apple Pest Control," J. Econ. Entomol.,
63(5):1528-1531 (October 1970).
2/ Moftitt, H. R., E. W. Anthon, and L. 0. Smith, "Toxicity of Several
Commonly Used Orchard Pesticides to Adult Hippodamia convergens,"
Environ. Entomol.. 1(1):20-23 (February 1972).
3_/ Lingappa, S. S., K. J. Starks, and R. D. Eikenbary, "Insecticidal
Effect on Lysiphlebus testaceipes, a Parasite of the Greenbug,
at Three Development Stages," Environ. Entomol., 1(4):520-521
(August 1972).
166
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10 days old and sprayed in the laboratory with parathion at the equiva-
lent of 0.25 Ib Al/acre, the common greenbug control dosage. Adult
parasites failed to emerge from the greenbugs that were exposed to
parathion 1 and 4 days after parasitism, while untreated controls had
94.1 and 93.9% emergence, respectively. Parasite emergence from the
greenbugs exposed to parathion 8 days after parasitization was 76.5%
(97.8% in the untreated control). The authors suggest that apparently
the host greenbugs were killed by the parathion treatment before the
parasite had completed larval development or, in the case of the 1-day-
old treatments, even before parasite eggs had hatched. Thus, field
sprays of parathion at these early states in the life cycle of the
parasite would be distinctly detrimental to parasite survival.
Several reports from overseas also deal with the effects of para-
thion on beneficial insects. Gupta and Kushwaha (1970)—' found that
parathion and several other insecticides were toxic to the aphid preda-
tor Menochilus sexmaculata. Satpathy et al. (1968)—' studied the
toxicity of parathion and seven other insecticides to the aphid preda-
tor Chilomenes sexmaculata by feeding adult beetles with insecticide
poisoned aphids. Parathion was among the insecticides most toxic to
the predator. Teotia and Tiwari (1972)—' also found parathion to be
among the insecticides most toxic to the aphid predator Coccinella
septembpunctata.
The reports summarized in this section indicate that parathion
would permit survival of beneficial insects in some crop pest predator/
parasite systems, but certainly not in all. The relative toxicity of
the insecticide to the pest and to the predators and parasites and
their respective life stages will have to be studied on a case-by-case
basis. At least some predators and parasites appear to be capable of
developing tolerance or resistance to parathion in the same manner as
many insect and mite pests.
I/ Gupta, R. S., and K. 8. Kushwaha, "Toxicity of Some Insecticides to
the Predator, Menochilus sexmaculata," Indian J. Entomol., 32(Pt.
4):379-381 (1970).
2_/ Satpathy, J. M., G. K. Padhi, and D. N. Dutta, "Toxicity of Eight
Insecticides to the Coccinellid Predator Chilomenes sexmaculata."
Indian J. Entomol., 30(1):130-132 (1968).
3_/ Teotia, T. P. S., and G. C. Tiwari, "Toxicity of Some Important
Insecticides to the Coccinellid Predator, Coccinella septempunctata,"
Labdev. Part B, 10(1):17-18 (1972).
167
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Interactions with Lower Terrestrial Organisms
Reviews - The relationships between insecticides and microorganisms
have recently been reviewed by several authors. Matsumura and Boush
(1971)—' point out that organic phosphate pesticides (including para-
thion) have thus far apparently neither presented serious problems in
soils as regards undesirable persistence, nor demonstrated an extra-
ordinary affinity for fat with resulting concentration within a food
chain. Although considerable variations exist between individual
organophosphates, most of them are readily degraded in soil, mainly
by hydrolytic and oxidative means.
These authors also point out that, although several workers have
demonstrated in the laboratory that some microorganisms are able to
degrade even the most stable and persistent organic insecticides, no
one has yet demonstrated whether or not this occurs in nature, or
even that these compounds serve as nutritional or energy sources for
organisms. "In fact there are no reports as yet that these chemicals
have been shown to serve as sole nutritional carbon sources." The
incredible biological and chemical complexity of the soil is a formid-
able obstacle to gaining an understanding of the fate of pesticides in
that habitat, and of the mechanisms involved in their metabolism and
degradation in situ.
Another recent review of the interactions between pesticides
(including parathion) and the soil fauna was authored by Drift (1970).—'
Ecology, degradation and movement of pesticides in the soil were
reviewed in an international symposium at Michigan State University
in 1970. The proceedings of this symposium have been published and
contain a wealth of general data and overviews of different aspects
of the subject, but no reports dealing specifically with parathion.
I/ Matsumura, F., and G. M. Boush, "Metabolism of Insecticides by
~" Microorganisms," Soil Biochem., Vol. II pp. 3.20-336, Marcel Decker,
New York (1971).
21 Drift, j., "Pesticides and Soil Fauna," Meded. Rijksfac. Land-
bouwwetensch..Gent, 35(2) : 707-716 (1970).
168
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Field Studies - Bollen et al. (1954)i/ investigated the effects of
field treatments of insecticides, including parathion, on the numbers
of bacteria, Streptomyces, and molds in field plots in Oregon. Para-
thion in the form of a wettable powder was incorporated with the soil
by rotary tillage at the rate of 10 Ib Al/acre. Composite soil sam-
ples at plow depth were taken on the day of application and trans-
ported to the laboratory in paper bags or friction-top tin cans.
These containers were opened and allowed to stand, well isolated
from each other, until sufficiently dry for screening. The samples
were then passed through a 10-mesh sieve and stored in friction-top
cans at room temperature for 10 to 20 days, when they were counted.
The counts of molds and bacteria in the parathion-treated samples
differed very little from those in the untreated controls.
Hubbell et al. (1973)-^ studied the effects of several pesti-
cides, including parathion, on the relative numbers of microbes and
on nitrification in field plots to which the pesticides, alone and
in combination, had been applied at times and rates of application
approximating current agronomic practice in the growing of shadeleaf
tobacco in the area of Quincy, Florida. Numbers of microbes and
nitrification were monitored at 2-week intervals for 16 weeks follow-
ing application. There were no significant effects from the pesticide
treatments on the relative numbers of bacteria and actinomycetes.
The count of fungi increased in the parathion + DDT + Zineb treatment.
There were no significant effects on nitrification.
Wolfe et al. (1973)2/ investigated the effects of very high
levels of parathion on soil microorganisms. The extreme concentra-
tions of parathion in the soil studied by these authors resulted from
simulated spillage of concentrated parathion emulsifiable liquid and
dilute sprays. Soil from a test plot that had received a topical
application of 45.5% emulsifiable concentrate of parathion 2 years
I/ Bollen, W. B., H. E. Morrison, and H. H. Crowell, "Effect of Field
Treatments of Insecticides on Numbers of Bacteria, Streptomyces,
and Molds in the Soil," J. Econ. Entomol.. 47(2):302-306 (1954).
2/ Hubbell, D. H., D. F. Rothwell, W. B. Wheeler, W. B. Tappan, and
F. M. Rhoads, "Microbiological Effects and Persistence of Some
Pesticide Combinations in Soil," J. Environ. Qual., 2(l):96-99
(1973).
3/ Wolfe, H. R., D. C. Staiff, J. F. Armstrong, and S. W. Comer,
"Persistence of Parathion in Soil," Bull. Environ. Contain. Toxicol..
10(1):1-9 (1973).
169
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earlier contained 3.47. parathion, a concentration equivalent to 136,000
Ib Al/6 acre-ft. Soil from this plot and soil from a comparable, un-
treated control plot were plated on nutrient yeast-dextrose agar con-
taining different levels of parathion, to determine if the soil organ-
isms might have developed resistance or tolerance to the insecticide.
The number of colonies that developed in 6 days at 70°F was used as an
indicator. Significantly fewer colonies of microorganisms were isolated
from the treated soil. Microorganisms from the treated soil showed no
evidence of resistance to parathion.
These data indicate that soil organisms survive extremely high
concentrations of parathion in the soil, even though they were adversely
affected.
Laboratory Studies - Several authors have investigated interactions
between parathion and isolated microorganisms under laboratory condi-
tions.
Mick and Dahm (1970)!' incubated parathion at concentrations in
the range of 10~^ to 10"^M with cultures of two species of Rhizobium
and found that these fungi metabolized the insecticide primarily by
nitroreduction. Eighty-five percent of the initial parathion was
reduced to aminoparathion. About 10% was hydrolyzed to the correspond-
ing phosphorothioic acid. Both of these degradation products have
negligible toxicity compared to parathion. No paraoxon was detected.
Populations of both Rhizobium species decreased somewhat in the pres-
ence of parathion in the incubation mixtures.
Mackiewicz et al. (1969)—' investigated the biodegradation of
parathion in a germ-free system. Bean roots grown under aseptic con-
ditions were exposed to parathion for 7 days with or without the alga
Chlorella. The only pesticide-related product found in extracts from
the aerial parts of plants exposed to the insecticide alone was parathion.
If Mick, D. L., and P. A. Dahm, "Metabolism of Parathion by Two Species
" of Rhizobium," J. Econ. Entomol.. 63(4):1155-1159 (August 1970).
21 Mackiewicz, M., K. H. Deubert, H. B. Gunner, and B. M. Zuckerman,
"Study of Parathion Biodegradation Using Gnotobiotic Techniques,"
J. Agr. Food Chem.. 17(1):129-130 (January/February 1969).
170
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By contrast, parathlon and a sulfur-containing parathion metabolite
were recovered from bean leaves and stems of plants whose roots were
exposed to both parathion and the algae. The authors conclude that
parathion metabolites found in plants may be a product of microbial
metabolism, rather than metabolism by the plant as has generally been
assumed by other authors. They emphasize the utility of, and often
the requirement for, germ-free systems in the study of the degradative
pathways of pesticides.
Cowley and Lichtenstein (1970)17 studied the toxic effects of
parathion and other insecticides on 17 species of fungi from Wisconsin
prairie soils. The fungi, including Aspergillus fumigatus and Fusarium
oxysorum, were grown on nutrient agar that had been treated with the
insecticides at six rates, ranging from 1 to 40 ug/ml. The pesticide-
containing inoculated culture media were incubated for 5 days at about
34°C. The dry weight of each colony was then determined as a measure
for the toxicity of the insecticides. In further, similar tests, yeast
extract, vitamins, and nitrogenous compounds were added to the cultures
to study possible counteractions of insecticidal effects. Relative
sporulation was evaluated by visual inspections, and the diameter of
each fungal colony was also recorded.
Parathion and all other insecticides inhibited the growth of most
of the fungal species. Threshold concentrations at which no decrease
in fungal growth occurred differed for each compound, and also for each
of the two fungal species. None of the fungi tested were able to use
parathion or any of the other insecticides as a source of carbon or
phosphorus.
2 /
Anderson (1971)—' investigated the capacity of several fungi iso-
lated from an agricultural loam soil to degrade DDT or dieldrin. He
reported that Mucor alternans in shake cultures partially degraded DDT
within 2 to 4 days into two water-soluble metabolites. At a concen-
tration of 1 ppm, parathion partially inhibited DDT degradation by this
fungus, although fungal growth was not drastically affected. A para-
thion hydrolysis product, p-nitrophenol, had no effect on fungal growth
or DDT degradation.
I/ Cowley, G. T., and E. P. Lichtenstein, "Growth Inhibition of Soil
Fungi by Insecticides and Annulment of Inhibition by Yeast Extract
or Nitrogenous Nutrients," J. Gen. Microbiol.. 62(l):27-34 (1970).
2/ Anderson, J. P. E., "Factors Influencing Insecticide Degradation
by a Soil Fungus, Mucor Alternans," Piss. Abstr. Int.. 32(6):3114B-
3115B (1971).
171
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Sethunathan and Yoshida (1972, 1973)!*^/ found that parathlon
and several other organic phosphate insecticides were rapidly hydro-
lyzedby a cell-free extract of a species of Flavobacterium isolated
from water of a rice field that had previously been treated with
diazinon. Most of the parathion was rapidly decomposed.(within 30
min), without a lag phase. The major metabolite formed was p-nitro-
phenol which was not further degraded by the organism. No appreciable
degradation of aminoparathion was observed.
Griffiths and Walker (1970)^ investigated the microbiological
degradation of parathion in soil percolation experiments. Parathion
in the soil was degraded by a heat labile agent which was transferable
in small amounts between soil cultures. This observation is consistent
with the effects of microorganisms, but the responsible organisms have
not been isolated in pure cultures.
Residues in Soil
4/
Laboratory Studies - Iwata et al. (1973)— investigated the persistence
of parathion in six California soils under laboratory conditions.
Each soil was fortified with 20 ppm (equivalent to 80 Ib AI/6 acre-foot)
of parathion, kept in enameled trays, and maintained at 30°C and a soil
moisture level of approximately 40% of saturation. In four of the six
soils (Mocho silt loam, Linne clay, Madera sandy loam, and Laveen loamy
sand), residues decreased rapidly, i.e., from 20 ppm to 0.2-2.0 ppm in
30 days. Chemical hydrolysis and microbial degradation were responsible
for the rapid decline. In Windy loam, the residue remained above 3,0
ppm after 8 months. In two experiments differing slightly in soil
I/ Sethunathan, N., and T. Yoshida, "Conversion of Parathion to Para-
nit rophenol by Diazinon Degrading Bacterium," Proc. Inst. Environ.
Scl. Annu. Tech. Meet. 18:255-257 (1972).
2j Sethunathan, N., "Degradation of Parathion in Flooded Acid Soils,"
J. Agr. Food Chem.. 21(4)-.602-604 (1973).
3/ Griffiths, D. C., and N. Walker, "Microbiological Degradation of
~" Parathion," Meded. Rijksfac. Landbouvwetensch., Gent, 35(2):805-810
(1970).
4/ Iwata, Y., W. E. Westlake, and F. A. Gunther, "Persistence of Para-
thion in Six California Soils Under Laboratory Conditions," Arch.
Environ. Contain. Toxicol., 1(1):84-96 (1973).
172
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moisture, the residue in Santa Lucia silt loam was about 1.5 ppm after
8 months in one experiment, and about 0.5 ppm after 6 months in the
other. The latter two soil types gave linear semilogarithmic per-
sistence curves, suggestive of degradation by hydrolysis. The degrada-
tion of the parathion residues remaining in Windy loam (3.2 ppm) and
Santa Lucia silt loam (2.2 ppm) 7.7 months after fortification was not
greatly accelerated by flooding with water. Parathion disappeared
more rapidly in soils with low organic matter, suggesting that binding
to organic matter may reduce the availability of parathion for degradation.
According to the authors, the results of this study support the
conclusion of other investigators that most of the parathion applied
to soil disappears rapidly, but that low levels may be retained by the
soil for extremely long periods. The persistence of parathion is par-
tially dependent on soil types. In soils with strong microbial activity,
rapid biological degradation tends to overshadow differences in soil
types. In situations where hydrolysis is the primary degradative mech-
anism, differences in soil type exert greater influence.
Campbell et al. (1971)—' studied the influence of organic matter
content of soils on the efficacy of parathion against the wireworm
(Melanotus communls)in the laboratory. Parathion and most of the other
insecticides tested were affected by the organic matter content of the
soil; wireworm control increased with decreasing organic matter content.
These observations support the results of other studies, including those
by Iwata et al. (1973) discussed above, that soil organic matter binds
parathion residues, reducing their availability for insect control as
well as degradation.
7 /
Weidhaas et al. (1961)—' reported on the adsorption of parathion
by soil from water dispersions and vermiculite granules. Different
volumes of water (100 or 250 ml) containing 0.02 ppm of parathion were
added to jars containing 50 g of soil that had been premoistened with
25 ml of untreated water. Changes in the insecticide content of the
supernatant water and of the soil were monitored by analyzing extracts,
0, 6, and 24 hr after preparation. Immediately after initiation of the
If Campbell, W. V., D. A. Mount, and B. S. Heming, "Influence of
Organic Matter Content of Soils on Insecticidal Control of the
Wireworm," J. Econ. Entomol., 64(l):41-44 (1971).
2_/ Weidhaas, D. £., M. C. Bowman, and C. H. Schmidt, "Loss of Para-
thion and DDT to Soil from Aqueous Dispersions and Vermiculite
Granules," J. Econ. Entomol., 54(1):175-177 (1961).
173
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test, most of the parathlon was found in the water, but the amount in
the soil increased as time elapsed, indicating soil adsorption. When
parathion was applied in formulations on vermiculite granules contain-
ing 0.01 and 0.0257. of AI (weight/weight), it was readily released
into water from the granules. The radiometric results were supplemented
by bioassay tests of extracts of water and soil with mosquito larvae.
The results show that parathion dispersed in water looses insecticidal
toxicity in the presence of soil, and that this loss results primarily
from adsorption on the soil.
Harris (1966)17 investigated the bioactivity of parathion and
other insecticides in 10 soil types, employing a bioassay technique
using first instar nymphs of the common field cricket (Acheta
pennsylvanicus) as the test insect. Soils were tested both dry and
moist. In most soils, bioactivity was dependent on the organic con-
tent of the soil. Parathion was 1,132 times less active in a muck
soil containing 64.6% organic matter as compared to quartz sand. There
was no direct correlation between organic content and bioactivity in
dry soils. The presence of moisture activated parathion in mineral
soils, but not in muck soils. The author concluded that in muck soils,
parathion (and other insecticides) appear to be sorbed in such a fashion
that they are not released from active sites on soil particles in the
presence of moisture. Between different pesticides (chlorinated hydro-
carbon and organophosphate insecticides) and different soil fractions
(clay, sand, silt, and organic), at least three different bonding
mechanisms appear to exist.
Burkhardt and Fairchild (1967a)-' also employed a cricket species,
Acheta domesticus, as bioassay test insects in laboratory studies de-
signed to determine the bioactivity of parathion and other insecticides
in five soil types, each at two moisture levels. The insecticidal
activity of parathion (and of the other insecticides tested) varied
with soil type and moisture content. Highest initial insect mortality
was obtained in the sandy soils, but the residual activity was shorter
in these. Increased moisture generally resulted in increased insect
mortality.
I/ Harris, C. R., "Influence of Soil Type on the Insecticidal Activity
of Insecticides in Soil," J. Econ. Entomol.. 59(5):1221-1225
(1966).
2/ Burkhardt, C. C., and M. L. Fairchild, "Toxicity of Insecticides to
House Crickets and Bioassay of Treated Soils in the Laboratory,"
J. Econ. Entomol.. 60(6):1496-1503 (1967a).
174
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Llchtenstein et al. (1966)17 studied the effects of detergents on the
persistence of parathion in the soil. The addition of alkyl benzene
sulfonate detergents to insecticide-treated soils increased the per-
sistence of parathion. Parathion was applied to Carrington silt loam
free of insecticidal residues at the rate of 10 ppm. The treated
soils, with and without detergents added, were incubated for 15 days
at 30°C. At that time, 28.57. of the amount of parathion applied was
recovered from the soil without added detergents, while 79.5 and 80.07,,
respectively, of the applied rate were recovered from soils to which
two different detergents had been added. Soils not treated with the
detergents had an average count of 4.33 million bacteria per gram of
dry soil, while those treated with the detergents contained 56.7 and
228 million, respectively, 15 days after incubation.
In a further experiment, parathion was applied to a loam soil
and a quartz sand at the rate of 10 ppm with or without detergents.
Two months after the insecticidal and detergent applications, 13 times
more parathion was recovered from the loam soil that had been treated
with detergent, as compared to the series free of detergents. In the
quartz sand, only 0.5 to 3 times more parathion was recovered from the
detergent-containing as compared to the detergent-free systems.
The effects of detergents and inorganic salts in water on the
persistence and movement of parathion in soils were investigated by
Lichtenstein et al. (1967).£/ Quartz sand of low sorptive capacity
and minimal microbiological activity served as control. The effects
of the sorptive capacities of a loam soil became evident. Water that
had been treated at the rate of 2 Ib of parathion per 6-in. acre con-
tained only small amounts of parathion after it had been percolated
through untreated loam soil. The amount of parathion found in the
percolated water was a function of the concentration of the insecticide
in the soil. When detergents (alkyl benzene sulfonates) were added to
the system, they increased the persistence of parathion in the soil
and the amount of parathion in the percolated water. When untreated
water, with or without added detergents, was percolated through soil
treated with parathion at the rate of 20 Ib Al/acre, parathion concen-
trations in the percolated water samples ranged from 0.2 to 0.8 ppb.
I/ Lichtenstein, E. P., K. R. Schulz, R. F. Skrentny, and Y. Tsukano,
"Toxicity and Fate of Insecticide Residues in Water," Arch. Environ.
Health, 12:199-212 (1966).
2_/ Lichtenstein, E. P., T. W. Fuhremann, K. R. Schulz, and R. F.
Skrentny, "Effect of Detergents and Inorganic Salts in Water on
the Persistence and Movement of Insecticides in Soils," J. Econ.
Entomol.. 60(6):1714-1721 (1967).
175
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These amounts are far below the water solubility of parathion, and the
water was not toxic to mosquito larvae. When salts were added to the
percolating water, it reduced the amount of parathion residues found in
it.
From these results, the authors conclude that it appears unlikely
that water in deeper soil strata could become contaminated with insec-
ticidal residues from the upper agricultural soil layers.
The behavior of parathion when applied to the surface of soils was
studied in flow-through lysimeters by Herzel (1971).U ' The lysimeters,
1.35 m long, were packed with sand or sandy loam, with or without a 20-cm
covering of humus, treated with parathion and the other insecticides at
recommended rates, and watered with the equivalent of normal or excessive
rainfall. Samples of the runoff and percolated water collected through-
out the test, and soil cores taken at the end of the 8-month test were
analyzed by gas chromatography. Parathion (as well as the other insec-
ticides studied) moved downward more easily in the sand than in the loam,
and was strongly retained in the humus covering. No parathion was found
in any of the soil or water samples after 8 months.
In a follow-on test, 10 ml of concentrated parathion was applied
to the center of the lysimeter surfaces. For an additional period of
15 months, one-half of the lysimeters were again watered with the equiva-
lent of normal rainfall, the other half at the excessive rate, equiva-
lent 0.4 in. of precipitation each day. After 15 months in this second
test, very little parathion was found at the 50- to 100-cm soil levels.
Sethunathan (1973) studied the persistence of parathion in India
in five acid soils under flooded conditions. The product degraded
faster in soils which had a high organic matter content. The fastest
degradation occurred in an acid sulfate soil with an organic content
of 12.2%. The author attributes this to microbial participation.
Hydrolysis of parathion to j^-nitrophenol was enhanced by repeated
additions of parathion to an alluvial soil. Heat treatment of this
system retarded the rate of hydrolisis of parathion, indicating the
role of biological agents in the process. A Bacillus species capable
of readily decomposing jo-nitrophenol was isolated from the parathion
enriched flooded alluvial soil.
if Herzel, F., "The Behavior of Several Persistent Insecticides in the
Soil," Bundesgesundheitsblatt 14(3):23-28 (1971).
176
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Sethunathan and Yoshida (1973)1.' studied the persistence and
degradation of parathion in Philippine rice soils in the laboratory,
simulating submerged and upland conditions. Parathion was incubated
in the different soils at 30°C, then extracted with a hexane-acetone
mixture and determined by gas chromatography. Parathion disappeared
more rapidly from submerged soils than from upland soils. In sub-
merged soils, it was reduced to aminoparathion. Autoclaving of the
soils increased the persistence of parathion under submerged condi-
tions, indicating microbial involvement in the degradation. Inocula-
tion of flooded soils with Flavobacterium species accelerated the rate of
degradation of parathion as compared to uninoculated soil. This bac-
terium, isolated from paddy water, had been shown to be highly efficient
in hydrolyzing parathion in previous tests.
2/
Chopra and Khullar (1971)— found that the following experimental
conditions accelerated the rate of degradation of parathion in soils
in laboratory tests: increased concentration of parathion; increased
temperatures; increased time of exposure to UV light; increased rela-
tive humidity; and increased pH. Hydrolysis was more rapid in alkaline
and acidic soils than in neutral ones. The authors point out that some
of the loss occurring with increasing temperature may have been due to
vaporization.
Swoboda and Thomas (1968)—' investigated the movement of para-
thion in eight important agricultural soils from various locations in
Texas in laboratory studies. ^^P-labeled parathion was applied at an
initial concentration of 16.5 ppm (equivalent to 66 Ib Al/acre-foot)
to laboratory columns prepared from the soils, and leached through the
columns with distilled water. Distribution coefficients for the adsorp-
tion of parathion were calculated, and the amount of rainfall required
to leach parathion to a depth of 60 in. was estimated. This amount
varied from 230 in. for a Nacogdoches clay subsoil to 1,725 in. for a
Houston Black clay surface soil. Desorption experiments indicate that
parathion is not effectively displaced by inorganic electrolyte salts,
or by aqueous solutions. However, it moved swiftly through the soil
JL/ Sethunathan,N., and T. Yoshida, "Parathion Degradation in Submerged
Rice Soils in the Philippines," J. Agr. Food Chem.. 21(3):504-
506 (1973).
2_/ Chopra, S. L., and F. C. Khullar, "Degradation of Parathion in Soils,"
J. Indian So. Soil Sci., 19(1):79-85 (1971).
3_/ Swoboda, A. R., and G. W. Thomas, "Movement of Parathion in Soil
Columns," J. Agr. Food Chem.. 16(6):923-927 (November/December
1968).
177
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columns when leached with ethanol. From the data obtained, the authors
conclude that it is very unlikely that parathion could contaminate
underground water supplies beneath any of these soils by leaching under
normal rainfall conditions.
Leenheer and Ahlrichs (1971)!/ performed kinetic and equilibrium
studies on the adsorption of parathion on soil organic matter surfaces,
using two types of Indiana soil, i.e., a silty clay loam and a muck
soil. They found that the differences in adsorptive characteristics
of various types of soil organic matter were small, but changing the
saturating cation from calcium to hydrogen greatly increased the adsorp-
tive capacity for parathion. The authors conclude that the fast adsorp-
tion rates, the low heats of adsorption, the reversibility of adsorption,
and the high adsorptive capacities on hydrophobic surfaces tend to rule
out chemisorption, pointing instead to physical adsorption with forma-
tion of Van der Waals bonds between the hydrophobic portions of the
pesticide molecules and the adsorbent surfaces in aqueous systems.
Saltzman et al.(1972),-' Saltzman and Yaron (1972)2/, and Yaron
and Saltzman (1972)*' used parathion labeled with 14C in the alkyl
chain in studies on the influence of soil organic matter on the adsorp-
tion of parathion. In aqueous solutions, parathion had greater affin-
ity for organic than for mineral colloid adsorptive surfaces. Parathion
bonding was stronger on organic than on mineral surfaces. When aqueous
and hexane solutions containing from 1 to 10 ug of parathion per milli-
liter were applied to three soil types under different conditions, there
was no appreciable thermic effect on the adsorption of parathion from
aqueous solutions after correction for increased solubility. Increasing
soil water content resulted in decreasing parathion adsorption.
\l Leenheer, J. A., and J. L. Ahlrichs, "A Kinetic and Equilibrium
Study of the Adsorption of Carbaryl and Parathion Upon Soil Organic
Matter Surfaces," Soil Sci. Am. Proc.. 35(5):700-705 (1971).
2_/ Saltzman, S., L. Kliger, and B. Yaron, "Adsorption-Desorption of
Parathion as Affected by Soil Organic Matter," J. Agr. Food Chem.,
20(6):1224-1226 (1972).
3/ Saltzman, S., B. Yaron, "Parathion Adsorption from Aqueous Solutions
as Influenced by Soil Components." In: Fate of Pesticides in
Environment, Gordon and Breach, London, pp. 87-100 (1972).
4_/ Yaron, B., and S. Saltzman, "Influence of Water and Temperature on
Adsorption of Parathion by Soils," Soil Sci. Soc. Am. Proc.,
36(4):583-586 (1972).
178
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In another test series, adsorption isotherms were obtained for
20 soils, Na-kaolinite, Na-montmorillonite, organic material, and
glass beads. The results showed that the main soil components affect-
ing parathion adsorption are the expanding-lattice clays and the
organic matter which present linear adsorption isotherms. Parathion
adsorption on nonexpanding-lattice clays and on noncolloidal soil
materials is reduced.
King and McCarty (1968)i/ developed a chromatographic model for
predicting pesticide migration in soils. For several insecticides,
including parathion, theoretical elution curves based on chromato-
graphic theory were developed and compared with experimental degrada-
tion and leaching data. Four soil types, and different column lengths
and pesticide application rates were employed. Analysis of the experi-
mental data and their correlation with the theoretically derived curves
establish the feasibility of predicting the extent to which organic
phosphate insecticides may be leached through soil columns. The equa-
tion describing the chromatographic movement of the pesticides takes
into account the noncontinuous flow conditions which would be expected
in typical agricultural practice. Critical variables include the
degradation rate of the pesticide, the distribution of the pesticide
in the soil water environment, and the decay reaction rate constant
under the environmental conditions prevailing. Problems may arise
when the water solubility of the pesticide is approached, if the
degradation of the pesticide increases due to biological acclimation,
and from similar factors.
Field and Combined Field-Laboratory Studies -
Short-term studies - Several authors have studied the persistence
of parathion under field conditions.
Lichtenstein and Schulz (1964)—' applied parathion at 5 Ib Al/acre
to Carrington silt loam field plots. Residue levels of parathion of
approximately 0.1 ppm (3.1% of the applied dosage) were reached under
field conditions within 90 days after the insecticidal application to
the soil.
I/ King, P., and P. L. McCarty, "A Chromatographic Model for Predicting
Pesticide Migration in Soils," Soil Sci.. 106(4):248-261 (1968).
2/ Lichtenstein, E. P., and K. R. Schulz, "The Effects of Moisture
and Microorganisms on the Persistence and Metabolism of Some
Organophosphorus Insecticides in Soils, with Special Emphasis
on Parathion," J. Econ. Entomol.. 57:618-627 (1964).
179
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Under laboratory conditions (30°C), 30% of the applied parathion
dose was lost within 12 days after application to a loam soil. In
further laboratory studies, the effects of moisture and microorganisms
on the persistence and metabolism of parathion in Carrington silt loam
soil were tested at 30°C. Parathion was most persistent in dry soil,
least persistent in soils with high moisture content. There was no
loss of parathion through volatilization. Parathion was degraded either
by hydrolysis or by reduction to its amino form, depending on popula-
tions of soil microorganisms. In autoclaved soils that had low numbers
of microorganisms, or in dry soils in which microorganism activity was
low, parathion residues persisted for a relatively long time. No amino-
parathion was formed in autoclaved soils. Paraoxon, a parathion metab-
olite, was hydrolyzed within 12 hr after its application to loam soil
at 20 ppm. During that time, the amount of paraoxon decreased con-
stantly, while the amount of j>-nitrophenol increased. Aminoparathion
or £-nitrophenol, added to soils, disappeared within 2 and 16 days,
respectively.
Burkhardt and Fairchild (1967b)i' applied parathion (from a
granular formulation) at 1, 2 and 4 Ib Al/acre in a 7-in. band at
planting time in field studies located in four counties in Missouri.
Soil samples were taken at various depths both in the treated row and
adjacent to the row, and bioassayed with 21-day old house crickets,
Acheta domesticus. to determine bioactivity and vertical and lateral
movement of the insecticide. Based on the bioassay results from all
field plots combined, parathion at 1 Ib Al/acre provided 78% mortality
after 1 day; 77% after 1 week; 86% after 2 weeks; 47% after 4 weeks;
37« after 6 weeks; 0% after 8 weeks. At the 4-lb Al/acre rate, para-
thion provided 1007. mortality during the first 2 weeks after applica-
tion; 98% after 4 weeks; 33% after 6 weeks; 25% after 8 weeks. Results
from the 2-lb Al/acre rate were intermediate. At all three applica-
tion rates, there was a sharp drop in bioactivity after the 4th week.
There was little downward movement of parathion; in the majority of
soil samples from the parathion-treated plots, very little or no bio-
activity was found more than 3 in. below the soil surface. Horizontal
movement of parathion likewise was minimal.
I/ Burkhardt, C. C., and M. L. Fairchild, "Bioassay of Field-Treated
Soils to Determine Bioactivity and Movement of Insecticides,"
J. Econ. Entomol.. 60(6):L1602-1610 (1967b).
180
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Sacher et al. (1972)1' studied the bioactivity and persistence of
several parathion formulations in the soil under laboratory and field
conditions. They found that moisture and soil type influenced the
rate of degradation of parathion, but this influence was mediated pri-
marily by the activity of microorganisms. Highest biological activity
against larvae of the Western corn rootworm, Diabrotica virgifera, in
soil was obtained with a low-concentrate formulation with minimum bind-
ing of parathion (1% kaolinite dust, insect 1*050 0.05 ppm), whereas
low activity resulted from a tightly bound, concentrated, thinly dis-
tributed formulation (10% on charcoal, LD^g 6.0 ppm). However, para-
thion applied by way of the kaolinite dust formulation had a half-life
in soil of only 6 days, compared to more than 72 days for the 107. char-
coal granules.
Microbial degradation appeared to be a major contributor to para-
thion breakdown in soil. Ray silt loam was treated with parathion 10%
granules on vermiculite at 20 ppm. Only about 30% of the applied rate
was still present, as determined by chemical assay, 6 weeks after
treatment. When the same soil was sterilized by treatment with methyl
bromide (1 g/100 g of soil) prior to the parathion application, there
was no appreciable parathion decline after 6 weeks.
The importance of microbial activity in the soil degradation of
parathion was further demonstrated in field tests in which it was
shown that the rate of parathion degradation was much slower in field
soils in the winter months when soil microorganisms are dormant. Most
rapid breakdown occurred in August and September when the half-life of
parathion in the soil was as short as 1.5 weeks.
2/
Knutson et al (1971)—' studied the relationships between insecticide
usage and resulting residues in a newly developed irrigation district
in central Kansas. This area had previously been under dry land farm-
ing practices with little exposure to insecticides. Parathion was
applied to irrigated corn at planting time at treatment rates ranging
from 0.79 to 1.40 Ib Al/acre each year during a 4-year period, 1966
to 1969. Soil samples taken immediately after each annual application
I/ Sacher, R. M., G. F. Ludvik, and J. M. Deming, "Bioactivity and
Persistence of Some Parathion Formulations in Soil," J. Econ.
Entomol., 65(2):329-332 (April 1972).
21 Knutson, H., A. M. Kadoum, T. L. Hopkins, 6. F. Swoyer, and T. L.
Harvey, "Insecticide Usage and Residues in a Newly Developed
Great Plains Irrigation District," Pest. Monit. J.» 5:17-27 (1971)
181
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had average parathion residues ranging from 0.5 ppm to 4.07 ppm. No
detectable parathion residues were found in samples obtained 1.5 and
2.5 months after treatment. No residues vere detected in corn; grain,
in capped wells from 13 to 71 ft deep, nor in surface water samples
from the Smoky Hill River and the Cedar Bluff Reservoir, the water
bodies draining the area.
Harris and Sans (1971)—' studied insecticide residues in soils on
16 farms in southwestern Ontario in 1964, 1966, and 1969. Residues of
organophosphate insecticides were determined qualitatively by a non-
specific enzymatic analysis, and quantitatively by 6LC where possible.
The use pattern of insecticides in the area showed that organophosphate
insecticides were used at an increasing rate from 1965 to 1969. Pre-
liminary findings indicated that the more extensive use of the organo-
phosphate insecticides resulted in residues of these products in
vegetable soils, while the enzyme inhibition tests in 1969 indicated
that inhibitory substances were generally below significant levels in
field crop, tobacco, and orchard soils. Parathion and paraoxon residues
were positively identified by GLC analysis on at least one of the 16
farms studied.
2/
Mol et al. (1972)=-' investigated the persistence of parathion
residues in the field after winter applications of parathion at 3.0
and 6.0 Ib/acre in Australia. Parathion residues in top soil de-
creased from 6.5 ppm initially to 4.7 ppm 3 months after application
of the lower rate, and from 10.7 ppm to 8.5 ppm at the higher rate.
No detectable residues were found in the soil at either application
rate after 8 months. Little soil penetration of parathion was found
below a depth of 1 in.
Kilgore et al. (1972)!/ analyzed soil samples from a vineyard
sprayed with parathion emulsifiable concentrate at 4 and 8 Ib. Al/acre
for parathion residues. Following the 4 Ib/acre application, parathion
I/ Harris, C. R., and W. W. Sans, "Insecticide Residues in Soils on 16
" Farms in Southwestern Ontario - 1964, 1966, 1969," Pest. Monit. J..
5(3):259-267 (December 1971).
2j Mol, J. C. M., D. L. Harrison, and R. H. Talfer, "Parathion: Toxicity
to Sheep and Persistence on Pasture and in Soil," N.Z. J. Agr. Res..
15(2):306-320 (1972).
3/ Kilgore, W. W., N. Marey, W. Winterlin, "Parathion in Plant Tissues:
New Considerations." In: Degradation of Synthetic Organic Molecules
in the Biosphere, National Academy of Sciences, pp. 291-312 (1972).
182
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concentration in the soil was 21 ppm at 0 days, 0.06 ppm at 46 days
after treatment. Following the 8-lb/acre treatment, parathion con-
centration in the soil was 70 ppm at 0 days, 0.13 ppm at 46 days after
treatment.
Long-term field studies - Stewart et al. (1971)!/ and Chisholm and
MacPhee (1972)2/ investigated the long-term persistence and effects of
parathion (and several other pesticides) in the soil in a field experi-
ment at Kentville, Nova Scotia. Parathion was applied to a sandy loam
at the rate of 31.4 Ib Al/acre (equivalent to 15.7 ppm in the upper
6 in. of soil) from a 15% wettable powder formulation. This rate was
intended to approximate the maximum concentration in the soil (neglect-
ing loss through volatilization, etc.) that might accrue from an inten-
sive spray program carried on over a 20- to 25-year period, and it was
applied each spring from 1949 to 1953 inclusive. Each time, the in-
secticide was thoroughly incorporated to a depth of 6 in. with a rotary
cultivator, and various crops were grown on the plots each year up to
1969. In the spring of 1969, 16 years after the last application, soil
samples were taken at various depths from the experimental plots and
analyzed for parathion residues. The 0.06 ppm of parathion was found
in the 0-to 4-in. soil layer; 0.063 ppm in the 4-to 8-in. layer, 0.008
ppm in the 8-to 12-in. layer, and a trace amount at the 12-to 16-in.
depth. Thus, about 0.1% of the total parathion applied to the plot
(157 Ib Al/acre) was still present 16 years after the last application.
Voerman and Besemer (1970)27 reported on an experiment started in
1953 at Wageningen, The Netherlands, and continued for 15 years, up to
1968. Parathion (and other insecticides) were sprayed in two concen-
trations on crops several times each year. In addition, soil treat-
ments of these insecticides were applied once a year. Soil and crop
samples were takenvand analyzed throughout the entire period. The
experiment was conducted in light, sandy soil. From 1963 to 1968, the
total quantities of parathion applied to three different plots were
10.4, 21.5 and 111.4 Ib Al/acre. Soil residues found in the 0-to 4-in.
I/ Stewart, D. K. R., D. Chisholm, and M. T. H. Ragab, "Long-Term
Persistence of Parathion in Soil," Nature, 229:47 (1971).
2f Chisholm, D., and A. W. MacPhee, "Persistence and Effects of Some
Some Pesticides in Soil," J. Econ. Entomol., 65(4):
1010-1013 (August 1972).
3_/ Voerman, S., and A. F. H. Besemer, "Residues of Dieldrin, Lindane,
DDT, and Parathion in a light Sandy Soil After Repeated Applica-
tion Throughout a Period of 15 Years," J. Agr. Food Chem., 18(4):
717-719 (1970).
183
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soil layer after 15 years of repeated applications were 0.01, 0.02 and
0.06 ppm, respectively, equivalent to 0.17. of the applied amount for
each application rate. No parathion residues.were detected in the
4-to 8-in. soil layer in the plots that had received the two lower
rates, while 0.02 ppm was found in that layer following the heaviest
parathion applications. No parathion residues were found in deeper
soil layers.
Massive soil contamination with parathion may result from the
spillage of pesticides, especially from repeated spillage in areas
where spray tanks are routinely loaded. Wolfe -.and Durham (1966)I/
set up a replicated field test to simulate spillage of undiluted para-
thion emulsifiable concentrate containing 45.6% Al/gal. In another
test, soil contamination from tank drainage on the ground with dilute
(Ix) and concentrate (8x) liquid sprays, using both wettable powder
and emulsifiable concentrate formulations, was simulated. The test
plots were in orchard silt-loam soil with high organic material con-
tent, and a pH ranging from 4.4 to 5.5. The plots were exposed to
weathering and regular sprinkler irrigation.
The top 1 in. of soil contaminated with the emulsifiable concen-
trate contained 59,000 ppm of parathion Initially. Forty-six percent
of this residue was still present after 2 years. The soil contaminated
with the dilute formulations had initial surface-soil concentrations
of parathion of 98 to 108 ppm from the Ix spray, and from 370 to 1,126
ppm from the 8x spray.
The authors then collected and analyzed top soil samples from 37
spray tank fill sites throughout the Wenatchee Valley, Washington area.
The time intervals between contamination of soil and sampling for analysis
were not known. Parathion residues found ranged from 0.3 to 330 ppm, with
a mean of 48.4 ppm. The authors conclude that parathion residues may
persist in the soil at relatively high levels for long periods of time.
The experimentally contaminated field plots described by Wolfe and
Durham (1966) were monitored further, and more recent findings were re-
ported by Wolfe et al. (1973). Farathion residues persisted at rela-
tively high levels for 5 years following the initial applications.
I/ Wolfe, H. R., and W. F. Durham, "Spillage of Pesticides and Residues
~~ In Soil," Wash. State Hort. Assoc. Proc., 62:91-92 (1966).
184
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The levels of parathion in the soil had declined considerably by the
end of the first year. The rate of disappearance vas much slower the
second year, and the decline curves indicate very little further dis-
appearance of residues beyond the third year. Six years after appli-
cation of the 45.67. concentrates, parathion residues ranging from
9,330 to 15,370 ppm were still present in the upper 3 in. of soil.
Residues found in the 3-to 9-d.n. soil layer ranged from 9.48 to 9,900
ppm, while concentrations ranging from 0.1 ppm to trace amounts were
found in five different layers of soil ranging from 9 to 24 in. in
depth. Residues from the dilute sprays disappeared more rapidly.
Where the Ix (0.03%) concentration had been applied, average parathion
levels after 5 years ranged from 0.6 to 1.2 ppm in the top 1 in. of
soil, and from 0.2 to 0.3 ppm in the 1- to 3-in. depth. Where the 8x
(0.24%) concentration was applied, average residue levels after 5 years
were 0.4 to 1.5 ppm in the top 1 in. of soil, and from 1.2 to 3.60 ppm
in the t to 3-in. level.
Monitoring studies - In the National Soils Monitoring Program for
pesticides, 1,729 samples of cropland soils from 43 states were col-
lected in 1969 (Wiersma et al., 1972b).!/ Of these, 66 samples were
analyzed for organic phosphate residues, and seven of the 66 (10.6%)
contained parathion residues ranging from 0.01 to 3.01 ppm, the mean
residue level being 0.06 ppm. One hundred ninety-nine samples of non-
cropland soil were also obtained, but none of these were analyzed for
organophosphate residues.
In the National Soils Monitoring Program for Pesticides in 1970
(Crockett et al., 1970)2/ soil and crop samples,were collected from
1,506 cropland sites in 35 states. Pesticide use records indicated
that parathion was used at 20 of 1,346 sites sampled, that is, 1.49%
of all sites. No analyses of soil samples for parathion residues are
reported. Samples of alfalfa, field corn kernels, cotton stalks and
green bolls, grass hay, field corn stalks, cotton seeds, mixed hay,
and soybeans (beans) were analyzed for organophosphate residues.
If Wiersma, G. B., H. Tai, and P. F. Sand, "Pesticide Residue Levels
in Soils, FY 1969 - National Soils Monitoring Program," Pest.
Monit. J.f 6(3):194-228 (December 1972b).
2/ Crockett, A. B., G. B. Wiersma, H. Tai, W. G. Mitchell and P. J.
Sand, "National Soils Monitoring Program for Pesticide Residues -
FY 1970," U.S. Environmental Protection Agency, Technical Services
Division, unpublished manuscript (1970).
185
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Parathion residues found were nondetectable in most instances; in some,
their mean concentration was 0.01 ppm or less.
Wiersma et al. (1972a)i/ monitored pesticide residues in commer-
cially grown onions and in the soil on which these onions were grown in
1969. A total of 76 sites in 10 major onion producing states were
sampled. According to pesticide use records, parathion had been used
on 34.4% (36.4%) of the farms sampled, at an average rate of 1.64 Ib
Al/acre. However, parathion residues (ranging from 0.02 to 2.55 ppm,
averaging 0.22 ppm) were found in 51.5% of the soil samples. In most
instances, the average amount of residue detected was considerably less
than the amount applied when converted to pounds AI per acre. Despite
the high residue levels in the soils, no residues of parathion (or of
any of the other pesticides) were detected in the onion samples.
Stevens et al. (1970).?-' reported on a pilot study conducted nation-
wide at 51 locations in 1965, 1966, and 1967 to determine pesticide
residue levels in soil. Samples were collected from 17 areas in which
pesticides are used regularly, 16 areas with a record of at least one
pesticide application, and 18 areas with no history of pesticide use.
This study was apparently aimed primarily at persistent chlorinated
hydrocarbon pesticides; only those organophosphates that were amenable
to chlorinated pesticide clean-up methods were detected, and no serious
attempts were made to quantitate metabolites or oxygen analogs of the
organophosphates. Pesticide use records indicated that parathion had
been used at a number of the sites sampled, but only one single detec-
tion of parathion is reported, i.e., a residue of 0.06 ppm in one of
seven fields sampled near Tulelake, California.
The data on parathion soil residues reported in the foregoing four
reports emanating from the National Soils Monitoring Program for Pesti-
cides are subject to question because in this program, soil samples are
being shipped and stored at room temperature until processed for analysis,
as reported by Stevens et al. (1970), and confirmed in a recent personal
communication to this reviewer by G. B. Wiersma. No information is
I/ Wiersma, G. B., W. G. Mitchell, and C. L. Stanford, "Pesticide
Residues in Onions and Soil - 1969," Pest. Monit. J.. 5(4):
345-347 (March 1972a).
2_/ Stevens, L. J., C. W. Collier, and D. W. Woodham, "Monitoring Pesti-
cides in Soils from Areas of Regular, Limited, and No Pesticide
Use," Pest. Monit. J., 4(3):145-164 (December 1970).
186
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given in these reports on the relationships between time of pesticide
application, time of sampling, and time of processing and analysis of
the samples. No information is available on the effects of shipping
and storage of the samples on the parathion residues that may have been
present at the time of sampling.
Applegate (1970)—' collected samples of soil, vegetation, birds,
rodents, and lizards from a large area of the Big Bend National Park,
Texas, and analyzed them for insecticide residues. Samples were
placed in an ice chest as quickly as possible after collection, main-
tained under refrigeration, then taken to Presidio, Texas, 3 to 5 days
later where they were placed in deep freezers and held for 10 to 14
days in frozen storage until processing and analysis. Parathion resi-
dues were found in 1 out of 9 samples of surface soil (0.01 ppm); in
1 out of 9 samples of leather stem, Jatropha dioica (0.01 ppm); in 2
out of 20 samples of muscle tissue of rodents (0.04, 0.11 ppm); in 3
out of 19 samples of whole lizards (0.01, 0.01, 0.10 ppm); and in 6 out
of 19 samples of bird muscle (0.01 to 0.21 ppm). There were no known
direct applicators of parathion in the park. The nearest areas using
insecticides are all south of the park in Mexico where parathion and
other pesticides have been applied routinely to cotton fields. It is
not known how the specimens that were found to contain parathion resi-
dues acquired these. The purpose of this study was to establish a
baseline for future investigations to show possible changes in the
level of pesticide pollution of this park.
The California Department of Water Resources (1969,
reported on pesticide concentrations in surface and subsurface drain
effluents in the San Joaquin Valley. In 1969, 14 samples of surface
drain effluents 'were analyzed for organophosphorus compounds. Para-
thion was detected in three of these, at concentrations ranging from
6 to 500 ppt (parts per trillion), averaging 37 ppt in all samples
analyzed, 173 ppt in the positive samples. In the same year (1969),
41 samples of subsurface drain effluents were analyzed for organo-
phosphate compounds. Residues were detected in 19 of these, but no
identification was made of specific pesticides involved.
If Applegate, H. G., "Insecticides in the Big Bend National Park,"
Pest. Monit. J.. 4(1):2-7 (1970).
2_/ California Department of Water Resources^ San Joaquin Valley Drain-
age Monitoring Program, 1969 Summary, Sacramento, California (1969)
(In: Li and Fleck, op. cit., 1972.)
3_/ California Department of Water Resources, San Joaquin Valley Drain-
age Monitoring Program, 1970 Summary, Sacramento, California (1970)
(In: Li and Fleck, op. cit., 1972.)
187
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In 1970, 18 samples of surface drain effluents were analyzed for
organophosphate compounds. Parathion was positively identified in one
of these; the concentration found was 190 ppt. Of 60 samples of sub-
surface drain effluents analyzed for organophosphates, 10 were found
to contain residues of undetermined members of this group.
These data show that only very small quantities of parathion and
of other organophosphate insecticides were present in these effluents.
The concentrations of these pesticides were somewhat higher in the sur-
face than in the subsurface drains. These findings are in good agree-
ment with those of other authors, indicating that organic phosphates
do not leach appreciably through soil profiles.
The results of the 1972 National Soils Monitoring Program have not
yet been published, and a computer printout of the analytical data by-
products is not expected to become available until later this summer.
Thus, data from the program is not included in this review.
Summary - Scientific data on the reviewed laboratory, field and monitoring
studies on residues and fate of parathion show that the persistence of this
chemical in the soil varies considerably, depending on a number of factors.
Parathion residues in the soil degrade by chemical hydrolysis as well as
by microbial action. Parathion is strongly adsorbed by organic matter.
Thus adsorbed, the chemical becomes unavailable for insecticidal action,
and appears to be protected to a degree against degradation. No data
are available on the fate of such adsorbed parathion residues; it is
not known whether they eventually degrade, or if the under what condi-
tions they might become reactivated by desorption. No information
appears to be available on the fate of the first degradation products,
especially _p_- nitrophenol and aminoparathion, or regarding effects on
organisms other than mammals and insects.
Parathion soil residues resulting from crop protection uses at
recommended dosage levels are apparently degraded in the soil, in most
cases, within a few weeks or months after application. However, small
fractions of originally applied quantities may persist in the soil for
prolonged periods of time. In the case of heavy soil contamination,
parathion soil residues have persisted for at least 16 years.
188
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Parathion degradation in the soil appears to be temperature-dependent
and proceeds much more slowly in colder climates. Thus, Canadian
investigators and one researcher from Australia who studied winter
application of parathion reported much slower decline rates than were
experienced in California.
Monitoring studies in which samples to be analyzed for parathion
residues are not frozen promptly after collection are of questionable
value in determining environmental residues of this pesticide. In
such studies, the time(s) and rate(s) of application in relation to
time of sampling should also be reported.
Residues in Water
Laboratory and Field Studies - Studies dealing with the fate of para-
thion residues in water are discussed in this section in approximate
chronological order.
Lichtenstein et al. (1966)i/ studied the toxicity of parathion
and several other insecticides in water to mosquito larvae after per-
colation of the water through insecticide-contaminated agricultural
loam soil. In distilled water, parathion caused 857. mortality of
mosquito larvae within 24 hr at 0.035 ppm. When water was percolated
through soil treated with parathion at the rate of 50 ppm, parathion
residues were present in the water as determined by gas liquid chroma-
tography and 100% mosquito mortality. Parathion was also present in
water percolated through soil treated at the rate of 1 ppm, when per-
colation took place on the day of treatment. The 0.013 ppm of para-
thion was found analytically in the percolated water. Seventeen days
after soil treatment, the parathion residue in the soil was 0.089 ppm;
in the percolated water 0.001 ppm. The percolated water was not toxic
to mosquito larvae at this time. The authors conclude that the con-
tamination of water by insecticidal soil residues is to a large degree
a function of the water solubility of a particular insecticide. Insec-
ticidal concentration in the soil and specific properties of a given
pesticide also are important.
I/ Lichtenstein, E. P., "Increase of Persistence and Toxicity of
Parathion and Diazinon in Soils with Detergents," J. Econ. Entomol.,
59(4):985-993 (1966).
189
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Graetz et al. (1970)!' Investigated the pathways and mechanisms
of parathion degradation in lake sediments. Lake sediment samples
were taken from two lakes in Wisconsin, and the mechanisms and rates
of parathion degradation were determined in dry-heat-sterilized lake
sediment, in aerobic and anaerobic peptone solutions in a peptone
enriched sediment system, and in intact sediments from the two lakes.
Parathion was readily susceptible to microbial degradation in aerobic
and anaerobic environments. Reduction of the nitro group to form
aminoparathion was a major microbial degradation pathway. Under
aerobic, but not under anaerobic conditions aminoparathion was de-
graded further, apparently by another microbial process. Parathion
degradation was slower in a slightly acid sediment than in a calcareous
one. The authors conclude that the persistence of parathion in the
natural aquatic environment is affected markedly by microbial activity.
Without microbial activity, parathion would remain in the environment
for several months, while in biologically active (aerobic or anaerobic)
environments, it would be degraded in a matter of weeks.
Eichelberger and Lichtenberg (1971)I/ investigated the persistence
of parathion and a number of other common pesticides in raw river water
over an 8-week period. Aliquots of 10 pig/liter of parathion from a
freshly prepared 0.1% solution in acetone were injected into samples of
raw water from the Little Miami River, a relatively small stream re-
ceiving domestic and industrial wastes and farm runoff. The dosed raw
river water was kept in the laboratory in closed glass containers at
room temperature, exposed to natural and artificial light. The same
concentration of parathion was also added to distilled water in the
same manner. In river water (alkalinity 98 ug/liter) 50% of the ori-
ginal concentration of parathion remained after 1 week, 30% after 2
weeks, less than 5% after 4 weeks. With the use of thin layer chroma-
tography, it was observed that parathion was hydrolyzed to p_-nitrophenol
and diethylthiophosphoric acid. Parathion remained stable in distilled
water for 3 weeks.
I/ Graetz, D. A., G. Chesters, T. C. Daniel, L. W. Newland, and G. B.
Lee, "Parathion Degradation in Lake Sediments," J. Water Poll.
Control Fed.. 42 (2, Pt. 2):R76-R94 (1970).
21 Eichelberger, J. W., and J. J. Lichtenberg, "Persistence of Pesti-
" cides in River Water," Environ. Sci. Tech., 5(6):541-544 (1971).
190
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Miller et al. (1966) investigated the persistence and movement
of parathion in cranberry bog irrigation waters. Irrigation water
from a cranberry bog that had been treated with parathion at a rate
equal to 1 Ib Al/acre through overhead sprinkler irrigation was
sampled immediately after application, and every 24 hr thereafter
for a period of 96 hr. The same experiment was repeated 14 days
later. The authors report data representing the mean of the two
experiments. Samples collected from an adjacent irrigation ditch
contained 750 ppb of parathion immediately after application; 60 ppb
after 24 hr; 25 ppb after 48 hr; 10 ppb after 72 hr; and 5 ppb after
96 hr. In an associated drainage canal, 30 ppb of parathion were
found immediately after application, indicating water seepage through
a flood gate. When this canal was resampled after 24 hr, 3.0 ppb of
parathion were detected. Twenty-four hours after the application (but
at no other time period), trace amounts of parathion were also detected
at two locations 50 and 150 yd from the application site in the drain-
age canal down from the point where seeping irrigation water would
enter the canal waters.
Schaefer and Dupras (1969)— studied the effects of water quality,
temperature and light on the stability of parathion used for mosquito
control. Samples of pasture water from pastures with a history of
mosquito control difficulties in alkaline soils in two California
counties were collected and passed through a coarse filter to remove
larvae and large pieces of organic matter. The 150-ml samples of
pasture water and distilled water in glass jars were treated with para-
thion from a 0.15-ug/ml acetone solution to give a concentration of
0.1 ppm of the insecticide, the concentration normally encountered in
pasture water following application of 0.1 Ib Al/acre. The jars were
moved to the field and placed into pasture water to expose them to the
same conditions of color, temperature and natural solar radiation as
field pasture water. Both pasture and distilled water samples were
extracted after 0, 2, 4, and 8 hr of exposure. Parallel tests were
carried out in the laboratory where samples were kept in the dark and
at constant temperatures of 24 and 38°C. Water quality had little, and
light had no, effect on the stability of parathion. This insecticide
was very stable both under field and laboratory conditions and was only
slightly influenced by temperature. After 8 hr, there was 10% more
loss of AI at 38 than at 24°C.
I/ Schaefer, C. H., and E. Dupras, Jr., "The Effects of Water Quality,
Temperature and Light on the Stability of Organophosphorus
Larvicides Used for Mosquito Control," Proc. Papers Ann. Conf.
California Mosquito Control Assoc.. 37:67-75 (1969).
191
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Paris and Lewis (1973)!/ recently presented a rather brief, but
fairly complete review of the current extent of knowledge on the chem-
ical and microbial degradation of 10 selected pesticides, including
parathion, in aquatic systems. They briefly cite many of the research
studies reviewed in greater detail in this report, but do not draw any
conclusions from their overview of the parathion data.
Several authors from abroad have contributed data on parathion in
aquatic systems. Greve (1972)£' identified parathion residues in Rhine
water at 0.01 to 0.1 ppb. Quentin (1972a, 1972b)l*f!/ dealt with the
analytical, decontamination, and hygienic problems associated with the
presence of residues of parathion and other pesticides in water, in-
cluding drinking water supplies. Adoption of a reduced maximum allow-
able concentration of parathion is being urged in West Germany. Pesti-
cide contamination of surface waters must be monitored more closely in
the future as the use of surface water for drinking water purposes in-
creases. The author emphasizes that maximum allowable concentrations
of single pesticides may be inadequate when several pesticides are
present in the same water.
Manescu (1971)— observed a decreased rate of oxygen consumption
by the self-purifying bacterial flora in surface water samples follow-
ing treatment with 100 mg/liter of parathion. Oxygen consumption was
determined by the micromanometric Warburg procedure. Compared to other
pollutants, metals, cationic detergents, or chlorine, pesticides ranked
low in their inhibitory action on the oxygen consumption of the bacteria,
The reports reviewed in this section indicate, and the recent
literature search by Paris and Lewis (1973) confirms,that relatively
little information is available on the persistence and fate of
parathion residues in water, especially under actual field conditions.
I/ Paris, D. F., and D. L. Lewis, "Chemical and Microbial Degradation of
Ten Selected Pesticides in Aquatic Systems," Residue Rev., 45:95-
124 (1973).
2/ Greve, P. A., "Toxic Organic Trace Pollutants in Surface Water,"
Chem. Weekblad. 41(68):11, 13, 15 (1972).
3/ Quentin, K. E., "Pesticides in Water - Determination, Removal, and
"~ Limiting Values," Chem. Ing. Tech.. 44(20):1172-1176 (1972a).
4/ Quentin, K. E., "Evaluation and Significance of Residue Values
from the Viewpoint of the Water Biocenosis and Drinking Water
Quality," Schriftenr. Ver. Wasser-Boden-Lufthyg.. 34:19-28 (1972b).
5_/ Manescu, S., "The Value of the Manometric Procedure in Studying the
Chemical Micropollutant Action Potential on the Self-Purifying Water
Flora," Igiena 20(5):275-286 (1971).
192
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Monitoring Studies - Dupuy and Schulze (1972)—' and Achulze et al. (1973)!/
reported a maximum of 1 ppb parathion In routine water monitoring. Butler
(unpublished)±' found a maximum of 170 ppb parathion in several marine fish
along the Atlantic and Gulf coasts.
Residues in Air
There is little information available on the origin, presence and
persistence of parathion residues in air.
Harris and Lichtenstein (1961)— exposed cages vinegar flies (Drosophila
melanogaster) and houseflies (Musca domestica) to vapors from soils that had
been treated with parathion in the laboratory or in the field. In the
laboratory tests, quartz was treated at the rate of 4 ppm of parathion.
There was no mortality of the insects that were kept in screened cages above
the parathion-treated sant for periods of 6 or 24 hr. Under the same, con-
ditions, 100% mortality was obtained with several other insecticides,
demonstrating the method's validity. Lichtenstein and Schulz (1970)A'
investigated the volatilization of parathion and other insecticides from
eight different substrates. It was generally assumed that low water solubility
and a relatively high vapor pressure would enhance volatilization from aqueous
substrates. However, no direct relationships were established by experimental
results between water solubility of a particular compound and its volatiliza-
tion. Glass beads, tap water, soil water, algae in nutrient media, buffer
solution, buffer solution plus 0.1% detergent, silt loam and silt loam
containing 0.1% detergent were treated with C-labeled parathion. The
material volatilized within 24 hr was collected in a vapor trap and deter-
mined. The volatilization rate of parathion was very low, ranging from
0.07% of the applied dose from the soil with or without the detergent, to
1.67% of the applied does from the buffer solution containing detergent.
Volatilization rates from the other substrates were intermediate between
these two extremes.
Sandi (1958)— studied the effects of direct sunlight compared to
dark conditions on parathion in a 2 x 10"^ M solution in a barbiturate buffer
at pH 8.0. The results observed by two different analytical methods show
that parathion is photochemically reduced, presumably to the corresponding
p_-amino compound.
I/ Dupuy, A. J., and J. A. Schulze, Selected Water-Quality Records for Texas
Surface Waters, 1970 Water Year. Texas Water Development Board,
Report 149, Austin, Texas (1972).
2J Schulze, J. A., D. B. Manigold and F. L. Andrews, "Pesticides in Selected
Western Streams - 1968-71, Pesticide Monitoring J., 9(2) 124-135 (1973).
3/ Butler, P. A., Unpublished report on Environmental Protection Agency
National Estuarine Monitoring Program.
4/ Harris, C. R., and E. P. Lichtenstein, "Factors Affecting the Volitilization
of Insecticidal Residues from Soils," J. Econ. Entomol., 54(5):
1038-1045 (1961).
5_/ Lichtenstein, E. P., and K. R. Schulz, "Volatilization of Insecticides
from Various Substrates," Agr. Food Chem.. 18(5):814-818 (1970).
6/ Sandi, E., "Reduction of Parathion Induced by Light," Nature. 181:499
(1958).
193
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Stanley et al. (1971)— conducted a pilot study to establish a
system for measuring the extent of atmospheric contamination of the
air by pesticides in nine localities throughout the United States.
Samples were analyzed for 19 pesticides and metabolites, including
parathion. Parathion was found in only one of the nine sampling loca-
tions, i.e., Orlando, Florida. At that location, 37 samples contained
detectable amounts of parathion, the maximum level found being 465 ng/
cu m of air. The majority of the Orlando air samples contained para-
thion levels ranging from about 10 to 25
") I
Tessari and Spencer (1971)—' analyzed air samples from human
environments in the Greeley, Colorado, area for pesticide residues.
Nylon chiffon cloth screens were exposed to the atmosphere for 5 days,
after which residues were extracted from them with suitable solvents
and determined by gas chromatographic analysis. Screens were deployed
inside and outside 12 homes of men occupational ly exposed to pesticides,
including parathion (farmers and pesticide f emulators) . Samples were
collected monthly for 1 year. Parathion residues were found in a sur-
prisingly high number of cases from test screens exposed for 5 days at
a time. In the positive indoor samples, parathion residues ranged
from 0.03 to 9.60 ug/m2 of filter; the means were 0.26 ug/m2 for the
farmers, 2.24 for the f emulators. The authors point out that these
results are surprising because "parathion is volatile and has a rela-
tively short environmental half -life. The farmer group had little or
no use of parathion, yet the occurrence of parathion in their environ-
mental samples, especially housedust and inside air samples, was high."
The outside air levels of parathion were very similar for both types
of homes sampled (means 0.75 and 1.11 ug/m , respectively; range 0.0 to
12.92 ug/m2).
I/ Stanley, C. W., J. E. Barney II, M. R. Helton, and A. R. Yobs,
"Measurement of Atmospheric Levels of Pesticides," Environ.
Set. Tech., 5(5):430-435 (1971).
2j Tessari, J. D., and D. L. Spencer, "Air Sampling for Pesticides
in the Human Environment," J. Assoc. Offlc. Anal. Chem., 54(6):
1376-1382 (1971).
194
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Search of the literature and of other information sources failed
to yield additional data on parathion air residues. The reports reviewed
above indicate that parathion residues may be present in air, but these
very limited data leave open many important questions, including origin
of such air residues, relationships to parathion use and handling patterns
in the area, persistence and transport patterns of such residues in air,
and their significance to human and environmental health.
Residues in Nontarget Plants
Search of the literature failed to yield any reports on parathion
metabolism or residues in or on nontarget plants. Fukuto and Sims
(1971)—' state in a recent text on the metabolism of insecticides and
fungicides: "Surprisingly few Investigations have been carried out on
the metabolism of parathion and related compounds in plants in spite
of its wide usage on a variety of crops."
Joiner and Baetcke (1973)—' studied the persistence of parathion
on cotton and identified its photoalteration products. ^C-labeled
parathion was applied to cotton four times in three successive weeks
in four environmental situations, i.e., environmental growth chamber,
greenhouse, controlled field exposure, and open field. After 28 days,
11.2 to 15.4% of the total radioactivity applied was recovered by
methanol extraction and was found to be 58 to 68% unchanged parathion.
There was a constant increase in photoalteration products, paralleled
by a consistent decrease in *^C-parathion over time. Photoalteration
products did not include any previously unreported metabolites. In
this set of experiments, parathion was found to be at least seven times
more persistent than previously reported on cotton, according to the
authors.
I/ Fukuto, T. R., and J. J, Sims, "Metabolism of Insecticides and
Fungicides," Pest. Environ.. R. White-Stevens (ed.) Vol. I, Parti,
Ch. 2, pp.147-155, Marcel Dekker, New York (1971).
2f Joiner, R. L., and K. P. Baetcke, "Parathion: Persistence on
Cotton and Identification of Its Photoalteration Products,"
J. Agr. Food Chem.. 21(3):391-396 (1973).
195
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Kilgore et al. (1972) studied the persistence of parathion follow-
ing treatment of field plots of grapevines at 2, 4 and 8 Ib Al/acre.
Parathion residues in bark, leaves, berries, and soil were monitored
at different time periods after application. From these field experi-
ments that were conducted in 1969 and 1971, the following conclusions
were drawn: (a) parathion tends to stabilize in grape bark for at
least 15 months at a level of 25 ppm; (b) no degradation of the parent
compound occurs on the surface of grape plants or within the tissue
after penetration; the parathion-paraoxon ratio found in the insecti-
cide at the time of application did not change over the entire experi-
mental period; (c) rapid loss of parathion occurs after application,
mostly attributable to volatilization, which was then followed by an
increasingly slower rate of disappearance; (d) parathion penetrates
cane bark and reaches wood as well as pith tissues; and (e) parathion
translocates via xylem into the emerging buds and the expanding new
shoots.
Further'tests on the absorption and translocation of-parathion
in roots were conducted in bean, barley and grape plants. The re-
sults obtained in this series of tests confirm reports of other authors
that parathion actually penetrates and translocates in plants. It is
suggested that the metabolites reported in earlier studies to be present
in foliage are due to microbial activity in the soil, and that no signif-
icant modification of parathion occurs in plant tissue. Parathion dis-
appears quite rapidly from the surface of plants after spraying. It
is estimated that over 90% of the initial deposit is lost by vola-
tilization during the first few days. The remainder is stabilized
in the bark (in the case of grapevine), or penetrates into plant tissue.
The amount of parathion that gains entry into plants is persistent,
not subject to significant metabolic or chemical modification, trans-
located within plants, and to decline primarily as a result of dilution
by plant growth. The authors conclude from their work and other studies
that parathion appears to be much more persistent in the environment
than previously believed.
Bioaccumulation, Biomagnification
Miller et al. (1966) found that mummichog (Fundulus heteroclitus)
and mussels (Elliptic? complanatus), in a model cranberry bog containing
0.07 ppm parathion, within 24 hours had levels of 1.68 and 0.99 ppm,
respectively. The ambient level of parathion in the water at the end
of 24 hours was 0.02 ppm. After 144 hours the ambient water level was
0.002 ppm, mummichog, 0.22 ppm and mussels, 0.04 ppm.
196
-------
Metcalf (1972)—' states: "Both the organophosphates and carbamates
are not persistent in soil and do not accumulate in body fat."
Thus, experimental data on possible bioaccumulation and biomagni-
fication of parathion appear to be almost nonexistent. However, the
physical, chemical, and biological properties of parathion make it
unlikely that biomagnification in food chains or food webs occurs,
and there is no evidence that it does.
Environmental Transport Mechanisms
The data reviewed in the preceding sections of this report in-
dicate that under field conditions, volatilization appears to be one
important mechanism by which parathion may move away from the target
site after application. Freed et al. (Unpublished data, quoted from
von RUmker and Horay, 1972)—' determined the propensity of parathion
for volatilization and leaching under simulated field conditions for
loam soils at 25°C at an annual rainfall of 59 in. (150 cm). Vola-
tilization of pesticides under these conditions, i.e., from a porous,
sorptive medium (loam soil) in a nonequilibrium situation, is dif-
ferent from volatilization from an inert surface or from the chemical's
own surface. Therefore, the environmental volatilization index
assigned to pesticides investigated in this manner may or may not
parallel a chemical's vapor pressure. By this method, parathion
rated a volatilization index of 3, indicating an estimated median
vapor loss from treated areas of 4.45 Ib/acre/year. This index number
indicates a relatively high propensity for volatilization from treated
fields, compared to many other pesticides.
Leaching index numbers for pesticides indicate the approximate
distance that the chemical would move through the standardized loam
soil profile under an annual rainfall of .59 in. (150 cm). Under
these conditions, parathion rated a leaching index number of 2,
indicating movement of 4 to 8 in.
I/ Metcalf, R. L., "DDT Substitutes," Grit. Rev. Environ. Contr..
3(1^:25-59 (Ref: 110) (1972).
2/ von Rumker, R., and F. Horay, Pesticide Manual, Vol. I, Depart-
ment of State, Agency for International Development (1972).
197
-------
These volatilization and leaching index numbers for parathion
are in excellent agreement with many laboratory and field observa-
tions reviewed in the preceding sections of this report.
It thus appears that volatilization and surface runoff adsorbed
on solids are the two most important environmental transport mech-
anisms for parathion. Surface runoff as a solute in water is likely
to occur only very soon after application, before substantial adsorp-
tion on soil solids, especially on organic matter, has occurred.
Leaching of parathion through soil profiles does not occur readily,
and is not likely to result following field applications at rates
recommended for insect control.
198
-------
References
Anderson, B. G., "The Toxicity of Organic Insecticides to Daphnta."
In: Transactions of the Second Seminar on Biological Problems
in Water Pollution, Cincinnati, Ohio, U.S. Public Health Service,
pp. 94-95 (1959). (In: Li and Fleck, 1972.)
Anderson, J. P. E., "Factors Influencing Insecticide Degradation by
a Soil Fungus, Mucor Alternans," Piss. Abstr. Int.. 32(6):3114B-
3115B (1971).
Anon., National Water Quality Laboratory (EPA), unpublished data
(24 May 1974).
Applegate, H. 6., "Insecticides in the Big Bend National Park,"
Pest. Monit. J.. 4(1):2-7 (1970).
Barker, R. J., "Cholinesterase Reactivators Tested as Antidotes for the Use
on Poisoned Honeybees," J. Econ. Entomol ., 63(6);1831-1833 (December 1970).
Battelle's Columbus Laboratories, "Effects of Chemicals on Aquatic
Life," Water Quality Criteria Data Book. Vol. Ill, p. B167-B186,
Environmental Protection Agency (1971).
Bejer-Petersen, B., R. R. Hermansen, and M. Weihe, "On the Effects
of Insecticide Sprayings in Forests on Birds Living in Nest Boxes,"
Dan. Ornithol. Foren. lidsskr.. 66(1,2):30-50 (1972).
Benke, 6. M., K. L. Cheever, F. E. Mirer, and S. D. Murphy, "Compara-
tive Toxicity, Anticholinesterase Action and Metabolism of Methyl
Parathion in Sunfish and Mice," Toxicol. Appl. Pharmacol.. 28:97-
109 (1974).
Bollen, W. B., H. E. Morrison and H. H. Crowell, "Effect of Field
Treatments of Insecticides on Numbers of Bacteria, Streptomyces,
and Molds in the Soil," J. Econ. Entomol.. 47(2):302-306 (1954).
Brodeur, J., and K. P. DuBois, "Comparison of Acute Toxicity of Anti-
cholinesterase Insecticides to Weanling and Adult Male Rats," Proc.
Soc. Exp. Biol. Med.. 114(2):509-511 (November 1963).
Bucknell, E. S., "Side-Effects of Granulated Insecticides in Canterbury,"
Proc. N. Z. Weed Pest. Contr. Conf.. No. 23:124-126 (1970).
Burkhardt, C. C., and M. L. Fairchild, "Toxicity of Insecticides to
House Crickets and Bioassay of Treated Soils in the Laboratory,"
J. Econ. Entomol.. 60(6):1496-1503 (1967a).
199
-------
Burkhardt, C. C., and M. L. Fairchild, "Bioassay of Field-Treated Soils
to Determine Bioactivity and Movement of Insecticides," J. Econ.
Entomol.. 60(6):L1602-1610 (1967b).
Buttiker, W., "Ecological Effects of Insect Control on Bird Populations,"
Int. Union Conserv. Nature Natur. Resources, Tech. Meeting, Warsaw
1960, Proc. 8:48-60 (1961). Quoted from: Pimentel (1971).
California Department of Water Resources, San Joaquin Valley Drainage
Monitoring Program, 1969 Summary, Sacramento, California (1969).
(In: Li and Fleck, 1972.)
California Department of Water Resources, San Joaquin Valley Drainage
Monitoring Program, 1970 Summary, Sacramento, California (1970).
(In: Li and Fleck, 1972.)
Chambers, J. E., and J. D. Yarbrough, "Parathion and Methyl Parathion
Toxicity to Insecticide-Resistant and Susceptible Mosquitofish
(Gambusia affinis)," Bull. Environ. Contarn. Toxicol.. 4:315-320 (1974).
Campbell, W. V., D. A. Mount, and B. S. Heming, "Influence of Organic
Matter Content of Soils on Insecticidal Control of the Wireworm,"
J. Econ. Entomol.. 64(l):41-44 (1971).
Chisholm, D., and A. W. MacPhee, "Persistence and Effects of Some
Pesticides in Soil," J. Econ. Entomol.. 64(4):1010-1013 (August 1972).
Chopra, S. L., and F. C. Khullar, "Degradation of Parathion in Soils,"
J. Indian So. Soil Sci.. 19(1):79-85 (1971).
Cope, 0. B., "Contamination of the Freshvater Ecosystem Pesticides,"
J. Appl. Ecol.. 3(Suppl):33-44 (A Special issue on Pesticides in
the Environment and Their Effects on Wildlife) (1966). (In: Li
Fleck, 1972.)
Coppage, D. L., "Characterization of Fish Brain Acetylcholinesterase
with an Automated Ph Stat for Inhibition Studies," Bull. Environ.
Contam. Toxicol.. 6:304-310 (1971).
Coppage, D. L., "Organophosphate Pesticides: Specific Level of Brain
AChE Inhibition Related to Death in Sheepshead Minnows," Trans. Am.
Fish. Soc.. 101:534-536 (1972).
200
-------
Coppage, D. L., and E. Matthews, "Short-Term Effects of Organophos-
phate Pesticides on Cholinesterases of Esturarine Fishes and Pink
Shrimp," Bull. Environ. Contain. Toxicol., 11:483-488 (1974).
Cowley, G. T., and E. P. Lichtenstein, "Growth Inhibition of Soil
Fungi by Insecticides and Annulment of Inhibition by Yeast Extract
or Nitrogenous Nutrients," J. Gen. Microbiol.. 62(l):27-34 (1970).
Crockett, A. B., G. B. Wiersma, H. Tai, W. G. Mitchell and P. J. Sand,
"National Soils Monitoring Program for Pesticide Residues - FY 1970,"
U.S. Environmental Protection Agency, Technical Services Division.
Unpublished Manuscript (1970).
Croft, B. A., and L. R. Jeppson, "Comparative Studies on Four Strains
of Typhlodromus occidentalis, II. Laboratory Toxicity of Ten Com-
pounds Common to Apple Pest Control," J. ECon. Entomol., 63(5):
1528-1531 (October 1970).
Dolphin, R. E., and R. N. Peterson, "Developments in the Research and
Control Program of the Clear Lake Gnat Chaoborus astictopus, D & S,"
Proc. and Papers of Twenty Eighth Ann. Conf., California Mosquito
Control Assoc., pp. 90-94 (1960).
Drift, J., "Pesticides and Soil Fauna," Meded. Rijksfac. Landbouwwetensch.,
Gent, 35(2):707-716 (1970)
Eichelberger, J. W., and J. J. Lichtenberg, "Persistence of Pesticides
in River Water," Environ. Sci. Tech.. 5(6):541-544 (1971).
Federal Water Pollution Control Administration, "Water Quality Criteria,"
Report of the National Technical Advisory Committee, p. 37 (1968).
Fukuto, T. R., and J. J. Sims, "Metabolism of Insecticides and Fungi-
cides," Pest. Environ., R. White-Stevens (ed.) Vol. I, Part I,
Chapter 2, pp. 147-155, Marcel-Dekker, New York (1971).
Gaufin, A. R., L. D. Jensen, A. V. Nebeker, T. Nelson and R. W. Teel,
"The Toxicity of Ten Organic Insecticides to Various Aquatic Inver-
tebrates," Water Sewage Works, 12:276-279 (1965). (In: Li and
Fleet, 1972.)
Gibson, J. R., J. L. Ludke, and D. E. Ferguson, "Sources of Error in
the Use of Fish-Brain Acetylcholinesterase Activity as a Monitor
for Pollution," Bull. Environ. Contarn. Toxicol.. 4:17-23 (1969).
201
-------
Gibson, J. R., "Comparative Biochemistry of Parathion Metabolism in
Three Species of Fishes," Piss. Abstr. Int.. 32(4):2365-B (1971).
Graetz, D. A., G. Chesters, T. C. Daniel, L. W. Nevland, and G. B. Lee,
"Parathion Degradation in Lake Sediments," J. Water Poll. Control
Fed., 42(2, Pt. 2):R76-R94 (1970).
Gregory, Jr., W. W., J. K. Reed, and L. E. Priester, Jr., "Accumulation
of Parathion and DDT by Some Algae and Protozoa," J. Protozool.,
16(1):69-71 (1969).
Greve, P. A., "Toxic Organic Trace Pollutants in Surface Water,"
Cfaem. Weekblad., 41(68):11, 13, 15 (1972).
Griffiths, D. C., and N. Walker, "Microbiological Degradation of
Parathion," Meded, Rijksfac. Landbouwwetensch., Gent 35(2):805-810
(1970).
Grzenda, A. R., G. J. Lauer, and H. P. Nicholson, "Insecticide Con-
tamination in a Farm Pond, Part II - Biological Effects," Trans.
Am. Fish. Soc.. 91(2):213-221 (1962).
Gupta, R. S., and K. S. Kushwaha, "Toxicity of Some Insecticides to
the Predator, Menochilus sexmaculata," Indian J. Entomol., 32(Pt. 4):
379-381 (1970).
Hamilton, E. W., and R. W. Kieckhefer, "Toxicity of Malathion and Para-
thion to Predators of the English Grain Aphid," J. Econ. Entomol.,
62(5):1190-1192 (October 1969).
Harris, C. R., "Influence of Soil Type on the Insecticidal Activity
of Insecticides in Soil," J. Econ. Entomol.. 59(5):1221-1225 (1966).
Harris, C. R., and E. P. Lichtenstein, "Factors Affecting the Vola-
tilization of Insecticidal Residues from Soils," J. Econ. Entomol.,
54(5):1038-1045 (1961).
Harris, C. R., and W. W. Sans, "Insecticide Residues in Soils on 16
Farms in Southwestern Ontario - 1964, 1966, and 1969," Pest. Monit.
J^, 5(3):259-267 (December 1971).
Heath, R. G., J. W. Spann, E. F. Hill, J. F. Kreitzer, "Comparative
Dietary Toxicities of Pesticides to Birds," Bureau of Sport Fish-
eries and Wildlife, Special Scientific Report, Wildlife No. 152
(February 1972).
202
-------
Henderson, C., and Q. H. Pickering, "Toxicity of Organic Phosphorus
Insecticides to Fish," Trans. Am. Fish. Soc.. 87:39-51 (1958).
Herzel, F., "The Behavior of Several Persistent Insecticides in the
Soil," Bundesquesundheitsblatt, 14(3):23-28 (1971).
Holland, H. T., D. L. Coppage, and P. A. Butler, "Use of Fish Brain
Acetylcholinesterase to Monitor Pollution by Organophosphorus
Pesticides," Bull. Environ. Contam. Toxicol.. 2(3):156-162 (1967).
Hubbell, D. H., D. F. Rothwell, W. B. Wheeler, W. B. Tappan, and F. M.
Rhoads, "Microbiological Effects and Persistence of Some Pesticide
Combinations in Soil," J. Environ. Qual.. 2(1); 96-99 (1973).
Hudson, R. H., R. K. Tucker, and M. A. Haegele, "Effect of Age on
Sensitivity: Acute Oral Toxicity of 14 Pesticides to Mallard Ducks
of Several Ages," Toxicol. Appl. Pharmacol., 22:556-561 (1972).
Iwata, Y., W. E. West lake, and F. A. Gunther, "Persistence of Para-
thion in Six California Soils Under Laboratory Conditions," Arch.
Environ. Contam. Toxicol.. 1(1):84-96 (1973).
Jensen, L. D., and A. R. Gaufin, "Effects of Ten Organic Insecti-
cides on Two Species of Stonefly Naiads," Trans. Am. Fish. Soc..
93-34 (1964a). (In: Li and Fleck, 1972.)
Jensen, L. D., and A. R. Gaufin, "Long-Term Effects of Organic Insec-
ticides on Two Species of Stonefly Naiads," Trans.' Am. Fish. Soc..
93:357-363 (1964b). (In: Li and Fleck, 1972.)
Johansen, D., "Spray Additives for Insecticidal Selectivity to In-
jurious vs Beneficial Insects," Environ. Entomol.. 1(1):51-54
(February 1972a).
Johansen, C. A., "Toxicity of Field-Weathered Insecticide Residues
to Four Kinds of Bees," Environ. Entomol.. l(3):393-394 (June 1972).
Joiner, R. L., and K. P. Baetcke, "Parathion: Persistence on Cotton
and Identification of Its Photoalteration Products," J. Agr. Food
Chenu. 2l(3):391-396 (1973).
Kaplan, H. M., and S. S. Glaczenski, "Hematological Effects of Organo-
phosphate Insecticides in the Frog (Rana Pipiens)," Life Sci.. 4(7):
1213-1219 (1965).
203
-------
Keith, J. 0., M. S. Mulla, "Relative Toxicity of Five Organo-
phosphorus Mosquito Larvicides to Ducks/1 J. Wildlife Manag..
30(3):553-563 (1966).
Kilgore, W. W., N. Marey, and W. Winterlin, "Parathion in Plant
Tissues: New Considerations," In: Degradation of Synthetic
Organic Molecules in the Biosphere, National Academy of Sciences,
pp. 291-312 (1972).
Kimmerle, G., and D. Lorke, "Toxicity of Insecticidal Organophos-
phates," Pflanz. Nachr. Bayer.. 21:111-142 (1968).
King, P., and P. L. McCarty, "A Chromatographic Model for Predict-
ing Pesticide Migration in Soils," Soil Set.. 106(4):248-261 (1968).
Knutson, H., A. M. Kadoum, T. L. Hopkins, 6. F. Svoyer and T. L.
Harvey, "Insecticide Usage and Residues in a Newly Developed Great
Plains Irrigation District," Pest. Monit. J.. 5:17-27 (1971).
Kortus, J., P. Macuch, J. Mayer, K. Durcek, and V. Kremery, "Uptake
of 32-P-Parathion and 32-P Imidan," J. Hyg. Epidemiol. Microbtol.
Inmunol. (Prague), 15(1):101-3 (1971).
Lahav, M., and S. Sarig, "Sensitivity of Pond Fish to Cotnion (Azin-
phosmethyl) and Parathion," Bamidgeh. 21(3):67-74 (1970).
Leenheer, J. A., and J. L. Ahlrichs, "A Kinetic and Equilibrium Study
of the Adsorption of Carbaryl and Parathion Upon Soil Organic Matter
Surfaces," Soil Sci. Am. Proc., 35(5):700-705 (1971).
Lewallen, L. L., and W. H. Wilder, "Toxicity of Certain Organophosphorus
and Carbamate Insecticides to Rainbow Trout," Mosquito News, 22 (4):
369-372 (1962).
Li, M., and R. A. Fleck, "The Effects of Agricultural Pesticides in
Aquatic Environment, Irrigated Croplands, San Joaquin Valley,"
Pesticide Studies Series - 6. Environmental Protection Agency,
Office of Water Programs, Applied Technology Division, Rural Waste
Branch TS-00-72-05, 268 pp. (1972).
Lichtenstein, E. P., "Increase of Persistence and Toxicity of Para-
thion and Diazinon in Soils with Detergents," J. Econ. Entomol.,
59(4):985-993 (1966).
204
-------
Lichtenstein, E. P., and K. R. Schulz, "The Effects of Moisture and
Microorganisms on the Persistence and Metabolism of Some Organo-
phosphorus Insecticides in Soils, with Special Emphasis on Para-
thion," J. Econ. Entomol., 57:618-627 (1964).
Lichtenstein, E. P., and K. R. Schulz, "Volatilization of Insecti-
cides from Various Substrates," Agr. Food Chem., 18(5):814-818 (1970),
Lichtenstein, E. P., K. R. Schulz, R. F. Skrentny, and Y. Tsukano,
"Toxicity and Fate of Insecticide Residues in Water," Arch. Environ.
Health. 12:199-212 (1966).
Lichtenstein, E. P., T. W. Fuhremann, K. R. Schulz, and R. F. Skrentny,
"Effect of Detergents and Inorganic Salts in Water on the Persis-
tence and Movement of Insecticides in Soils," J. Econ. Entomol.,
60(6):1714-1721 (1967).
Lingappa, S. S., K. J. Starks, and R. D. Eikenbary, "Insecticidal
Effect on Lysiphlebus testaceipes, a Parasite of the Greenbug, -at
Three Development Stages," Environ. Entomol., 1(4):520-521 (August
1972).
Lowe, J. I., P. D. Wilson, and R. B. Davison, "Laboratory Bioassays,"
Progress Report for Fiscal Year 1969, Bureau of Commercial Fish-
eries Center for Estuarine and Menhaden Research, Pesticides Field
Station Gulf Breeze, Florida, U.S. Dept. Interior, Circular 335,
pp. 20-28 (1970).
Lowe, J. I., P. D. Wilson, and A. J. Wilson, "Chronic Exposure of
Oysters to DDT, Toxaphene and Parathion," Proc. Nat. Shellfish
Assoc., 61:71-79 (1971).
Mackiewicz, M., R. H. Deubert, H. B. Gunner, and B. M. Zuckerman,
"Study of Parathion Biodegradation Using Gnotobiotic Techniques,",
J. Agr. Food Chem., 17(1)-.129-130 (January/Febraury 1969).
Manescu, S., "The Value of the Manometric Procedure in Studying the
Chemical Micropollutant Action Potential on the Self-Purifying
Water Flora," Igiena. 20(5):275-286 (1971).
205
-------
MatIda, Y., and N. Kawasaki, "Study on the Toxicity of Agricultural
Control Chemicals in Relation to Freshwater Fisheries Management/'
No. 2 Toxicity of Agricultural Insecticides to Daphnia carinata,
King. Bull. Freshwater Fish. Res. Lab.. Tokyo, 8:1-6 (1968). (In:
Li and Fleck, 1972.)
Matsumura, F., and 6. M. Boush, "Metabolism of Insecticides by Micro-
organisms," Soil Biochem.. 320-336, Marcel Dekker, New York (1971).
McFarland, L. Z., and P. B. Lacy, "Acute Anticholinesterase Toxicity
in Ducks and Japanese Quail," Toxicol. Appl. Pharmacol,, 12:105-114
(1968).
Metcalf, R. L., "DDT Substitutes," Crit. Rev. Environ. Contr.. 3(1):
25-59 (Ref: 110) (1972).
Mick, D. L., and P. A. Dahm, "Metabolism of Parathion by Two Species
of Rhizobium," J. Econ. Entomol.. 63(4):1155-1159 (August 1970).
Miller, C. W., B. M. Zuckerman, and A. J. Charig, "Water Translocation
of Diazinon-C ^ and Parathion-S*-* off a Model Cranberry Bog and
Subsequent Occurrence in Fish and Mussels," Trans. Am. Fish. Soc.»
95:345-349 (1966).
Moffitt, H. R., E. W. Anthon, and L. 0. Smith, "Toxicity of Several
Commonly Used Orchard Pesticides to Adult Hippodamla convergens,"
Environ. Entomol., l(l):20-23 (February 1972).
Mol, J. C. M., D. L. Harrison, and R. H. Talfer, "Parathion: Toxicity
to Sheep and Persistence on Pasture and in Soil," N. Z. J. Agr. Res.,
15(2):306-320 (1972).
Moore, R. B., "Effects of Pesticides on Growth and Survival of
Euglena gracilis Z., Bull. Environ. Contain. Toxicol.. 5(3):226-230
(1970).
Mulla, M. S., "Vector Control Technology and Its Relationship to
the Environment and Wildlife," J. Appl. Ecol., 3^ (Supplement on
Pesticides in the Environment and Their Effects on Wildlife):
21-28 (1966). Quoted from: Pimentel (1971).
Mulla, M. S., J. St. Amant, and L. D. Anderson, "Evaluation of Organic
Pesticides for Possible Use as Fish Toxicants," Prog. Fish-Cult.,
29(1):36-42 (1967).
206
-------
Mulla, M. S.f and L. W. Isaak, "Field Studies cm the Toxiclty of
Insecticides to the Mosquitofish, Gambusta affinis," J. Econ.
Entpmol., 54(6):1237-1242 (1961).
Mulla, M. S., L. W. Isaak, and H. Axelrod, "Field Studies on the
Effects of Insecticides on Some Aquatic Wilflife Species,"
J. Econ. Entomol.. 56(2):184-188 (1963).
Muncy, R. J., and A. D. Oliver, Jr., "Toxicity of Ten Insecticides
to the Red Crawfish, Procambarus clarki (Girard)," Trans. Am.
Fish. Soc., 92:428-431 (1963). (In: Li and Fleck, 1972.)
Murphy, S. D., R. R. Lauwerys, and K. L. Cheever, "Comparative Anti-
cholinesterase Action of Organophosphorus Insecticides in Verte-
brates," Toxicol. Appl. Pharmacol.. 12:22-35 (1968).
Nagvi, S. M., and D. E. Ferguson, "Levels of Insecticide Resistance
in Freswater Shrimp, Palaemonetes kadiakensis," Trans. Am. Fish
Soc.. 99:696-699 (1970). (In: Li and Fleck, 1972.)
Nagvi, S. M., and D. E. Ferguson, "Levels of Insecticides Resistance
in Freshwater Shrimp, Palaemonetas kadiakensis," Trans. Am. Fish.
Soc.. 99:697 (1970).
Nicholson, H. P., H. J. Webb, 6. J. Lauer, R. E. O'Brien, A. R.
Grzenda, and D. W. Shanklin, "Insecticide Contamination in a Farm
Pond. Part I - Origin and Duration," Trans. Am. Fish. Soc..
91(2)-.213-221 (1962).
Nishiuchi, Y., and Y. Hashimoto, "Toxicity of Pesticides to Some
Freshwater Organisms," Rev. Plant Protec. Res.. 2:137-139 (1969).
Paris, D. F., and D. L. Lewis, "Chemical and Microbial Degradation
of Ten Selected Pesticides in Aquatic Systems," Res. Rev.. 45:
95-124 (1973).
Pickering, Q. H., C. Henderson, and A. E. Lemke, "The Toxicity of
Organic Phosphorus Insecticides to Different Species of Warmwater
Fishes," Trans. Am. Fish. Soc.. 91(2)-.175-184 (1962).
Plmentel, D., "Ecological Effects of Pesticides on Nontarget Species,"
Executive Office of the President, Office of Science and Technology,
U.S. Government Printing Office, Washington, D.C. (1971).
207
-------
Poorman, A. E., "Effects of Pesticides on Euglena gracilts. I.
Growth Studies," Bull. Environ. Contain. ToxLcol.. 10(l):25-28
(1973).
Priester, L. E., "The Accumulation in Metabolism of DDT, Parathion
and Endrin by Aquatic Food Chain Organisms," Ph.D. Thesis, Clemson
University (1965). (In: Li and Fleck, 1972.)
Quentin, K. E., "Pesticides in Water - Determination, Removal and
Limiting Values," Chem. Ine. Tech.. 44(20)-.1172-1176 (1972a).
Quentin, K. E., "Evaluation and Significance of Residue Values from
the Viewpoint of the Water Biocenosis and Drinking Water Quality,"
Schriftenr. Ver. Wasser-Boden-Lufthyg.. 34:19-28 (1972b).
Robel, R. J., C. D. Stalling, M. E. Westfahl, and A. M. Kadoum,
"Effects of Insecticides on Populations of Rodents in Kansas -
1965 to 1969," Pest. Monit. J.. 6(2):115-121 (September 1972).
Rudd, R. L., and R. E. Genelly, Pesticides; Their Use jand Toxicity
in Relation to Wildlife. State of California Department of Fish
and Game, Game Bull. No. 7, pp. 108-113 (1956).
Sacher, R. M., G. F. Ludvik, and J. M. Deming, "Bioactivity and
Persistence of Some Parathion Formulations in Soil," J. Econ.
Entomol.. 65(2):329-332 (April 1972).
Saltzman, S., L. Kliger, and B. Yaron, "Adsorption-Desorption of
Parathion as Affected by Soil Organic Matter," J. Agr. Food Chem..
20(6):1224-1226 (1972).
Saltzman, S., B. Yaron, "Parathion Adsorption from Aqueous Solutions
as Influenced by Soil Components," In: Fate of Pesticides in Environ-
ment , Gordon and Breach, London, pp. 87-100 (1972).
Sanders, H. 0., "Toxicity of Pesticides to the Crustacean Gammarus
lacustris," Technical Papers No. 25, pp. 18, United States Depart-
ment of the Interior Fish and Wildlife Service (1969).
Sanders, H. 0., "Pesticide Toxicities to Tadpoles of the Western
Chorus Frog Pseudacris triseriata and Fowler's Toad Bufo woodhousii
fowleri, Copeia, 2:246-251 (1970).
208
-------
Sanders, H. 0., and 0. B. Cope, "Toxicities of Several Pesticides to
Two Species of Cladocerans," Trans. Am. Fish. Soc., 95(2):165-169
(1966).
Sanders, H. 0., and 0. B. Cope, "The Relative Toxicities of Several
Pesticides to Naiads of Three Species of Stoneflies," Limnology
and Oceanography, 13(1):112-117 (1968).
Sandi, E., "Reduction of Parathion Induced by Light," Nature, 181:
499 (1958).
Satpathy, J. M., G. K. Padhi, and D. N. Dutta, "Toxicity of Eight
Insecticides to the Coccinellid Predator Chilomenes sexmaculata,"
Indian J. Entomol.. 30(1):130-132 (1968).
Schaefer, C. H., E. Dupras, Jr., "The Effects of Water Quality,
Temperature and Light on the Stability of Organophosphorus
Larvicides Used for Mosquito Control," Proc. Papers Ann. Conf.
California"Mosquito Control Assoc. 37:67-75 (1969).
Schafer, E. W., "The Acute Oral Toxicity of 369 Pesticidal, Pharma-
ceutical and Other Chemicals to Wild Birds," Toxicol. Appl.
Pharmacol., 21:315-330 (1972).
Schafer, E. W., and R. B. Brunton, N. F. Lockyer, and J. W. DeGrazio,
"Comparative Toxicity of 17 Pesticides to the Quelea, House
Sparrow, and Red-Winged Blackbird," Toxicol. Appl. Pharmacol.,
26:154-157 (1973).
Sethunathan, N., "Degradation of Parathion in Flooded Acid Soils,"
J. Agr. Food Chem.. 21(4):602-604 (1973).
Sethunathan, N., and T. Yoshida, "Conversion of Parathion to Para-
nitrophenol by Diazinon Degrading Bacterium," Proc. Inst. Environ.
Sci. Annu. Tech. Meet.. 18:255-257 (1972).
Sethunathan N., and T. Yoshida, "Parathion Degradation in Submerged
Rice Soils in the Philippines," J. Agr. Food Chem.. 21(3):504-506
(1973).
Sreenivasan, A., and G. K. Swaminathan, "Toxicity of Six Organo-
phosphorus Insecticides to Fish," Curr. Sci., India, 36:397-398
(August 1967).
209
-------
Stanley, C. W., J. E. Barney II, M. R. Helton, and A. R. Yobs,
"Measurement of Atmospheric Levels of Pesticides," Environ. Sci.
Tech.. 5(5):430-435 (1971).
Stephen, W. P., "The Effects of Chronic Sublethal Doses of Pesticides
on Behavior and Longevity in Arthropods," Oregon State Univ. Environ.
Health Sci. Cent. Annu. Prog. Rep.. 161-167 (1972).
Stevens, L. J., C. W. Collier, and D. W. Woodham, "Monitoring Pesti-
cides in Soils from Areas of Regular, Limited, and No Pesticide
Use," Pest. Monit. J., 4(3):145-164 (December 1970).
Stewart, D. K. R., D. Chisholm, and M. T. H. Ragab, "Long-Term Per-
sistence of Parathion in Soil," Nature. 229:47 (1971).
Swoboda, A. R., and G. W. Thomas, "Movement of Parathion in Soil
Columns," J. Agr. Food Chem., 16(6) -.923-927 (November/December 1968).
Teotia, T. P. S., and G. C. Tiwari, "Toxicity of Some Important Insec-
ticides to the Coccinellid Predator, Coccinella septempunctata,"
Labdev. Part B, 10(1):17-18 (1972).
Tessari, J. D., and D. L. Spencer, "Air Sampling for Pesticides in
the Human Environment," J. Assoc. Offic. Anal. Chem.. 54(6)-.1376-
1382 (1971)
Tucker, R. K., and D. G. Crabtree, "Handbook of Toxicity of Pesticides
to Wildlife," U.S. Department of the Interior, Fish and Wildlife
Service, Denver Wildlife Research Center, Resource Publication
No. 84, p. 82 (1970).
Tucker, R. K., and M. A. Haegele, "Comparative Acute Oral Toxicity
of Pesticides to Six Species of Birds," Toxicol. Appl. Pharmacol.,
20:57-65 (1971).
USDI, "Wildlife Research; Problems, Programs and Progress, Pesticide-
Wildlife Relations," Fish Wildlife Service, Bur. Sport Fish Wildl.
Circ. 43, 117 pp. (1966). Quoted from: Pimentel (1971).
Voerman, S., and A. F. H. Besemer, "Residues of Dieldrin, Lindane,
DDT, and Parathion in a Light Sandy Soil After Repeated Applica-
tion Throughout a Period of 15 Years," J. Agr. Food Chem.. 18(4):
717-719 (1970).
210
-------
von Rumker, R., and F. Horay, Pesticide Manual, Vol. I. Department
of State, Agency for International Development (1972).
WADC, Wright-Patterson Air Force Base, Ohio, Air Force Systems
Command, "The Handbook of Toxicology, Vol. Ill, "Insecticides"
WADC Tech. Report 55-16 (1959).
Ware, 6. W., and C. C. Roan, "Interaction of Pesticides with Aquatic
Microorganisms and Plankton," Residue Rev., 33:15-45 (1971).
Weidhaas, D. £., M. C. Bowman, and C. H. Schmidt, "Loss of Parathion
and DDT to Soil from Aqueous Dispersions and Vermiculite Granules,"
J. Econ. Entomol.. 54(1):175-177 (1961).
Wiersma, 6. B., W. G. Mitchell, and C. L. Stanford, "Pesticide Residues
In Onions and Soil - 1969," Pest. Monit. J., 5(4):345-347 (March
1972a).
Wiersma, G. Bn H. Tai, and P. F. Sand, "Pesticide Residue Levels in
Soils, FY 1969 - National Soils Monitoring Program," Pest. Monit.
J._, 6(3): 194-228 (December 1972b).
Wolfe, H. R., and W. F. Durham, "Spillage of Pesticides and Residues
in Soil," Washington State Hort. Assoc. Proc.. 62:91-92 (1966).
Wolfe, H. R., D. C. Staiff, J. F. Armstrong, and S. W. Comer, "Per-
sistence of Parathion in Soil," Bull. Environ. Contarn. Toxicol..
10(1):1-9 (1973).
Wood, E. M., "The Pathology of Pesticide Toxicity in Fish," Unpublished,
USDI, Columbia, Mo.
Yaron, B., and S. Saltzman, "Influence of Water and Temperature on
Adsorption of Parathion by Soils," Soil Sci. Soc. Am. Proc.. 36(4):
583-586 (1972).
Zuckerman, B. M., K. Deubert, M. Mackiewicz, and H. Gunner, "Studies
on the Biodegradation of Parathion," Plant Soil, 33(2):273-281 (1970).
211
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SUBPART II. D. PRODUCTION AND USE
CONTENTS
Page
Registered Uses of Parathion 213
Federally Registered Uses 213
State Regulations 237
Production and Domestic Supply of Parathion In the U.S 238
Volume of Production 238
Imports 239
Exports 239
Domestic Supply 240
Formulations 240
Use Patterns of Parathion in the United States 241
General 241
Parathion Use Patterns by Region 244
Parathion Use Patterns by Crops 244
Parathion Uses in California 245
Summary 251
212
-------
This subsection contains data on the production and uses of parathion;
it is organized according to three subject areas: registered uses, produc-
tion and domestic supply, and use patterns.
Registered Uses of Parathion
Federally Registered Uses - Parathion has a very broad spectrum of effective-
ness against insects and mites. It is registered and recommended in the
United States for use on a large number of crops, including fruit, nut,
vegetable and field crops. Tolerances for parathion residues have been
established on about 100 raw agricultural commodities.
All registered uses of parathion by crops, target pests, dosage rates,
formulations, type of use, established tolerances, and use, timing, and pre-
harvest interval limitations are summarized in the "EPA Compendium of
Registered Pesticides," pages III-P-2.1 through 2.164. This section on
parathion, comprising 164 pages, makes up more than 15% of all listings of
all registered insecticides, acaricldes, molluscidles and antifouling com-
pounds in Volume III of the EPA "Compendium of Registered Pesticides." This
fact illustrates the large number and variety of pest control uses for which
parathion formulations are currently registered in the U.S.
The registered uses of parathion are detailed in this section by a set
of four tables:
Table 29: Parathion - Summary of registered Uses by Crops,
Application Rates, and Rate and Time Registration.
Table 30: Pest Insects and Mites against which parathion is
recommended, in alphabetical order by common name.
Tables 31 and 32: Registered uses of one of the common formula-
tions of parathion, i.e., emulsifiable liquid containing
4 Ib of active ingredient per gallon, by crops; insects
and other pests controlled on each crop; recommended
dosage rates; and general and specific directions for,
and limitations of use.
In these tables, rates of application are given in
terms of pints or quarts of formulated product per
acre or per volume of spray. These rates are readily
convertible into active ingredient units.
213
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TABLE 29. PARATHION - SUMMARY OF REGISTERED USES BY CROPS, APPLICATION RATES,
AND RATE AND TIME RESTRICTIONS.
Target crops
Rate per Maxium
application permissible
AI rate.
(Ib. AI) (Ib./acre)
Minimum time, last treatment
to harvest.
(days)
Agricultural crop
Alfalfa
Almonds A/
Apples
Apricots
Artichokes
Avacados
Barley
Beans
(soil appl.)
Beets
(soil appl.)
Blackberries
(soil appl.)
Black-eyed peas
(soil appl.)
Blueberries
Boy senberr ies
(sell appl.)
Broccoli
(soil appl.)
Brussels sprouts
(soil appl.)
Cabbage
(soil appl.)
Cantaloupes
(soil appl.)
Carrots
(soil appl.)
Cauliflower
0.25-0.8/A
0.25-0.5/100gal. 2.6
1.0-2.6/A
0.12-0.5/100gal. 6.0
0.3-3.0/A
0.15-0. 5 /lOOgal. 3.6
1.0-3.0/A
0.35-0. I/A
0.18-0.37/100gal. 2.5
0.25-0.75/A
0.25-0.8/A
5.0-6.0/A
0.15-0.6/A
2.0-6.0/A
0.11-1.0/A
1.0/A
0.25-0.5/A
3.0-4.0/A
0.25-0.5/A
0.15-1.0/A
1.0/A
0.15-1.0/A
3.0-6.0/A
0.15-1.0/A
3.0-6.0/A
0.15-1.0/A
3.0-6.0/A
0.15-0.5/A
3.0-6.0/A
0.2-0.6/A
2.0-5.0/A
0.15-1.0/A
15days thru 0.8 Ib/A
thru 2.6 Ib/A
lAdays thru 6.0 Ib/A
14days thru 3.6 Ib/A
7days thru 1.0 Ib/A
21days thru 2.5 Ib/A
ISdays thru 0.85 Ib/A
7days thru 0.5 Ib/A
15days> 0.5 thru 0.8 Ib/A
ISdays thru 0.6 Ib /A
21days thru 0.6 Ib/A If
ISdays thru 1.0 Ib/A
ISdays thru 0.5 Ib/A
14days thru 0.5 Ib/A
ISdays thru 1.0 Ib/A
7days thru 0.5 Ib/A
21days>0.5 thru 1.0 Ib/A
7days thru 0.5 Ib/A
21days 0.5 thru 1.0 Ib/A
7days thru 0.25 Ib/A
10days>0.25 thru 0.5 Ib/A
21days>0.5 thru 1.0 Ib/A
7days thru 0.5 Ib/A
ISdays thru 0.6 Ib/A
7days thru 0.5 Ib/A
(soil appl.)
3.0-6.0/A
21days 0.5 thru 1.0 Ib/A
Source: U.S. Environmental Protection Agency, EPA Compendium of Registered Pesticides.
Vol. Ill, (1973).
214
-------
Table 29. (Continued)
Celery
(soil appl.)
Cherries
Citrus
Clover
Collards
(soil appl.)
Corn
(soil appl.)
Corn (sweet)
(soil appl.)
Cotton
Cow peas
Cranberries
Cucumbers
(soil appl.)
Currants
Dewberries
Eggplant
(soil appl.)
Endive
(Escarole)
(soil appl.)
Figs
Filberts!/
Garlic
Gooseberries
Grapefruit
Grapes
Grass (forage)
Hops
Rale
(soil appl.)
Kohlrabi
Kumquats
Lemons
0.15-0.75/A
3.0-5.0/A
0.11-0.5/100gal. 2.0
0.4-1.4/A
0.0625-2.0/100gal. 4.0
1.0-10.0/A 10.0
0.12-0.75/A
0.15-0.5/A
3.0-4.2/A
0.16-0.75/A
0.015/1,OOOsq.ft.
1.0-6.0/A
2.0-5.0/A
0.1-1.0/A
0.45/A
0.5-1.0/100gal. 1.0
0.5-1.0/A
0.1/5xlO*cu.ft.
0.15-0.5/A
3.0-4.2/A
0.11-0.8/A
0.2-0.5/A
0.2-0.6/A
3.0-5.0/A
0.1/5x100 cu.ft.
0.35-0.5/A
3.0-4.2/A
0.25-0.5/100gal. 2.5
0.25/100gal. 2.5
0.4/A
0.25-0.5/A
0.11-0.8/A
0.0625-2.0/100gal. 4.0
1.0-10.0/A 10.0
0.25-1.0/lOOgal. 2.5
0.25-2.5/A
0.25-0.8/A
0.25-0.8/A
0.15-0.5/A
3.0-5.0/A
0.2-1.0/A
0.0625-2.0/100gal. 4.0
1.0-10.0/A 10.0
0.0625-2.0/100gal. 4.0
1.0-10.0/A 10.0
ISdays thru 0.25 Ib/A
21days3T 0.25 thru 0.5 Ib/A
30days>- 0.5 thru 0.75 Ib/A
14days thru 2.0 Ib/A
I4days thru 4.0 Ib/A
SOdays^- 4.0 thru 10.0 Ib/A
ISdays thru 0.8 Ib/A
7days thru 0.25 Ib/A
10days2" 0.25 thru 0.5 Ib/A
12days thru 1.0 Ib/A
7days thru 1.0 Ib/A
ISdays thru 0.45 Ib/A
ISdays thru 0.8 Ib/A
SOdays^ 0.8 thru 1.0 Ib/A
ISdays thru 0.1/SxlO4 cu.ft.l/
ISdays thru 0.5 Ib/A
30days thru 0.8 Ib/A
ISdays thru 0.5 Ib/A
ISdays thru 0.6 Ib/A
21days70.il thru 5x10 cu.ft.-/
21days thru 0.5 Ib/A
30days thru 2.5 Ib/A
thru 2.5 Ib/A
ISdays thru 0.5 Ib/A
ISdays thru 0.8 Ib/A
lAdays thru 4.0 Ib/A
30days ^4.0 thru 10.0 Ib/A
14days thru 1.5 Ib/A
1.5 thru 2.5 lb/Al/
ISdays thru 0.8 Ib/A
ISdays thru 0.8 Ib/A
7days thru 0.25 Ib/A
lOdays 0.25 thru 0.5 Ib/A
7days thru 0.8 Ib/A
21days^ 0.8 thru 1.0 Ib/A
14days thru 4.0 Ib/A
30days:=- 4.0 thru 10.0 Ib/A
14days thru 4.0 Ib/A
30daysxr4.0 Ib. thru 10.0 Ib/A
215
-------
Table 29. (Continued)
Lettuce
(soil appl.)
Limes
Loganberries
Mangoes
Melons
(soil appl.)
Mustard greens
Nectarines
Oats
Okra
Olives
Onions
(soil appl.)
Oranges
Pastures see Grass
(soil appl.)
Pastures
(irrigated)
Peaches
Peanuts
(soil appl.)
Pears
Peas
(soil appl.)
Pecans
Peppers
(soil appl.)
Pineapples
(preplant dip)
Plums/Prunes
Potatoes
(soil appl.)
Pumpkins
Quince
0.1/5x10* cu.ft.
0.25-0.5/A
3.0-6.0/A
0.0625-2.0/100g
0.25-1.0/A
0.5/100gal.
0.15-0.5/A
4.0-6.0/A
0.15-0.5/A
0.18-0.5/100gal.
0.6-2.0/A
0.25-0.75/A
0.25-0.75/A
0.25-0.62/100gal.
0.2-0.8/A
0.38-0.6/A
0.0625-2.0/100gal.
1.0-10.0/A
(forage)
0.5-1.0/A
O.I/A
0.18-0.5/100gal.
0.6-2.0
0.2-0.5/A
2.0-3.0/A
0.15-0.38/100gal.
0.4-1.0/A
0.25-0.5/A
3.0-6.0/A
0.25-0.38/100gal.
0.6-0.7/A
0.15-0.8/A
5.0-6.0/A
0.45-0.75/A
0.15/100gal.
0.25-0.5/100gal.
1.0-1.5/A
0.25-1.0/A
2.0-6.0/A
0.2-0.5/A
0.3-0.38/100gal.
10.0
3.0
5.0
5.0
4.0
10.0
5.0
3.6
5.4
4.0
21days 0.1 Ib. thru 5x10* cu.ft.i'
7days thru 0.5 Ib/A (head)
lAdays thru 0.25 Ib/A (bibb & head)
21days^> 0.25-0.5 Ib/A (bibb & head)
14days thru 4.0 Ib/A
ISdays thru 1.0 Ib/A
21days thru 3.0 Ib/A
7days thru 0.5 Ib/A
7days thru 0.25 Ib/A
IQAaya^ 0.25 thru 0.5 Ib/A
14days thru 4.0 Ib/A
21days thru 2.5 Ib/A*/
ISdays thru 0.75 Ib/A
21days thru 0.75 Ib/A
ISdays thru 0.8 Ib/A5-/
14days thru 4.0 Ib/A
30daysjx" 4.0 thru 10.0 Ib/A
7days thru 0.1 Ib/A
7days thru 0.116/A
14days thru 4.0 Ib/A
21days thru 2.5 lb/A±'
ISdays thru 0.5 Ib/A
14days thru 3.6 Ib/A
lOdays thru 0.5 Ib/A (peas)
ISdays thru 0.5 Ib/A (forage)
ISdays thru 5.4 Ib/A
ISdays thru 0.8 Ib/A
7days thru 0.75 Ib/A
14days thru 4.0 Ib/A
Sdays thru 1.0 Ib/A
lOdays thru 0.5 Ib/A
14days thru 3.6 Ib/A
216
-------
Table 29. (Continued)
Radishes
Raspberries
Rice
Rutabagas
(soil appl.)
Safflower
Sorghum
Soybeans
(soil appl.)
Spinach
(soil appl.)
Squash
Strawberries
(soil appl.)
Sugar beets
(soil appl.)
Sugarcane
(soil appl.)
Sweet potatoes
(soil appl.)
Swiss chard
Tangelos/
Tangerines
Tobacco
(soil treat)
Tomatoes
(soil appl.)
Turnips
(soil appl.)
Vetch
WalnutsiH/
Watermelons
(soil appl.)
Wheat
0.1/5xl04cu.ft.
0.2-1.0/A
0.094-0.I/A
0.15-0.75/A
3.0-5.0/A
0.5/A
0.25-1.01 Ib/A
0.2-0.8/A
3.0-4.2/A
0.2-0.5/A
4.0-6.0/A
0.15-0.5/A
0.2-0.8/A
1.0/Al/
0.4-5.0/A
0.3-0.8/A
4.0-5.0/A
2.0-6.0/A
0.5-1.0/A
2.0-4.0/A
0.2-0.5/A
0.0625-2.0/100gal.
1.0-10/A
0.01-0.05/lOOsq.ydJi'
0.15-0.5/A
2.0-6.0/A
0.1/5x10 sq.ft.
0.25-1.0/A
3.0-6.0/A
0.25-0.5/A
3.0-5.0/A
0.25-0.8/A
0.075-0.5/100gal
0.3-0.8/A
0.2-0.5/A
3.0-4.0/A
0.25-0.8/A
4.0
10.0
5.0
ISdays thru 0.1/5xl04 cu.ft.-2/
ISdays thru 1.0 Ib/A
Iday thru 0.1 Ib/A
7days thru 0.75 Ib/A
thru 0.5 Ib/A6-/
12days thru 1.0 Ib/A
20days thru 0.8 Ib/A
14days thru 0.5 Ib/A
ISdays thru 0.5 Ib/A
14days thru 0.8 Ib/A
ISdays thru 0.8 Ib/A
ISdays thru 11.0 Ib/A
21days thru 0.5 Ib/A
14days thru 4.0 Ib/A
3days^>4.0 thru 10.0 Ib/A
Sdays thru 0.5 Ib/A (by priming)
ISdays thru 0.5 Ib/A (by cutting)
lOdays thru 0.1/104 sq.ft.^/
lOdays thru 1.0 Ib/A
7days thru 0.25 Ib/A
lOdays^ 0.25 thru 0.5 Ib/A
ISdays thru 0.8 Ib/A
ISdays thru 0.8 Ib/A
7days thru 0.5 Ib/A
ISdays thru 1.0 Ib/A
Ornamentals
Gladiolus (soil appl.)
Flowering plants
(soil appl.)
5.0/A
0.15-0.75/A
2.0-5.0/A
217
-------
Table 29. (Continued)
Woody Shrubs, Trees and Vines
Christinas trees
Shrubs/Trees/Vines
(soil appl.)
Greenhouse Plants
Chrysanthemums
Lilies
Greenhouse
ornamentals
Aquatic Areas
Standing water
0.25/100gal.
0.15-0.75/A
2.0-5.0/A
0.1/5xl04 sq.ft.
0.1/5xl04 sq.ft.
0.1/5xl04 sq.ft.
0.04/A
For commercial use only.
For commercial use only.
For commercial use only.
See restrictions listed in Compendium.
Notes:
1. Do not apply after hulls begin to open thru 2.6 Ib/A.
2. 30 day spray/harvest interval if tops are to be used as food or feed.
3. Apply dosages^=^1.5 thru 2.5 Ib./A before fruit is the size of buckshot or after
harvest.
4. California: Do not apply 5.01b/A between Jan.1 and harvest.
5. Do not apply later than Aug. 1 through 5.0 Ib/A.
6. Do not apply after flowering through 5.0 Ib/A.
7. For post-harvest only.
8. Seed bed treatment.
9. For commercial greenhouse use only.
10. Do not apply after husks open through 5.0 Ib/A.
218
-------
TABLE 30. PEST INSECTS AND MITES AGAINST WHICH
FARATHION IS RECOMMENDED
(IN ALPHABETICAL ORDER BY COMMON NAMES)
Alfalfa caterpillar
Alfalfa looper
Alfalfa seed chalcid
Alfalfa weevil
American cockroach
American plum borer
Ants
»Aphids
Apple flea veevil
Apple lace bug
Apple maggot
Apple redbug
Armyworm
Artichoke plume moth
Asiatic garden beetle
Avocado lace bug
Avocado leafhopper
Azalea leafminer
Bagworm
Banded cucumber beetle
Beet armyworm
Bean leaf beetle
Beet leafhopper
Bean leafroller
Black grass bugs
Black vine weevil
Blackheaded fireworm
Black vine weevil
Blister beetles
Blossom anomala
Blossom weevils
Blueberry maggot
Boll weevil
Boll worm
Cabbage looper
Cankerworms
Carrot rust fly
*Casebearers
Catfacing insects
Celery leaftier
Cherry fruitworm
Cherry maggot
Chinch bug
Citrus root weevil
Climbing snails
Clover head weevil
Clover leaf weevil
Codling moth
Colorado Potato beetle
Consperse stinkbug
Colias eurytheme
Autographa californica
Bruchophagus roddi
Hypera postica
Periplaneta americana
Euzophera semifuneralis
Family Formicidae
Family Aphididae
Rhynchaenus pallicornis
Corythueha caelata
Rhagoletis pomonella
Lygi de a mendax
Pseudaletia unipuncta
Platyptilia carduidactyla
Maladera castanea
Pseudacysta perseae
Idona minuends
Gracillaria azaleelia
Thyridopteryx ephemeraeformis
Diabrotica baiteata
Spodoptera exigua
Erynephala puncticollis
Circulifer teneJLlua
Urbanus proteus
Family Miridae
Otiorhynchus sulcatus
Rhopobota naevana
Otiorhynchus sulcatus
Family Meloidae
Anomala undulata
Anthonomus spp.
Rhagoletis mendax
Anthonomus grandis
Heliothis zea
Trichoplusia ni
Family Geometridae
Psila rosae
Family Coleophoridae
Order Hemipter a/Heteroptera
Udea rubigalis
Grapholitha packardi
Rhagoletis cingulata
Plissus leucopterus
Pachnaeus litus
Class Gastropoda
Hypera meles
Hypera punctata
Laspeyresia pomonella
Leptinotarsa decemlineata
Euschistus conspersus
Source: List of pest Insects and mites from: U.S. Environmental Protection
Agency, EPA Compendium of Registered Pesticides, Vol. Ill (1973);
scientific names from: Supplement 13 to EPA Compendium, Vol. III.
219
-------
Table 30. (Continued)
Corn earworm
Corn rootworms
Corn silk fly
Cotton leafperforator
Cotton leafworm
Cranberry fruitworm
Cranberry tipvorm
Crane flies
Cri ckets
Cucumber beetles
Current borer
*Cutworms
Darkling beetles
Diamondback moth
Earwigs
European apple sawfly
European Corn borer
Eyespotted bud moth
Fall armyworm
Fall webworm
False celery leaftier
False chinch bug
Flea beetles
Fruittree leafroller
Fuller rose beetle
Grape berry moth
Grape bud beetle
Grape leaffolder
Grasshoppers
Green clovervorm
Green fruitworm
Green June beetle
Greenhouse leaftier
Harlequin bug
Hoplia beetles
Hornworms
Imported cabbageworm
Japanese beetle
Juniper webworm
Katydids
Lace bugs
Leafhoppers
Leaffooted bug
*Leafminers
*Leafrollers
*Leaftiers
Lesser appleworm
Lesser cornstalk borer
Lesser peachtree borer
Limabean pod borer
Little fire ant
Heliothis zea
Diabrotica spp.
Euxesta stigmatias
Bucculatrix thurberiella
Alabama argillacea
Acrobasis vaccinii
Dasineura oxycoccana
Family Tipulidae
Family Gryllidae
Family Chrysomelidae
Synanthedon tipuliformis
Family Noctuidae
Family Tenebrionidae
Plutella xylostella
Family Dermaptera
Hoplocampa testudinea
Ostrinia nubilalis
Spilonota ocellana
Spodoptera frugiperda
Hyphantria cunea
Udea profundalis
Nysius ericae
Family Chrysomelidae
Archips argyrospilus
Pantomorus cervinus
Paralobesia viteana
Glyptoscelis squamulata
Desmia funeralis
Family Acrididae
Plathypena scabra
Lithophane antennata
Cotinis nitida
Udea rubigalis
Murgantia histionica
Hoplia
Family
Pieris
spp.
Sphingidae
rapae
Popillia Japonica
Dichomeris marginella
Family Tettigoniidae
Family Tingidae
Family Cicadellldae
Leptoglossus phyllopus
Class Insecta
Class Insecta
Order Lepidoptera
Grapholitha prunivora
Elasmopalpus lignosellus
Synanthedon pictipes
Etiella zinckenella
Wasmannia auropunctata
220
-------
Table 30. (Continued)
Lygus bug
Mealybugs
Mellonworm
Midges
*Mites
Mosquitoes
Obsure root weevil
Omnivorous leaf roller
Onion maggot
Orangedog
Orange worm
Orange tortrix
Oriental fruit moth
Pameras
Pandemis moth
Peach bark beetle
Peach twig borer
Peachtree borer
Pea moth
Pea weevil
Pearslug
Pear psylla
Pecan leaf casebearer
Pecan nut casebearer
Pepper maggot
Pickleworm
Pink scavenger caterpillar
Plant bugs
Plum curculio
Potato psyllid
Potato tuberworm, Splitowrm
Psyllids
Raspberry crown borer
Readbanded leafroller
Readnecked cane borer
Readnecked peanutworm
Rice leafminer
Rindworms
Rose chafer
Saltmarsh caterpillar
Sand wireworm
Sapbeetles
Sawflies
"Scales
Seedcorn maggot
Shothole "borer
Sixspotted leafhopper
Sorghum midge
Sorghum webworm
Sowbugs
Lygus spp.
Family Pseudococcidae
Diaphania hyalinata
Family Chironomidae
Class Acarina
Family Culicidae
Sciophithes obscurus
PIatynota stultana
Hylemya antiq.ua
Papilio cresphontes
Class insecta
Argyrotaenia citrana
Grapholitha molesta
Pachybrachius bilobata
Family Tortricidae
Philoeotri'bus liminaris
Anarsia lineatella
Sanninoidea exitiosa
Laspeyresia nigricana
Bruchus pisorum
Caliroa cerasi
Psy11a pyricola
Acrobasis Juglandis
Acrobasis caryae
Zonosemata electa
Diaphania nitidalis
Sathro'brota rileyi
Family Miridae
Conotrachelus nenuphar
Paratioza cockerelli
Phthorimaea operculella
Family Psyllidae
Bembecia marginata
Argyrota.enia velutinana
Agrilus ruficollis
Stegasta bosquella
Hydrellia griseola
Order Lepidoptera
Macrodactylus subspinosus
Estigmene acrea
Horistonotus uhlerii
Family Nitidulidae
Order Hymenoptera
Superfamily Coccoidea
Hylemya platura
Scelytus rugulosus
Macrosteles fascifrons
Contarina sorghicola
Gelama sorghiella
Order Isopoda
221
-------
Table 31. REGISTERED USES OF PARATHION EMULSIFIABLE LIQUID
(A LB ACTIVE INGREDIENT PER GALLON) - CROPS AND
OTHER USES, PESTS, DOSAGE RATES AND USE LIMITATIONS^'
NI ran
E-4
Hazards and Ingredients
INSCCIKIOC BY
Monsanto.
Emulsifiable insecticide for
controlling certain insects
on the listed field, forage,
fruit and vegetable crops.
NOT FOR HOME USE
Complete Directions for Use
EPA Reg. No. 524-132
Use only according to these label instructions.
READ "LIMIT OF WARRANTY AND LIABILITr BE-
FORE BUYING OR USING. IF TERMS ARE NOT
ACCEPTABLE RETURN AT ONCE UNOPENED.
RESEALABLE BAG
TPull flaps apart to open.
Press along ridge to close.
STOP! READ THE LABEL
DANGER! POISON
Keep Out of Reach of Children
CAN KILL YOU
ACTIVE INGREDIENTS:
•Paratfiion: 0,0-diethyl 0-p-nHrophenyl
phospborothioate 45J%
Aromatic petroleum derivative solvent .. 49.4%
INERT INGREDIENTS: 5JK
100.0%
•Equivalent to 4.0 Ibs. of 100%
parathion per gallon.
Combustible: Do net store or use near beat or opn
HUM. In case of fire, use water spray, foam, dry
chemical or C02.
a/ Sample label of Monsanto Company, St. Louis, Missouri, EPA Reg.
No. 524-132.
This formulation Is not currently marketed by Monsanto, but the
label is being made available to Monsanto1s formulator customers
for parathion technical (J. M. Magner, Communication, 10 May 1974.
222
-------
Table 31. (Continued)
LIMIT OF WARRANTY AND LIABILITY
Monunto Company warrants that this material con-
forms to the chemical description on the libel ind
is ntsonabhr fit for the purposes referred to in the
directions for use. This product is sold subject to
the understanding that the buyer assumes all risks
of use or handling which may result in loss or dam-
tfe which are beyond the control of the seller, such
as for example incompatibility with other products.
the manner of its use or application, or the presence
of other products or materials in or on the soil or
crop. MONSANTO MAKES NO OTHER EXPRESS OR
IMPLIED WARRANTY OF FITNESS OR MERCHANT-
ABILITY. The exclusive remedy of the user or buyer.
and tte limit of the liability of Monsanto Company
or any other seller for any and all losses, injuries or
damatts resulting from the use or handling of this
product shall be the purchase price paid by the user
or buyer for the quantity of this product involved.
The buyer and all users are deemed to have accepted
the terms of this notice which may not be varied by
any verbal or written agreement
CAM KILL YOU BY SB* CONTACT
INt product an UK IN if fowled by knxb or
ipilM or lebsfltd on stiff, in eye or on cMftutf
(tqrt t»et ttroutk dottti). 4«^B> .
»
*
00 NOT TOUCH
CAM PU YOU If BREATHED
Wl product an kM |ta h* nporv nw» ma) or dint
tnbneftoi.
00 NOT BREATHE
CM PU YOU IF SWALLOWED
nil product on kin you il iwflowtd MM in
vnt Mmmti: ipny not or dutt ray bt MM if
00 NOT SWALLOW
Precautions
POISONOUS TO FISH AND WILDLIFE
This product is toiic to fish and wildlife. Birds and
other wildlife in treated areas may be hilled. Keep
out of any body of water. Do not apply when weather
conditions favor drift .from treated areas. Do not
apply when runoff is likely to occur. Do not con-
taminate water by cleaning equipment or disposal
of wastes.
MSrOSAL OF EMPTY CONTUMEI-Do not re-use
this container. Completely empty the contents and
bury the unused chemical at least 18 inches deep
• an isolated location away from water supplies.
Rinse out the inside of the container with water to
which has been added detergent and caustic soda.
Carefully discard the rinse solution by burying at
least It inches deep in an isolated area away from
water supplies. Puncture and crush empty metal
container and bury at least 18 inches deep in a
supervised public or private dump.
USE ONLY WHEN WEARING THE FOLLOWING
PROTECTIVE EQUIPMENT AND CLOTHING
(1) Wear water-proof pants, coat hat, rubber boob
or rubber overshoes. (2) Wear safety goggles. (3)
Wear mask or respirator approved by the U5. Bureau
•f Mines for parathion protection. (I) Wear heavy
My. natural robber gloves.
WORK SAFETY RULES
Keep alt unprotected persons and children away from
treated area or where there is danger of drift.
Do not rub eyes or mouth with hands. If you feel sick
in any way, STOP work and get help right away. Call
a doctor (physician), clinic or hospital—immediately.
Explain that the victim has been exposed to para-
thion and describe his condition. After first aid is
given (see Tint Aid Treatment Section) and if a doc-
tor cannot come, take victim to clinic or hospital.
IMPORTANT! Before removing gloves, wash them
with soap and water. Always wash hands, face and
arms with soap and water before smoking, eating or
drinking.
AFTER WORK, take off all work clothes and shoes.
Shower, using soap and water. Wear only dean
clothes when leaving job. Do not wear contaminated
clothing. Wash protective clothing and protective
equipment with soap and water after each use. Res-
pirator should be cleaned and filter replaced accord-
ing to instructions included with respirator.
•fc POISON SIGNS (Symptoms)
Parathion is a very dangerous poison. It rapidly en-
ters the body on contact with all skin surfaces and
eyes. Clothing wet with this material must be re-
moved immediately. Exposed persons must receive
prompt medical treatment or they may die.
Work Safety Rules and Poison Signs (Symptoms) 9
223
-------
Table 31. (Continued)
First Aid Treatment
10
Some of the signs and symptoms of poisoning ire:
Headache, nausea, vomiting, cramps, weakness,
blurred vision, pin-point pupils, tightness in chest
labored breathing, nervousness, sweating, watering
of eyes, drooling or frothing of mouth and nose.
muscle spasms and coma.
+ FIRST AID TREATMENT +
Call a doctor (physician), clinic or hospital immedi-
ately. Explain that the victim has been exposed to
parathion and describe his condition.
H breathing has stopped, start artificial respiration
immediately and maintain until doctor sees victim.
If swallowed and victim is awake (conscious) make
him vomit quickly. Induce vomiting by sticking finger
down throat or by giving soapy or strong salty water
to drink. Repeat until vomit is dear. Never give any-
thing by mouth to an unconscious person. Have victim
lie down and keep quiet. See doctor immediately
ta ox of contact, immediately flush' eyes or skin
with plenty of water for at least 15 minutes while
removing contaminated clothing and shoes. See doc-
tor immediately.
ATROPINE IS AN ANTIDOTE.
CONSULT PHYSICIAN FOR EMERGENCY SUPPLY.
If symptoms or signs of poisoning include blurred
vision, abdominal cramps, and tightness in the chest,
do not wait for a doctor but give two atropine tablets
(each 1/100 grain or 0.65 milligrams) at once. (One
tablet to children under five years of age.)
Prevent Injury
12
TO PREVENT PERSONAL INJURY AND POSSIBLE
FATALITIES:
Keep all persons and animals out of treated areas for
48 hours.
Vacated areas should not be re entered until drifting
insecticide and volatile residues have dissipated.
Do not use in any manner other than recommended
on this label.
To avoid excessive residues of parathion on food or
forage crops, always observe the statements found
under "Directions for Use," limiting the time before
harvest when parathion may be applied.
If handled indoors, provide mechanical exhaust
ventilation.
Do not apply or allow drift to areas occupied by
unprotected humans or beneficial animals.
Do not use or store in or around the home. Keep out
of reach of children and domestic animals. Do not
store near food or feed products. Bury spillage;
dean up area with strong lye solution.
This product is highly toxic to bees exposed to
direct treatment or residues on crops. Protective
information may be obtained from your Cooperative
Agricultural Extension Service.
NOTE TO PHYSICIAN
Antidote—administer atropine sulfate in large doses,
TWO to FOUR mg. intravenously or Intramuscularly as
soon as cyanosis is overcome. Repeat at 5 to 10 min-
ute intervals until signs of atropinization appear.
2-PAM chloride is also antidotal and may be admin-
istered in conjunction with atropine. DO NOT GIVE
MORPHINE OR TRANQUILIZERS. Parathion is a
strong chofinesterase inhibitor affecting the central
and peripheral nervous systems and producing car-
diac and respiratory depression. At first sign of
pulmonary edema, the patient should be given sup-
plemental oxygen and treated symptomatically. Con-
tinued absorption of the poison may occur and fatal
relapses have been reported after initial improve-
ment VERY CLOSE SUPERVISION OF THE PATIENT
IS INDICATED FOR AT LEAST 48 HOURS.
POST TREATED AREA
Consult your State Agricultural Extension Service or
Experiment Station regarding posting treated areas.
DIRECTIONS FOR USE
Be sure to read the precautionary statements before
using!
This product is designed for application after dilu-
tion with water and for use by trained operators
using airplane or power ground equipment The
hazards and precautions for handling the product in
this container are equally applicable to it after dilu-
tion with water for spray application. Add the con-
centrate to the spray tank while filling with water,
and mix thoroughly either by means of a tank agi-
tator or pump by-pass. For best results, thoroughly
cover all surfaces to be treated with spray. Rates of
app|ication given below should not be exceeded.
Never apply later than indicated to assure residue
levels at harvest are below tolerances established
by the Food and Drag Administration.
Consult the State Agricultural Extension Service or
Experiment Station for specific recommendations
regarding application, dosage and timing of sprays.
For application by ground equipment add the de-
sired amount of concentrate to sufficient water to
apply at least 3 gallons of water per acre. For appli-
cation by aircraft, add the amount of concentrate
desired per acre to Vt to 3 gallons of water con-
sistent with crop growth and good coverage. Greater
quantities of water may be required to give sufficient
coverage of orchard trees.
Note to Physician
11
Directions for Use
13
224
-------
Table 31. (Continued)
Fnit Insects
14
FRUIT
DO NOT USE TREATED CITRUS PEEL FOR
FOOD PURPOSES.
CITRUS (Calfhraia)-Grapefruits. Kumqvats,
lemons. Limes, Oranges, Tinf does and Tangerines.
Sah-For purple, black, brown soft, California
no*, citricola, cottony-cushion and yellow scales, use
H to H pint in 100 pllons of water applied at petti
fall to prevent fruit scattering.
Mar amcts Use 1 to 2 quarts in 100 pllons
of water for control of the following additional
kneels infesting citrus: climbing cutworms, fruit
tree leaf rollers, katydids, omnivorous leaf rollers,
Fuller rose beetles, pink scavenger caterpillars,
orange tortrix, orangeworms and Western tussock
moths. Do not use more than 2H gallons of this
product per acre up to 30 days of harvest. Do not
tse more than 1 gallon of this product per acre
from 30 days up to 15 days of harvest Consult agri-
cultural experimental authorities for specific recom-
mendations in your area.
CtnUS (fctas ifttr nan CaHforma)-€rapefniits,
Kumqoats, Lemons, Limes, Oranges, Tangeloes and
Treat for mealybugs: chaff, cottony-cushion, Glover's,
purple, Florida red, yellow, snow scales; aphids;
oranp dog and plant bugs, using H to H pint In 100
pllons of water. For control of mites and whHeffies.
Fruit Insects cont'd.
16
control whHeflies, use H pint with 1 gallon of emul-
sive oil concentrate in 100 gallons of water. To con-
trol Florida red scales. Florida wax scales, dictyo-
spermum scales and avocado leafhoppers. use %
pint in 100 gallons of water. To control pumpkin bugs
and mealybugs, use 'A to % pint in 100 pllons of
water. To control latania scales, use % pint In 100
pllons of water. Do not use more than 2H quarts
of this product per acre.
DO NOT APPLY TO THE FRUITS LISTED
BELOW WITHIN IS DAYS OF HARVEST.
CANEBEMUES (Raspberries, Loganberries. I
berries and Blackberries) - For control of two-
spotted spider mites, use K pint per acre. For control
of obscure and woods weevils, use at 1 quart per
acre as a post harvest application to the soil or
ground cover over roots of plants. For crown borers,
use at 1 quart per acre but apply to crown area and
lower canes.
CMMBDMES—For control ot fireworms, fruit-
worms, fa'pworms and Itcanium scales, use IK pints
per acre.
GOOSEBERRIES—f or control of currant aphids, use
H to IVi pints per acre. For control of two-spotted
spider mites, use 1 to I'A pints per acre. For
currant borers, use I*/, pints per acre.
ose tt to X pint with 1 gallon of emulsive oil concen-
trate in 100 pllons of water. For controlling grass-
hoppers, use 1 pint per acre. Thorough coverage is
essential for best results. Do not use more than
2tt pllons of this product per acre up to 30 days
of harvest Do not use more than 1 gallon of this
product per acre from 30 days up to 15 days of
b*Mu*4
MiYCSL
DO NOT APPLY TO CURRANTS AND FIGS
WITHIN 30 DAYS OF HARVEST.
COMMITS—For control of currant aphids, use H
to I'A pints per acre. For control of two-spotted
spider mites, use 1 to IV, pints per acre. For
currant borers, use l'/i pints per acre.
FIGS—for two-spotted and Pacific mites, use M to 1
pint per 100 pllons of water. For fig scales, use 1
pint per 100 pllons of water. Do not use more than
TA quarts of this product per acre.
DO NOT APPLY TO AVOCADO WITHIN 21
DAYS OF HARVEST.
WOCADO—To control banded cucumber beetles,
grasshoppers, citrus root weevils, red-banded Ihrips,
avocado lace bugs, pyriform scales, webbing worms,
Mossom anomala, little fire ants, greenhouse thrips
and tortridds, use X pint in 100 pllons of water. To
DO NOT APPLY TO THE FRUITS LISTED
WITHIN 14 DAYS OF HARVEST.
MflES— For control of, European sawflies, San
lose, Forbes or scurfy scales, mealybugs, European
red and two-spotted mites, bagworms, Japanese
beetles, shot-hole borers, orange tortra and apple
lace bugs, dilute tt pint in 100 gallons of water and
spray to cover foliage thoroughly. For codling moths,
use % pint in 100 pllons of water, 3 to 4 appli-
cations, 10 to 14 days apart, starting 10 to 14 days
after petal fall; for second and third broods, spray 1
to 3 times at 10 to 14 day intervals. For fruit tree
leaf rollers, use Vi pint per 100 pllons of water at
petal nil and for red-banded leaf rollers, apply tt
pint per 100 pllons of water at petal fall and at
first, fifth and sixth cover spray. For plum curculio,
apply at H pint per 100 pllons of water at petal fall
and 1 or 2 additional times each 7 to 10 days apart
For grasshoppers, use V pint in 100 pllons. For the
following insects. H pint per 100 pllons of water is
adequate: bud moths: dover, Pacific. Willamette or
Schoenii mites; flea weevils; rosy, mxrty and green
apple aphids; leafhoppers; leaf miners; and red
bugs. Certain insects, such as two-spotted Willamette
mites, may require repeat treatments at 7 to 10 day
intervals during the summer months. Parathion
sprays may injure the foliage and fruit of Mclntosh
apples and related varieties, such as Cortland, Ken-
dan, Macoun, Melba, ate, and Golden Delicious or
Fruit Insects confd.
15
Fruit Insects cont'd.
17
225
-------
Table 31. (Continued)
Fruit hotels confd
18
Fnut Insects court
20
Jonathan. Consult the State Apkuttunl Extension
Service or Experiment Station for advice on posa-
biity of mjory and safening the spay by uio| acti-
vated carbon. Do not use more than IK gaBons of
this product per acre.
AfBJCOTS—To control aphids. mites, bod moths.
peach tree borers, Japanese beetles and leaf rollers,
use < pint per 100 (aflons of water. Control of
coding moths, lesser peach tree borers, grass
happen, and tortrii requires K to % pint per 100
gaBons. To control Oriental fruit moths, ose K to %
pint per 100 pOons of water at shock spit, 10 to 12
days later and if needed 6 and 3 weeks before har-
vest For peach tree borers and lesser peach tree
borers, apply 2 or 3 sprays to trunk from {round to
scaffold tabs toned with moth emergence. Use *
pint»100 gallons of water for control of Panderms
moths. Avoid injury to bees by delaying spray tiB
after fuflbleonx to not use more than 3K quarts of
this product per acre.
BUJEKMJES-f or thrips, maggots, curcafio and
Up borers, use K pint in 100 gallons of water. For
lecaoium vales, use 1 pint per 100 gallons of water.
Use before froft sets or after harvest. Use from 100
to 300 gaOons of diluted spray per acre, but do not
apply more than I1/, pints of this product to one
acre of blueberries at any application.
rWCHB AND NECTMUIES (teas other than Caf-
fareia)—For control of green peach aphids, use X
pint in 100 gallons of water. For peach tree borers,
leaf rollers, mites, catfacug insects, tarnished plant
hues, shot-hole borers, peach bark beetles, states
and bod moths, on K pint per 100 gallons of water.
and repeat if re-infestation occurs. For Oriental fruit
moths, see under apricots. For plum cnrcuBo, oseK
pint per 100 gaflons of water. In the South, treat at
petal faB, 10 days later and repeat at 7 to 10 day
intervals up to 3 weeks before harvest In the North.
treat 3 to 4 tunes, 7 to 10 days apart, beginning at
shuck-off. For lesser peach tree and American pturn
borers and grasshoppers, use V to 1 pint per 100
gallons. For peach tree borers and lesser peach tree
borers, apply 2 or 3 sprays to trunk from ground to
scaffold tabs timed with moth emergence. Do not
apply more than 4 quarts of this material per acre at
any appfcation, and do not use more than 5 quarts
per acre per year.
KKHES AND NECnmiES (CaHoruiaJ-Use as
shown for other areas except do not appty within 21
days of harvest Do not apply more than once after
bloom. Do not apply more than 2% quarts of this
product per acre at any application, and do not use
more than 5 quarts per acre between January 1 and
harvest
CHHWES-For aphids and mites, mix % pint in 100
gaflons of water. For sawffies, use X to K pint in 100
(aflons of water. Use % pint per 100 gallons for
thrips, cherry fnutwwuis, pear slags, Pandemu
moths, bud moths, cankerworms, rose chafers, San
Jose scale crawlers, fruit ffies and tortrii. For fruit
tree leaf rollers, use K pint per 100 gallons of water
at petal fall or shuck spit; for plum curcuio, use
V, port per 100 gallons of water, 2 or 3 appOcatJons,
8 to 10 days apart beginning at petal fafl or shuck
spit for Oriental fruit moths, use K pint in 100
gallons of water at shock spSt and 10 to 12 days
later. For Japanese beetles, use K to 1 pint per 100
gaOons. Do not use more than 2V» quarts of this
product per acre.
(BATES—For mites, aphids, mealybugs and berry
moths, use H pint per 100 gaHons of water. For
leaf roBers, Japanese beetles and leaf folders, use
K pint per 100 gallons of water. For false chinch
bugs, use 1 pint in 100 gaOons of water per acre
fay ground equipment or in 10 gallons of water by
aircraft For eonsperse stink bugs, use IK quarts
per acre. For grape leafhoppers, use IK to 2K
quarts per tat for Mack vine weevils, use 2K
quarts per acre. Do not use more than IK quarts
of this product per acre after the fruit is the size of
buckshot Use 300 to 500 gallons of water per acre
depending on age of vineyard and stage of plant
growth.
control of leaf miners, aphids, leaf
roflers, grasshoppers, states, mealybugs and certain
mites, use the dosage described for those insects
on apples. For pear psyfla, use % pint per 100
gallons of water. For pear Mister mites, pear sJugs,
green fruitworro and plant bugs, use K pint per 100
gatons of water. For coding moths, use K pint in
100 gallons of water in 2 to 4 cover sprays, begin-
ning with the first cover. For phim curcuio, apply
K pint in 100 gattons of water at petal fafl and 10
days later. Some injury may occur on Bosc pears,
under some conditions. Do not use more than 3K
quarts of tab product per acre.
PUJMS AND nUNES-Appry K to % pint per 100
gaBoos of water for control of these insects: pear
thrips. flower thrips, mites, aphids, tearnoppen. leaf
rollers, peach tree borers, shot-hole borers, bod
moths, tortrii, mealy plum Gee and scales. Apply
scale treatment when crawlers emerge. For plum
curcuio nuke 3 to 4 applications, begMoing at
petal f* at rate of K pint • 100 gaBoos ef water.
For coding moths, use K to 1 pint per 100 gaBons
of water at petal fad and a summer ippfcafiM
tamed with moth emergence. For peach twig borers.
use 1 pint per 100 gaBons of water. Do not use more
thai 4 quarts ef this product per acre.
Fruit Insects eanf d.
19
Fruit Insects cunTd.
a
226
-------
Table 31. (Continued)
fa* hatch CMM
•To control Aovtf thrift, cncfcfd,
tabeehs. red spio* mites. aplmfeLrrB tap.
bjomoppen. wMtdSts and tot rates, at H to 1
pmt • 100 to ISO picas if water per acre. To
OMM korcn and strawberry led
, m * pmt m 100 to 150 ptas of water
per ten. As a Mar veatmeot do not use awn
IBM If, pints of Ifeis product per acre. To control
i srmpkjtois, use 5 worts • 40 poom of
r per acre as a prtpbot Mi treatment
00 NOT APPLY TO THE FRUITS LISTED
BELOW WITHIN 7 DAYS OF HARVEST.
control of crickets and mealy
tan o» M pmt per 100 ptas of '
apply 300 ptas of spray ptr acre.
00 NOT USE PARATHION ON OLIVES AFTER
AUGUST 1.
OUKS-for Mack, oleander aid partttoria safes.
m 1 pM • n ptas iptmedwi frade summer
•i umaiinn. or 1 plot itM-medwn pade sow-
Vtptaotehseds
VEGETABLES
DO NOT APPLY WITHIN 21 DAYS OF HARVEST
ON THE FOLLOWING CROPS UNLESS OTHER-
WISE SPECIFIED.
COOT—To control ipotdv mites, celery worms
aid tarnished plant tap, use 1 pot per acre. To
control leaf UMTS. •Metes and leafboppers. me
lKpmtsperacre.tatdoMiise wUm 30 dap
ofkanest
-To caofrol peen peach aphidi aid aHalb
11 pint per acre.
IfrroCE (Uat ami 8mb>-For aphids. i
mstar, cabbap kwoers. uwported cab-
banded cucumber beetles and Lypv
tap, ne H to 1 pmt per acre. To control six-spotted
leafhoppers, cse * pmt per acre. For harlequin tap
and feptabte wee*, use 1 pmt per acre. At the fc
pmt rat*, harvest can be made wram 14 days of
•or tmallin oi m 100 pBoas of trater. post-bloom.
-To control leaf miners and spider mites, use
H to 1 pmt per acre. For aphids and stink tap. use
1 pmt per acre.
SMSS CHAW-To control apbds and serpentine
leaf miners, «st 1 pmt per acre
DO NOT APPLY WITHIN 15 DAYS OF HARVEST
ON THE FOLLOWING CROPS UNLESS OTHER-
WISE SPECIFIED
NUTS
DO NOT APPLY AFTER HULLS OR HUSKS
BEGIN TO OPEN. DO NOT FEED TREATED
HULLS OR HUSKS TO LIVESTOCK.
UMOKDS-To eorinl frwt tree leaf roBers. M
catorpOan «nd ptocfc Mf bom. ne 1 pM per
100 ptas of water. As a dormant spray for par
htm and SM Jose scaks. gse 1 plot mth 3 p*«
darmant Ml emrisioi or 2M pBon dormait e«wl-
sivt oi m 100 fillORS of «ater. Do Ml ne more
tiM 3 •jwrts of ttis predict ptr lot
RUOnS-For appte mahrbap. fittert tphids. bod
•o*s Md spider mites, axe H pmt per 100 pHon
of vKr. Do Ml use more IBM 3 Marts of ttis
predict per acre.
•fCMS-For control of apMs. ne * to « pint in
100 ptas of mttr. To control antes, pecan Mt
casebtarers aid peoa leaf casebeartrs. sst * pmt
m 100 ptas of wter To control Mack and »eflo»
pocan apbids. fal mttaorms and hri| firalen. •»
1 ijart per 100 ptas of water. Do Mt me more
ton SK warts of tte pradKt per acre.
MUOTS-To control tphids. tecamim scales and
•afewt bust fSes. ne H pmt • 100 ptoos of water.
Do Mt «se more than » paws of tkis pnxtoet
per acre.
Nwftoacts »
KMS—For control of bean leaf beetles awl tmo-
spotted miles, use H pint per acre. Use H to * pmt
per acre to control tkrips aid fema pod borers. To
control stnk tap. plant tap. Uenoa bean beetles.
leaf rofcrs. leaf OHNTS. leifhopoers. apbids. red
spider mites and armyworms op to tttrd mstar. use
1 pmt per acre.
BEETS—To control flea beetles and leaf miners, ne
'A pmt per acre. For apbjtfs. bister beetles aid
•ebworau. «s* I pmt per acre. If (reeas are ned
for food, do not tat •*•• 21 dap of hanest
HJUEYED POS-To control aphids. leaf Men.
beta leaf roflers and stink bop. us* 1 pint per acre
CMMIS-To control leaf men. ne K to * pmt
per acre. To control teifhoppers. ise t pmt per
acre. Use 1 pmt ptr acre to control apbids. «cp>
tabk weenb. stak bup and petrobia mites. To tm-
tret rust DT manots (first brood), mii 1 pmt wrt*
100 ptorts per acre tat dribble into rarrow at
pbwtmf time. To control rust By mafpts (second
brood), use 1 pmt per acre as a Map spray. Do
Mt feed tops.
CUCUttBaS—f or squash vine borers, apbids. cn-
om«er beetles, leaf mmers. picUeworms, mites aid
thrips. ose K to 1 pmt per acre. For squash tap.
stmk tap. flea beetles and (eafnoppers. use I pint
per am. Do not apply prior to «WM{-
ftfftabte msects confd
227
-------
Table 31. (Continued)
VepbMe loseds cooTd.
EGOUKT-To control ttrips, leaf OMen, bister
beetles, aod flea beetles, KM % to * pint per acre.
To control Colorado potato beetles, OK * pM per
acre. To total spider Mites art lace bop, ne
Xto 1 pint per aae. To caotrol aphids, •Mefies
tod sM bop, ose 1 port per acre.
ttWJC-To control onion thrips, ose M port per
acre. To cootrol leaf OMen and pesroba onto*, ose
1 port per acrt-
MKMS—To control onion tbrips, tse H port per
acre. To coolrol OHM Mtjot fies, ose « pM per
acre. To coolrol apoids, sbok bop, leaf i
aod petrobia •ices, ose 1 plot per acre. To coon*
Iran •heat oofes. ose W piots per acre.
rOTOS-To control ftrips, ose 7/16 to M pM per
acre. To coolrol aphids, leaf mam aod mntera
potato flea beetles, ose 1 pint per acre.
MNSHES-To control apkids, false chinch bop
aod barteoM bop, ne tt to 1 port per acre. To
ose 1 port per acre.
SnMC8-To control aphids. leaf OMen. anoy-
MHOS op to third iostar, cabbafe topers, veptaMe
•eetfc, harieojM bop, seed con onffots, crowo
OHBB aod tejlBoppers. BK 1 pM per acre.
Yepteble oMuft cooT d.
To coolrol apUds,
boron, ose Via 1 port per acre.
fffllBBPt Mf rtl
M aphids, teofooMn,
optafJMov
pen, ose Ipiot per acre. Oofal aod rtoter crops, do
oot ose MUM 15 days of honest
par acre. To cooirot oonHOjnos, HoPJioppon aod
psyMs, ose % port per acre. For aphids, bjnf onncn,
•hrtefies, anoyvonos op to third outer, (rasshop-
sank bop, loopen and pbot bop. ose 1 port
par acre.
false
bop aod hatlaoaio bop, ose % to 1 plot per acre.
To coolrol cabbap loopen, ose 1 pM per acre. M
^MBS tWC BSM lOf lOOOf W M* tpfty VRHI Zl
dojs of harvest
DO NOT APPLY WITHIN 7 DAYS OF HARVEST
ON THE FOLLOWING CROPS UNLESS OTHER-
WISE SPECIFIED.
-To coolrol arochote
ose 1 ooart per acre.
SQMSH-To control cocamber beetles, aphids,
sint bop. OMloooomii. pieUenoron, cioiBioicit-
•omo, serpeofioe leaf OMen aod sooasb vioe
borers, ose % to 1 pnt per acre. To cootrol sqoasn
bop, flea beetles and leafluppen, ose 1 pint
per acre.
SHEET POnroES-To control aphids, spider OHles.
leaflMppm and sfiok bvp, use 1 port per acre. To
cootrol serpeofioe leaf OMen and owraiouJofy
leaf OMen, «e 1 to 1H pints per acre.
DO NOT APPLY WITHIN 12 DAYS OF HARVEST
ON THE FOLLOWING CROPS.
SHEET COW-To control com etrwonw feednf
m the bod, fal araqrwonn. aphids aod s*fBes, ose
K pM per acre. To control sap beetles and spider
antes, ne 1 pint per acre. To control duoch bop,
ose Hi pints per acre.
DO NOT APPLY WITHIN 10 DAYS OF HARVEST
ON THE FOLLOWING CROPS UNLESS OTHER-
WISE SPECIFIED
fBB-To control aphids, pea neenb, spider nates,
sfok bop, ttrips, anajwoms up to third Mar,
ctabioc otMnos. leaf OMen, alfaKa loopen aod
cotey loopen. ose 1 pint per acre. If noes art to be
osed for forap, do oot harvest lor 15 days after
CWMOE AND C0l£ CUPS (bVoeeol,
Sproots, Cio«inu)-To cootrol aphids, thrips. db-
cobbap loopen and anayworou op to third iostar,
ose % to 1 pint per acre. To control harleqwi bop,
^^^^•iVJ^ . ^-«- j;_«.--_ - ^-- j m
fff^BDIC ofBCVIo^ CMoWMf ConVOim JM 1KI
beetles, ose 1 pint per acre. Rates above fc port
short not be appfod to eobbop closer than 10
•tys MO ioWcsl,
WHUBW-To coolrol aphids, ose 1 pM per acre.
inTUtt (HeadMa control aphids, cabbap loop-
Mcocs, LypD oTitp. vcftponiis oWo oWywofws i^
to third iostar, ose % to 1 pint per acre. To control
six-spotted teaftoppen. ose * pint per acre. For
harleqM bop, vegetable wevos and leaf miners,
ose 1 port per acre. To control prdeo stjojphytaos,
broadcast IV pMoos per acre pot prior to ptonfiof
aod flMroefUy incorporate into upper 6 to 9 aches
of sol.
PJEUNB-for sojoash vine borers, leaf onocn aod
Use chjoch bop, ose W pint per acre. For aphids,
IftflMMtffi^ cvcvMbCf fcfftfCTt Bicklcvonw Md
oiiles, ose H to 1 pM per acre. To cootrol thrips,
sojoash bop and stink bop, ose 1 port per acre.
•VTMAttS-To cootrol apoids, cattop loopen
oiid cfcobnn cotMflos, «e 1 port per acre
VepbMehBects cooTd.
27
VeptaMe Inseds coofd
228
-------
Table 31. (Continued)
Field aod fanfi ***** <***
DO NOT APPLY WITHIN 5 DAYS OF HARVEST
ON THE FOLLOWING CROP
cart* apMs. bfister beetles,
Colorado poMo beetles. leaf *«om win. ptart
piffed, flpfvpf, vcfRiMc wccns 9M
H to 1 pi* per acre Fir anoy
to ffcird Mstar, csboofe toppers, aod
obMraB, KM * p*rt per acre For leaf
boppers. sfc* top aod flea keete. me I port
per acre.
SOTKMS—To cortol wswonv*. ose M pfeet per
acre T* ca«tre4 whet kea* oterpdbrj, pea
ehMtmauB, too-spotted Milei wd itat b«fj OK
1 pat per acre Te cartel can tanranm aod fall
arafiOTu. nt 1 to 1'A pMs per acre T* a*
tool «Me jn*» aid iwniwoB. broadtail 1 fatal
per acre jMt prior to ptofltaf a
corporate Mo «pper 4 to 6 wckes of toil.
HELD AND FORAGE CROPS
00 NOTAPPLYWTTHIN 15 DAYS OF HARVEST,
CUTTING OR FORAGE USE ON THE FOLLOW
INC CROPS.
9NM KETS-for aMatta (oopen.
•wm ip to ttird wt*. feafhoppen. kfester beetles.
te keetki, leaf Men, Lrpn bop. stMi tup. Mb
•mn^dMnf orl»orm art piirtoppen, at I
9* per acre For tabe celerj leaf Sen. at ft p«b
per acre Far beet crom borera, ne 1% pate per
acre, (mead appicattoa owr Ike nw dwwf iced
i«C itace To cwrtrol wtate puks Md mre«n«
broaden! 1 fata per acre pot prior to ptMtMf
aod thorMfMr iKoporate «t« opper 4 to i •<*«
ofioiL
-To CMtrol »>re«omv «e 2 ojaarb
Utol2iKiiha«d«theopet terra* at fioM of
, OMB, VETCH MB Ctt8-f or Meet
d**tr apkidi tkree-eenered aMatfa keppe
catoraflers, aod iptffiekop. ose % port per tot For
opbids. aNato wetii lame. aod ad* weevils.
anyvonoa op to tttrd onto, clover leaf VJMVOS,
DO NOT APPLYWTTHIN12 DAYS OF HARVEST.
CUTTING OR FORAGE USE ON THE FOLLOW
ING CROPS.
«rfcA MM tortriod Motta, OK H to 1 piat per acre
For aWfa teed dttkids eootrol M atfoKa from tor
Mod, OK M to 1 port per acre. Cattoraia aod Menda
nfrfriton tmt »e ow of On natenal to oot owre
fbjo) v pvt per aort. For doMr bead geeMh. spider
dooer Meiii. ao4 free* AM beeflei «te 1 piat
pw acre. Far bed anayvonojs aaid corn earvoran
ose 1 to IV5 oMi per acre. Do oot spray hymu
djriag Moo* period to avoid iopjry to beaey bees.
KMm— To cootrol
-------
Table 31. (Continued)
HeM and Forage Insects cont'd.
34
COTTON—To control aphids, mites, cotton leaf
worms, cotton fleahoppers, garden webworms and
thrips, use Vi pint per acre. For some spider mites,
use 'A to Vt pint per acre. For cabbage loopers, use
% to 1 pint per acre. For boll weevils and stink bugs,
ose 1 to l'/i pints per acre. For salt-marsh cater-
pillar*, use 1 to 2 pints per acre. For bollworms,
cotton leaf perforators, Lygus bugs, false chinch
bugs, serpentine leaf miners and southern garden
leafhoppers, use 1 quart per acre. Use enough water
for complete coverage. Make first application when
insects appear and repeat at 7 day intervals if re-
quired. If desired, this formulation may be combined
with other insecticides in a complete cotton spray
program.
TOBACCO—For control of aphids, stink bugs and
tobacco suckflies, use H pint per acre. Do not apply
within 5 days of priming or 15 days of cutting. Avoid
plant juices coming in contact with the skin or other
parts of the body of those who are engaged in
cutting the crop.
MISCELLANEOUS
CABBAGE—For application to cabbage grown for
seed only to control cabbage seed pod weevils, use 1
quart per acre.
CHRISTMAS TREES—To control aphids and mites,
use W pint per 100 gallons of water.
Soil Insects cont'd.
CORN ROOTWORMS-To control on:
Peanuts
Apply 2 to 2% qt. per acre as a row soil treatment
at planting or pegging time, work lightly into soil.
GARDEN SYMPHLAN—To control on:
Bern Lettuce Sugar Beets
Corn Potatoes Tomatoes
Apply 5 qt per acre to soil surface before planting
time and thoroughly work into upper 6 to 9 inches.
CUTWORMS—To control on:
Cora Cmnben
Broadcast 3 qt to 1 gal. per acre before planting
and thoroughly work into upper 1 to 3 inches.
WHfTE GRUBS—To control on:
Con Soybeans Sugar Beets
Broadcast 3 qt to 1 gal. per acre before planting
and thoroughly work into upper 4 to 6 inches.
NOTE: Consult the State Agricultural Extension
Service or Experiment Station concerning specific
usage, dosages and methods of application.
896.09-000.13/53
(EPA Reg. No. 524-132)
MONSANTO COMPANY
AGRICULTURAL DIVISION
ST. LOUIS. MO. 63166
HOPS—For control of hop aphids, use 1 to !'/»
pints per acre. For spider mites, use !'/> pints
per acre. Do not apply within 15 days of harvest
SAFFFOWER —To control aphids, Lygus bugs and
grasshoppers, use 1 pint per acre. Do not use para-
thion after (lowering.
SOIL INSECTS
WIREWORMS—To control on:
Rutabagas
Soybeans
Sugar Beets
Sugarcane
Sweet Corn
Sweet Potatoes
Tomatoes
Turnips
Watermelon
Broadcast 3 qt to 1 gal. per acre on soil before plant-
ing and thoroughly work into upper 4 to 9 inches.
HIREWORMS-To control on:
Tobacco
Broadcast 2 qt. per acre on soil at least 3 weeks
before planting and work into top 6 to 9 inches.
WIREWORMS-To control on:
Potatoes
Broadcast 1 to IVt gal. per acre on soil before plant-
ing and thoroughly work into upper 4 to 9 inches.
Beans
Beets
Broccoli
Brussels Sprouts
Cabbage
Cantaloupe
Carrots
Cauliflower
Celery
Com
Endive
Egg Plant
Escarole
Kale
Lettuce
Onions
Peas
Peppers
Soil Insects
35
230
-------
Table 32- REGISTERED USES OF PARATHION EMULSIFIABLE LIQUID
(4 LB ACTIVE INGREDIENT PER GALLON) - CROPS AND
OTHER USES, PESTS, DOSAGE RATES AND USE LIMITATIONS-
STOP - READ THE LABEL
See Side Panels
for Antidote &
Precautions
Keep Out of
Reach of
Children
ORGANOPHOSPHORUS INSECTICIDE
Active Ingredient — Parathion:
O,O-diethyl O-p-nitrophenyl phosphoro-
thioate 46.4%
Xylene-range solvent — 47.7%
Inert Ingredients _ ~ 5.9%
Contains 4 Ib. Parathlon/Gal.
COMBUSTIBLE — Keep away from heat & open
flame.
Read Label Folder for additional use precautions,
directions for use, recommendations and container
disposal. E.P.A. Reg. No. 476-603-AA
EMULSIFIABLE
LIQUID
NOT FOR HOME USE
See side panels for poison precautions, symptoms.
first aid treatment, information for physician and
posting treated areas.
NOTICE: Stauffer Chemical Company makes no war-
ranties, express or implied, Including the warranties
of merchantability and/or fitness for any particular
purpose concerning this material, except those which
are contained on Stauffer's label. ARC 710325
Made in USA By
STAUFFER CHEMICAL COMPANY
NEW YORK, NY IOOI7
aj Sample label of Stauffer Chemical Company.
EPA Registration No. 476-603-AA.
231
-------
Table 32. (Continued)
DANCER - POISON - PRECAUTIONS
Don
SWAUOW
^"
POISONOUS IF SWALLOWED
Even in small amounts!
DON'! 10DCN 11
I
POISONOUS BY SKIN CONTACT
Poisonous if touched by hands or spilled or
splashed on skin, in eyes or on clothes (liquid
goes through clothes).
POISONOUS IF BREATHED
Poisonous if vapor or mists from sprays are
breathed. Vapors are not visible. Never work
with parathion or in parathion treated areas
without protective clothing and equipment.
POISONOUS TO FISH & WILDLIFE: Toxic to fish and wildlife. Birds and other wildlife in
treated areas may be killed. Shrimp and crab may be killed at application rates recom-
mended on this label. Do not apply where these are important resources. Keep out of any
body of water. Do not apply when weather conditions favor drift from treated areas. Do
not apply where run-off is likely to occur.
232
-------
Table 32. (Continued)
WORK SAFETY RULES
USE ONLY WHEN WEARING THE FOLLOWING PRO-
TECTIVE CLOTHING 4ND EQUIPMENT: (1) Wear water-
proof pants, coat, hat, rubber boots or rubber overshoes.
(2) Wear safety goggles. (3) Wear mask or respirator ap-
proved by the U. S. Bureau of Mines for parathion protec-
tion. (A) Wear heavy duty natural rubber gloves.
Keep unprotected persons and children away from treat-
ed area or where there is danger of drift.
Do not rub eyes or mouth with hands. Do not smoke.
Before removing gloves, wash them with soap and water.
If you feel sick in any way STOP work and get help right
away. Tell foreman or have someone call him. Call a
physician, clinic or hospital immediately.
ALWAYS wash hands, face and arms with soap and wa-
ter before smoking, eating or drinking.
AFTER WORK, lake off all work clothes and shoes.
Shower, using soap and water. Wear only clean clothes
when leaving job. DO NOT wear contaminated work
clothing.
All protective clothing and equipment should be washed
with soap and water after each use. Respirators should
be cleaned and filter replaced according to instructions
Included with respirator.
POISON SIGNS (Symptoms)
Parathion is a very dangerous poison. It rapidly enters
the body on contact with all skin surfaces, eyes and
by contact with skin through wet clothes. Worker who
shows any of the following poisoning signs must receive
Immediate medical treatment or he may die.
Slgni and Symptoms of Poisoning Are: Headache, nau-
sea, vomiting, cramps, blurred vision, pin-point pupils,
tightness of chest, labored breathing, weakness, nervous-
ness, sweating, watering of eyes, drooling or frothing
of mouth and nose, muscle spasms and coma.
POSTING TREATED AREA: Consult state regulatory
agencies for posting regulations and requirements.
FIRST AID TREATMENT
Speed is essential to slop absorption of poison.ll
It possible, one person should make telephone
calls while another begins treatment.
Call a physician, clinic or hospital immediately In all
cases of suspected poisoning. Explain victim exposed
to parathion; describe his condition. Until medical help
is available take following steps.
IF BREATHING HAS STOPPED, start artificial respiration
immediately and continue until physician sees victim.
IF SWALLOWED and victim is awake (conscious) make
him vomit quickly. First, give soapy water or strong
salty water to drink then stroke back of throat with
finger to make victim vomit. Repeat by giving more water
and make vomit again until vomit fluid is clear. Never
give anything by mouth to an unconscious person. Have
victim lie down and keep quiet
IN CASE OF SKIN CONTACT, immediately remove wet
clothing and shoes and flush skin with water for at least
15 minutes.
EYE CONTACT: If splashed in eyes, immediately flush
eyes with water for at least 15 minutes.
After first aid is given and physician can
not come take victim to clinic or Hospital.
Bring "Label Folder." Give to physician.
NOTE TO PHYSICIAN
ANTIDOTE—Administer atropine sulfale in large doses,
2.0 to 4.0 mg. intravenously or intramuscularly as soon
as cyanosis is overcome. Repeat at 5 to 10 minute inter-
vals until signs of atropinization appear. 2-PAM chloride
is. also antidotal and may be administered in conjunction
with atropine. Do not give morphine or tranqulllzer*.
Parathion Is a strong chollnesterase Inhibitor affecting
the central and peripheral nervous system, producing
cardiac and respiratory depression.
At first signs of pulmonary edema, the patient should be
given supplemental oxygen and treated symptomatically.
Continued absorption of the poison may occur and fatal
relapses have been reported after initial improvement.
Very close supervision is indicated for ut least 48 to
72 hours.
233
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Table 32. (Continued)
LABEL FOLDER
CONTAINS
ALL DIRECTIONS FOR USE
Organophosphorus Insecticide
Emulsifiable Liquid
POISON
DANGER
NOT FOR
HOME USE
Before Using Read All Precautions
and Directions for Use
E.P.A. Reg. No. 476-603-AA ARC-710426
RESEALABLE BAG
I Pull flaps apart to open.
V Press along ridge to close.
IMPORTANT
SEE REVERSE SIDE OF FOLDER
CONTAINS SAFETY LABELING
INFORMATION
• Active Ingredient Statement
o Primary Statements of Hazard, Precaution-
ary Instructions.
• Fish and Wildlife Precautions
• Work Safety Rules
o Poison Symptoms
• First Aid Treatment
• Note to Physician
STAUFFER CHEMICAL COMPANY
NEW YORK, N. Y. 10017
234
USE PRECAUTIONS
READ ALL PRECAUTIONS AND DIRECTIONS BEFORE
USING. Use only for crops and claims recommended.
This product is toxic to fish and wild life. Keep out of
lakes, streams, and ponds. Birds and other wildlife in
treated areas may be killed. Do not apply when weather
conditions favor drift from areas treated.
This product is highly toxic to bees exposed to direct
treatment or residues on crops. Protective information
may be obtained from your Cooperative Agricultural Ex-
tension Service.
In order that pesticidal residues on food and forage crops
will not exceed tolerances established by the Federal
Food and Drug Administration, use only at recommended
rates and intervals, and do not apply closer to harvest
than specified. Do not apply or allow to drift to areas
occupied by unprotected humans or beneficial animals
or onto adjoining food, fiber or pasture crops. The grow-
er is responsible for residues on his crops as well as
for damages caused by drift from his property to that of
others.
Consult state agricultural extension service or state agri-
cultural experiment stations for additional information.
as the timing, number, and rate of applications needed
will vary with local conditions.
CONTAINER DISPOSAL
Destroy Empty Container — Never Re-Use
Completely empty contents and bury unused chemical
18 inches deep in an isolated location away from water
supplies.
Glass Container: Break container and bury 18 inches
deep.
Metal Containers: 1 gal. drum: Pour 1 qt. of water into
empty drum. Add 1 tablespoon of household detergent.
Rotate drum carefully until all inner surfaces are wet
Bury rinse solution 18" deep. Punch holes ir. top and
bottom of container, crush and bury. 5 gal. drum: Pour
2 qt of water into empty drum. Slowly add Vi cup caustic
soda (lye) and 2 tablespoons of household detergent. Fol-
low the same rinsing, destruction and burial procedures
given for 1 gal. drum. 55 gal. drum: Follow same proce-
dures as for 5-gal. drum except use 5 gal. of water, 2 Ib,
of lye and cup of detergent
CAUTION: Do not get rinse solution on hands, in eyes
or on clothing. Wear protective clothing and equipment
In case of contact wash immediately with soap and water.
DIRECTIONS FOR USE
Application can be made by aircraft or ground power
equipment by trained personnel only using approved pro-
tective equipment. Do not apply with hand equipment
Pour specified amount of this product into nearly filled
spray tank. Add balance of water to fill tank. Keep agita-
tor running during filling and spraying operations. If mix-
ture does not mix readily, but tends to separate as an oily
layer, do not use as injury to plants may result. Do not
combine with wettable powders unless previous use of
the mixture has proven physically compatible and safe
to plants. Always thorough^ emulsify this product with
at least half of total water before adding wettable
powder.
SUGGESTED WATER RATES FOR AIRCRAFT AND
GROUND APPLICATION. (The actual rate required to pro-
vide thorough, uniform coverage varies with plant growth
at time of application. Except as specified for certain
uses, the following rates are therefore intended to cover
a broad range of conditions.)
Crop Aircraft
Vegetable and Field Crops ...... ------- - 1-20
Orchard, Grapes -------------------------- ...... — - 5-25
Orchard Crops (See exceptions below) ._.
Citrus - ____ ....... __________ —
Grapes '""""'
Ground
5- 125
500-3000
100- 200
Maximum permissible rate per acre, expressed as Para-
thion 4-E, is given in parenthesis ( ), after each crop
claim.
-------
Table 32. (Continued)
RECOMMENDATIONS
FRUIT AND NUT CROPS
(Also Read Directions for Use)
Unless otherwise specified, rates are given in terms of
Parathion 4-E per 100 gal. of water for thorough coverage
application. Unless otherwise specified, apply at the first
sign of infestation and repeat at 7-10 day intervals as
needed to maintain control, but observe use limitations
given for specific crops.
APPLES
Codling moth, European red mite, fruit tree leaf roller,
mealybug, orange tortrix, plum curculio, red-banded leaf
roller (1st, 2nd and 3rd broods), two-spotted mite. Use
Vfept
Aphids (rosy apple, green apple), bud moth, Pacific mite,
red bug, Schoenii mite and Willamette mite. Use % pt
CAUTION: Injury to fruit and foliage may result from use
of this material on Mclntosh and related varieties. Do not
apply within 14 days of harvest. (1V4 gal.)
APRICOTS
Codling moth, Oriental fruit moth, tortrix. Use Vi-lV% pt.
Bud moth, fruit tree leaf roller, spider mites, aphids. Use
% pt. Do not apply until danger of bee poisoning has
passed. Do not apply within 14 days of harvest. (7-1/5
pt)
CHERRIES
Black cherry aphid, eye-spotted bud moth, lesser apple
worm, mites, shot-note borer, Western cherry fruit fly.
Use n pt For fruit fly control, begin applications at fly
emergence and repeat at 7 day intervals. Do not apply
within 14 days of harvest (4-1/5 pt.)
CITRUS
CALIF. RECOMMENDATIONS: Citrus thrips. Use 3 pt in
10-20 gal. water when applied by aircraft; 100-200 gal.
water by ground equipment. Apply at petal fall; repeat in
late summer and early fall to protect new growth and pre-
vent fruit scarring. Citrus scales. Parathion 4-E is recom-
mended for control of California Citrus Scales. The prod-
uct may be used in conventional high-pressure ground
sprayers or boom sprayers and airblast equipment when
the latter are capable of providing thorough coverage.
Black Scale—Use 1 pt. Make a full coverage spray during
Aug.-Nov. California Red and Yellow scales—Use IV* pt
alone or with 1V4-1% gal. of a light or light medium oil
emulsion in a full coverage spray at recommended times.
Citricola and Cottony-Cushiony scales—Use 3 pt. Apply
100-400 gal. spray per acre. Or use Vt pt in a full cover-
age spray during Aug.-Nov.; increase dose to V* pt. during
Feb.-Mar. and to Vi pt. during May and June applications.
Purple scale—Use 1 pt or % pt. with lVi-1% gal. of a
light or light medium oil emulsion in a full coverage spray
n recommended times. Max. Rate/ Acre and Date Limita-
tion: (1 gal. up to 14 days of harvest; 2Vz gal. up to 30
days of harvest).
GRAPES
Calif. Recommendations: Mealybug. Use 2 pt plus 2
gal. dormant oil emulsion. Apply during dormant period.
Spray vines after pruning but before budding. Refer to
Extension bulletin for complete spray program. Leaf
folder. Use 2 pt Mites. Use Vi pt Repeat applications
at 5-7 day intervals. Max, Rate/Acre and Date Limitation:
3 pt. up to 14 days of harvest; 5 pt. if applied before fruit
is the size of buckshot or after harvest
NECTARINES, PEACHES
Catfacing insects, Oriental fruit moth, peach twig borer,
thrips (on Nectarines only), San Jose scale. Use 1 pt. Cot-
tony peach scale, fruit tree leaf roller, green peach aphid,
spider mites. Use % pt. Limitations: Areas other than
Calif.: Full coverage spray for control of scale insects.
Do not apply within 14 days of harvest. Do not apply more
than 4 qt. per acre per application or more than 5 qt. per
acre per year. Calif.: Do not apply within 21 days of har-
vest. Do not apply more than once after bloom. Do not
apply more than 2Vx qt. per acre per application or more
than 5 qt. per acre between Jan. 1st and harvest.
PEARS
Codling moth, mealybug, pear blister mite, woolly aphid.
Use Vi pt. in pre-blossom spray. Pear psylla, spider mites.
Use % pt. Make either pre-blossom or post-blossom
sprays for the pear psylla. Under some conditions, injury
may occur on Bosc pears in the Northeast. Do not apply
within 14 days of harvest. (7-1/5 pt)
PLUMS, PRUNES
Aphids, bud moth, leafhopper, leaf roller, mealy plum
louse, spider mites, tortrix. Use Vi pt. Peach twig borer.
Use 1 pt. Do not apply within 14 days of harvest. (1 gal.)
OLIVE
Scales (parlatoria, oleander, black). Use 1 pt. with regu-
lar oil spray during June or July. Do not apply after Aug.
1. (2V4 gal.)
STRAWBERRIES
Southeast Region: Field crickets, flea beetles, flower
thrips. leaf rollers, pameras. Use Vi-\ pt Spider mites.
Use % pt. Do not apply within 14 days of harvest. (2 pt.)
Other Areas: Aphids. Use 1-1-3/5 pt Do not apply within
14 days of harvest. (1-3/5 pt.) Post-harvest control of
root weevil. Use 2 pt. (2 pt)
WALNUT
Aphids, red spider. Use Vz pt. Repeat at 7-10 days for
red spider. Codling moth. Use % gal. Do not apply after
husks open. (2Vi gal.)
VEGETABLE AND FIELD CROPS
(ALSO READ DIRECTIONS FOR USE)
Unless otherwise indicated, dosages are given in pints
of Parathion 4-E per acre in sufficient water to provide
thorough coverage. Begin applications when insects first
appear and repeat at 7-10 day intervals as needed to
maintain control, but observe use limitations given for
specific crops.
ALFALFA
Alfalfa Weevil
Calif.: Apply Vi-% pt. per acre in 15-20 gal. water per
acre. Make application when 75% of terminals show
feeding damage. Make no application within 15 days of
cutting or forage use. (% pt.)
Areas Other Than Calif.: Apply V4-1 pt. per acre as speci-
fied and limited above. (1-3/5 pt)
ALFALFA SEED CROPS
Alfalfa chalcid, alfalfa weevil larvae, aphids, armyworms,
blister beetles, lygus stinkbugs. Areas Other Than Calif.:
Use Vi-1-3/5 pt.; Calif., use %-l pt Use in early morning
or late evening to avoid injury to pollinators. Birds and
other wildlife in treated areas may be harmed. Do not
apply within 15 days of harvest. Do not use Parathion if
field to be cut for hay. (Areas Other Than Calif., 1-3/5 pt;
Calif., 1 pt.)
235
-------
Table 32. (Continued)
ALFALFA, CLOVER, VETCH
Aphids (including yellow clover aphid), armyworms. blis-
ter beetles, grasshoppers. Apply Vz-V* pt. per acre. Make
no application within 15 days of cutting or forage use.
(Calif.—% pt. for all crops)
(Areas Other Than Calif.—1-3/5 pt. for alfalfa and vetch;
3 pt. for clover)
ARTICHOKE
Aphids. plume moth. Use 2 pt. Do not apply within 7
days of harvest. (2 pt.)
BEANS (Dry and Green)
Aphids, armyworms, leafhopper, leaf miner, leaf roller,
Mexican bean beetle, spider mites, stinkbugs, whitefly.
Use 1-1-3/5 pt. (1 pt.—7 days of harvest; 1-3/5 pt—15
days.)
BEETS
Aphids, armyworms, blister beetle, flea beetle, leafhop-
per, leaf miner, webworm. Use 1-1-3/5 pt. Do not apply
within 15 days of harvest; 21 days if treated tops are to
be used for food or feed. (1-3/5 pt.)
CABBAGE, CAULIFLOWER, BROCCOLI,
BRUSSELS SPROUTS, KALE, MUSTARD,
TURNIPS
Aphids, armyworms, cabbage looper, flea beetle, dia-
mond-back moth larvae, imported cabbageworm, ser-
pentine leaf miner, thrips. Use 1 pt.
Rates and Use Limitations: Broccoli, Brussels sprouts,
cauliflower: 1 pt.—7 days; 3 pt.—21 days. Cabbage, kale,
mustard, turnips: Vz pt—7 days; 1 pt—10 days (cabbage
only 3 pt.—21 days).
CARROTS
Aphids. Use 3,i>-% pt. per 100 gal. Apply 300 gal. per
acre. Do not use treated carrot tops for food or feed.
Do not apply within 15 days of harvest. (2 pt.)
CELERY
Aphids, celeryworms, celery leaf tier, leafhoppers, spider
mites. Use 1-2 pt (1 pt—21 days of harvest; 2 pt.—30
days.)
CORN
Armyworms, corn rootworm adults (make full coverage
applications to foliage when adult beetles become nu-
merous and repeat as necessary). Use Vi pt. European
corn borer. Use 1-2 pt Do not apply within 12 days of
picking or cutting for forage. (2 pt.)
COTTON
Aphids, armyworms (up to 3rd instar), brown cotton leaf-
hopper, false chinch bug, salt-marsh caterpillar, ser-
pentine leaf miner, southern garden leafhopper, stink
bugs, spider mites, thrips. Use 1 pt.
Bollworm, cotton leaf perforator, fleahopper, lygus bugs,
tobacco budworm. Use 2 pt.
Limitations. For all uses listed above do not exceed
2% pt per acre. Do not apply within 5 days of hand-
picking. Workers entering treated fields within 24 hours
of application should wear protective clothing.
CUCUMBER, SQUASH, MELONS
Aphids cucumber beetle, cutworms, darkling ground bee-
tle (lea beetle, leafhopper, leaf miner, melonworm, pic-
kle'worm, serpentine leaf miner, squash bug, spider
mites, petrobia mite, thrips. Use 1 pt. Do not apply unless
plants are dry nor before plants start to vine. Do not
apply within 15 days of harvest on cucumber and squash;
7 days of harvest on melons. (1 pt.)
EGGPLANT
Aphids. leaf miner, red spider mites, thrips. Use %-Vz
pt Do not apply within 15 days of harvest (1-3/5 pt)
LETTUCE, ENDIVE
Aphids, leafhoppers. Use 1 pt. Do riot apply within 7
days of harvest on head lettuce; 21 days on endive, leaf
and bibb lettuce. (1 pt.)
MOSQUITO CONTROL
In Rice Fields and Irrigated Pastures: Apply 3.2 fluid
ounces in 5-20 gal. water by aircraft or in 25-100 gal.
water by ground equipment. Do not apply to water drain-
age areas where run-off or flooding will contaminate
ponds, lakes or streams. Keep out of tidal marshes and
estuaries. Do not apply with 1 day of harvest of rice;
7 days of pasturing or harvest of grass pasture. (3.2 fluid
ounces)
OKRA
Aphids, flea beetle, leaf miner, stinkbugs. Use Va-1 pt
Do not apply within 21 days of harvest (1-3/5 pt.)
ONIONS
Thrips: Apply 1-1-3/5 pt. and repeat at weekly intervals
as necessary for control. Do not apply within 15 days of
harvest. (1-3/5 pt)
PEAS
Aphids, armyworms, climbing cutworms, pea weevil, ser-
pentine leaf miner, thrips: Use 1 pt Do not apply within
10 days of harvest. (1 pt)
PEPPERS
Aphids, pepper maggot, flea beetle, serpentine leaf min-
er, thrips. Use 1-1-3/5 pt. Do not apply within 15 days of
harvest. (1-3/5 pt)
POTATOES
Aphids, armyworms, Colorado potato beetle, flea beetle,
green stinkbug, leafhopper, leaf miner, spider mites.
Use 1-2 pt Do not apply within 5 days of harvest (2 pt)
RICE
(CALIF. ONLY)—Rice leaf miner, tadpole shrimp. Use 1/5
pt. in 5-10 gal. water. Apply by aircraft at the first sign
of infestation after planting. Restrict spill from rice fields
for 2 days following application. Do not apply within 1
day of harvest. Caution: Do not use within 14 days of ap-
plication of Stam F.34 or Rogue. Injury may result. Do
not spray over canals or laterals. (1/5 pt)
SMALL GRAINS
(BARLEY, OATS, WHEAT)—Aphids, armyworms. grass-
hoppers, greenbug. Use Vz-% pt Do not apply within 15
days of harvest. (3 pt)
SORGHUM
False chinch bug, grasshoppers. Use V4-% pt Corn ear-
worm, sorghum webworm. Use Vi-1 pt Sorghum midge.
Use 1 pt. and make 2 applications 3-5 days apart when
approximately 90% of the heads have emerged from the
boot. Aphids, mites. Use 2 pt. Do not apply within 12
days of harvest or cutting for forage. (2 pt.)
SPINACH
Aphids, leaf miner. Apply Vz-1 pt Do not apply within 14
days of harvest. (1 pt)
SUGAR BEETS
Aphids, armyworms, blister beetle, flea beetle, leafhop-
per, leaf miner, mites, webworm. Use 1-1-3/5 pt Do not
apply within 15 days of harvest (1-3/5 pt)
TOMATOES
Aphids, flea beetle, leafhopper, serpentine leaf miner,
spider mites, stinkbugs, tomato pinworm. Use 1V4-2 pt
Do not apply within 10 days of harvest. (2 pt)
236
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One quart of parathion 4 Ib/gal formulation contains
1 Ib of active ingredient; 1 pt contains 0.5 Ib of
active ingredient. Thus, recommendations given in
terms of quarts are equivalent to pounds of active
ingredient; recommendations given in terms of pints
convert into active ingredient by multiplication with
the factor 0.5.
Parathion is also available to users in the form of emulsifiable liquids
containing 2, 6 and 8 Ib of active ingredient per gallon; furthermore, in the
form flowable liquids containing 4 or 8 Ib of active ingredient per gallon;
as wettable powders containing 15 or 25% of active ingredient, and as dusts,
granulars and pressurized sprays of various active ingredient concentrations.
In addition, a number of dry and liquid formulations combining parathion
with other insecticides and/or fungicides are registered.
For most registered uses of parathion, the rate of active ingredient
recommended per acre or per volume of spray for a given use is the same,
regardless of the type of formulation in which the product is applied.
State Regulations - In many of the states that currently regulate the use of
pesticides, parathion is subject to use restrictions. For instance, in
California, parathion is one of 42 pesticides that have been designated as
"injurious or restricted materials." The use of pesticides in this category
is subject to special restrictions under regulations administered by the
State Department of Agriculture. A permit from the County Agricultural
Commissioner must be obtained for the use of parathion. The product may not
be applied in any location where damage, illness or injury appears likely to
result through direct application, drift, or residue, to persons, other crops,
or animals (including honeybees) other than the pest(s) which the application
is intended to destroy.
Before parathion is applied, the person responsible for the application
must give warning to all persons known to be on the property to be treated.
After any formulation containing parathion has been applied at a rate
greater than 1 Ib of active ingredient per acre, the treated property must
be posted for 2 weeks to provide adequate warning to persons at the point or
points of normal entry. The warning notice must be readable at a distance
of 25 ft.
Under this code, it is unlawful to sell or deliver parathion-containing
pesticide products to any person who is required to have a permit, unless
the person or his agent signs a statement that he has a valid permit to use
the product.
237
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Similar restrictions on the use of parathion are in effect in a number
of other states, although California appears to have the most specific and
best enforced regulations. In some states, parathion can be used only by
licensed applicators.
Details of the pesticide use and application laws on a state-by-state
basis have been summarized by EPA, Office of Pesticides Programs, in a
publication entitled "guide for Analyzing Pesticide Legislation/Digest of
State Pesticide Use and Application Laws." This pesticide law digest is
being kept up to date by addition and replacement pages issued to holders
from time to time.
In addition to restrictions on the use of parathion Imposed by
state statutes and regulations, many states augment parathion product label
requirements with specific recommended uses designed to accommodate local or
regional requirements. These are usually issued Jointly by the State
Agricultural Experiment Station and Extension Service in cooperation with
the U.S. Department of Agriculture. The state insecticide use recommenda-
tions are issued or revised annually.
Production and Domestic Supply of Parathion in the United States
Volume of Production - The United States Tariff Commission, named
three basic producers of parathion in the United States: Monsanto Co.,
Stauffer Chemical Co., and Kerr-McGee Chemical CorpJL' Parathion is
currently produced by Monsanto.
In that report, the production and sales volumes of parathion are not
reported individually. Parathion is included in a group consisting of
seven other specified, and additional unspecified cyclic phosphorothioates
and phosphorodithioates. The reported production volume for this entire
group in 1972 was 44,385,000 Ib of active ingredients. Through a process
of careful analysis of the use patterns of all organophosphate insecticides
in this group, supported by information from trade sources, Midwest
developed estimates on the volume of production of all major products in
the group. The estimated volume of production of parathion in 1972 is 14
million pounds of active ingredient.
I/U.S. Tariff Commission, Synthetic Organic Chemicals, U.S. Production and
Sales, 1972, TC Publication 681 (1973).
238
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According to Midwest Research Institute/RvR Consultants, 1974-
about 10 million pounds of this total were produced by Monsanto Company,
the balance by Stauffer and Kerr-McGee.
Imports - Imports of pesticides that are classified as "benzenoid chemicals"
(including parathion) are reported by the U.S. Tariff Commission in its
annual report on "Imports of Benzenoid Chemicals and Products" (TC 1973, and
covers the calendar year 1972. According to this source, there were no imports
of parathion into the United States in 1972.
Exports - Pesticide exports are reported by the Bureau of the Census in
its annual report FT 410. Technical (unformulated) parathion and methyl
parathion are included in this report in Schedule B, Section 512.0652.
Formulations of parathion (and of all other cyclic and acyclic organic
phosphate insecticides) are included in Schedule B, Section 599.2035,
entitled "Organic phosphate containing pesticidal preparations, except
household and industrial and except fly sprays and aerosols."
Total exports of organic phosphate insecticides in these two categories
for 1972 are as follows:
Section 512.0652 (parathion and methyl parathion technical) -
16,533,940 Ib
Section 599.2035 (organic phosphate containing formulations) -
15,898,884 Ib
To derive the 1972 export volume of parathion from these totals,
Midwest Research Institute made a thorough analysis of these two pesticide
export categories by unit dollar values and by countries of destination.
This Information was then matched against the crop protection problems
and the pesticide trading patterns of the countries of destination.
Additional information was obtained from confidential trade sources.
Estimates from this data place the 1972 export volume of parathion at 4
million pounds of active ingredient.
I/ Midwest Research Institute/RvR Consultants, "Production, Distribution,
Use, and Environmental Impact Potential of Selected Pesticides,"
(draft), Council on Environmental Quality, Contract No. EQC-311
(15 March 1974).
239
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Domestic Supply - The information presented in the preceding three sections
estimates the domestic supply of parathion in the United States in 1972.
Subtracting exports from total production, Midwest Research Institute concludes
tnat about 10 million pounds of active ingredient were used domestically in
1972. ~~
It is not possible at this time to make comparable estimates for 1973,
because the U.S. Tariff Commission report on the production and sales of
pesticides and related products in 1973 will not become available until the
late fall of 1974.
Formulations - Parathion is available to users in the United States in a
variety of different formulations, and through a considerable number of
suppliers. The basic domestic producers of technical parathion sell a
large share, or all of their production, as technical to f emulator-customers
who prepare and sell different formulations of parathion under a variety
of different labels and brand names to end users, either directly, or
through wholesalers ., and/or retailers.
Frear (1972)—' lists almost 100 products containing parathion, offered
by many different suppliers, as follows:
Products
Aerosols (concentration not given) 2
Sprays (emulsifiable liquids containing
2, 4, 6, or 8 Ib of AI per gallon;
flowable liquids containing 4 or 8 Ib
of AI per gallon; wettable powders
containing 15 or 25% of AI) 60
Dusts (varying concentrations) 22
Granulars (varying concentrations) 4
Manufacturing concentrates 4
I/ Frear, D. E. H., Pesticide Handbook Entoma, 24th Edition, College
Science Publishers, State College, Pennsylvania (1972).
240
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In addition to these formulations containing parathion only, the product
is also offered in combination formulations with other insecticides and/or
fungicides, in dry and liquid formulations. Among these, an emulsifiable
liquid containing 6 Ib of parathion and 3 Ib of methyl parathion per gallon
has recently gained in popularity and use volume.
Use Patterns of Parathion in the United States
General - Essentially all of the quantities of parathion used in the
United States were in agriculture. There were no significant uses of
parathion by industrial, commercial or institutional pesticide users;
by Federal, state, county, local, or other governmental agencies; or
by home and garden users.
Surveys on the use of pesticides by farmers were conducted by the U.S.
Department of Agriculture in 1964 (Agricultural Economic Report No. 131,
published in January 1968), in 1966 (Agricultural Economic Report No. 179,
published in April 1970), and 1971 (Agricultural Economic Report No. 252,
in press). Data on the uses of parathion in 1972 were obtained by RvR
Consultants.
The following farm uses of parathion were reported:
Year Source Farm Use
1964 USDA 6,426,000 Ib of active ingredient
1966 USDA 8,425,000 Ib of active ingredient
1971 USDA 9,481,000 Ib of active ingredient
1972 RvR 10,000,000 Ib of active ingredient
These figures indicate an upward trend in the quantities of parathion
used by farmers during the 8-year period covered by the surveys.
As outlined earlier in this subsection, parathion has a very broad
spectrum of effectiveness and is registered and recommended in the United
States for use on a large number of fruit, nut, vegetable and field crops.
241
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Table 33 presents a breakdown of the estimated uses of parathion in the
United States in 1972, by regions and major crops. The following informa-
tion sources were used in arriving at these estimates:
1. The three USDA surveys of pesticide uses by farmers mentioned above.
2. The annual USDA publication "Pesticide Review" (Agricultural
Stabilization and Conservation Service).
3. Results of a survey of the Federal/State Cooperative Extension
Services in all 50 states and in Puerto Rico conducted by RvR
Consultants in 1973.
4. Analyses of state pesticide use recommendations.
5. Local and regional estimates on pesticide use volumes obtained from
State Research and Extension personnel in personal communications.
6. Pesticide use reports from the States of Arizona, California, Illinois,
Indiana, Michigan, Minnesota, and Wisconsin.
7. Data on pesticide uses supplied by the EPA Community Pesticide Studies
Projects in Arizona, Hawaii, Idaho, Mississippi, South Carolina,
Texas, and Utah.
8. Estimates and information obtained from basic producers of parathion
and other pesticides, and from pesticide trade sources.
9. Pesticide use surveys conducted recently by Wallaces' Farmer, Des
Moines, Iowa; Prairie Farmer, Chicago, Illinois; and Wisconsin
Agriculturist, Madison, Wisconsin.
10. "Agricultural Statistics," an annual publication of the U.S. Depart-
ment of Agriculture.
Data from all of these numerous and diverse sources were carefully
analyzed, correlated cross-checked and cross-validated. The resulting
estimates as summarized in Table 33 are believed to be the best and most
up-to-date information on the use patterns of parathion in the United States
currently available.
242
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Table 33. ESTIMATED USES OF PARATHION ON THE U.S. BY
REGIONS AND MAJOR CROPS (1972)
Region
Other
grains ,
Cotton Corn sorghum
Crop
Citrus
Vegetables fruits
Other
fruits,
nuts
All
other
Tobacco crops
Totals,
all
uses
Northeast^
Southeast-'
East North Central^/
West North Central^
East South Central—^
West South Central!'
Northwest^'
Southwest"-'
Totals, 50 States
500
Negl.
Negl.
700
600
500
2,300
Negl,
150
200
200
50
Negl,
Negl.
Negl.
600
Thousands of Pounds of Active Ingredient
Negl.
Negl.
Negl.
1,050
Negl.
1,100
50
50
100
100
100
Negl.
50
400
200
650
2,250 1,600
—
100
--
•**»
Negl.
««•
200
300
250
100
100
Negl
100
300
150
650
1,650
Negl.
300
Negl.
50
150
100
50
100
100
100
350
400
1,400
500
1,300
1,000
2,500
500
2,400
300 1,000 10,000
Source: RvR estimates, see text.
a/ New England States, New York, New Jersey, Pennsylvania
b/ Maryland, Delaware, Virginia, West Virginia, North Carolina, South Carolina, Georgia, Florida
cV Ohio, Indiana, Illinois, Michigan, Wisconsin
-------
Parathion Uae Patterna by Regions - Analyzing parathlon uses on a geo-
graphical basis, It Is Interesting to note that about one-half of the
total quantity of the product used in the U.S. In 1972 (alaost 5 million
pounds AI) was used In the Southwestern United States, i.e., in the West
South Central and Southwest regions (Table 33). In these areas, about
1.2 million pounds of parathion AI were used on grain crops other than
corn (primarily sorghum); 1.1 million pounds AI on cotton; and about 1
million pounds AI each on vegetable and fruit crops.
The Southeastern states used an estimated 1.4 million pounds of
parathion AI. Of this total, about 500,000 Ib was for cotton, another
300,000 Ib for tobacco. The balance was used on vegetables, citrus
and other fruits, and other crops.
An estimated 1.3 million pounds of parathion AI were used in the
West North Central region, primarily on sorghum and other small grains.
In the East South Central region, a combined total of about 1
million pounds of parathion AI was used on all crops, primarily on
cotton (700,000 Ib).
The Northeastern, East North Central and Northwestern regions of
the country eaehiused an estimated 500,000 Ib of parathion AI or less.
There were no single major uses on individual crops in these areas.
Parathion Use Patterns by Crops - Analyzing the parathion use pattern by
crops, it appears that cotton Is the single largest "consuming" crop.
Parathion is registered and recommended against 19 different insect and
mite pests on cotton.
The use of parathion on grain crops, especially sorghum, has increased
substantially during the last few years and is almost equal to the volume used
used on cotton in 1972. Increased use Is largely due to infestation of the
greenbug, Schlzaphis graminum. This insect, recorded in the United States
as early as 1882, for the first time severely damaged sorghum crops in a
number of states in 1968. This development has been attributed to a new bio-
type of the species, known as "Biotype C".^' The primary use of parathion
to control the greenbug was on sorghum in Southern Nebraska, and in Kansas,
Oklahoma and Texas.
I/ See Eight, S. C., R. D. Eikenbary, R. J. Miller, and K. J. Starks,
"The Greenbug and Lysiphelbus testaceipes." Environmental Entomology
1(2):205-209 (1972).
244
-------
Paratblon uses cm vegetable and fruit crops each amounted to about
1.6 Billion pounds of active ingredient in 1972, with the largest amounts
of product used in the Southwestern states.
Approximately 600,000 Ib of parathion AI were used on corn in 1972;
and about 300,000 Ib AI each on citrus fruits and on tobacco. The remain-
ing 1 million pounds of AI went on a large variety of other crops, with
no single one outstanding.
Parathion Uses in California - The State keeps detailed records
of pesticide uses by crops and commodities. They are published quarterly
and summarized annually. Table 34 summarized the uses of parathion In
California by major crops for the 4-year period 1970 to 1973. The total
volume of parathion used during this period varied relatively little, but
there were considerable changes in the uses on different crops from year
to year. For instance, the use of parathion on citrus fruits increased
from 137,000 Ib AI in 1970 to 234,000 Ib in 1973. Parathion uses on stone-
fruits (peaches, nectarines, apricots) varied from a low of 83,000 Ib AI
in 1971 to a high of 227,000 Ib in 1970.
Tables 35 and 36 present parathion uses In California by crop, number
of applications, pounds of active ingredient, and number of acres treated,
for 1972 and 1973, the two most recent years for which such data are avail-
able. In both years, parathion was used In California on close to 100
different crops.
Incongruities and inconsistencies were found In statistics on parathion
uses on California crops.
A significant amount, 90,000 Ib, of parathion AI was reportedly used
on cotton in California in 1972, and 107,000 Ib in 1973. However, the
University of California Extension Service recommends the use of parathion
on cotton only against the false chinch bug, described as an "occasional
Insect problem," but not against major California cotton pests such as the
cotton bollworm, the pink bollworm, the cotton leafperforatort Lygus bugs,
or mites.
The California Department of Agriculture reported using 186,000 Ib of
parathion AI on citrus crops (oranges, lemons, grapefruit) in 1971 (Table 34)
However, the U.S. Department of Agriculture in Quantities of Pesticides
Used by Farmers in 1971 (Agricultural Economic Report No. 252; in press)
reports only 68,000 Ib of parathion used on citrus fruits in the entire U.S.
During the 1971 to 1972 season, California produced about 22% of all citrus
fruits in the United States.*'
I/ U.S. Department of Agriculture, Agricultural Statistics. 1973. Table 314,
p. 219.
245
-------
Table 34.* PARATHION USES IN CALIFORNIA BY MAJOR CROPS
AND OTHER USES (1970-1973)
Crop
Citrus (oranges, lemons,
grapefruit)
Peaches, nectarines,
apricots
Plums, prunes
Almonds
Olives
Tomatoes
Lettuce
Beans
Artichokes
Cotton
Sugar beets
Alfalfa
Rice
Vector control
All other uses
Totals, all uses
1973
Thousands
234
157
58
82S/
9
90
90
30
49
107
71
23
29
26
159
1,214^
Year
1972
of Pounds
185
170
68
87
30
55
80
29
60
90
48
24
37
20
114
1,097
1971
of Active
186
83
22
11
11
85
180
23
49
108
71
32
37
29
142
1,069
1970
Ingredient
137
227
83
70
9
62
84
28
19
87
54
42
20
51
199
1,172
California Department of Agriculture, Pesticide use reports for
1970, 1971, 1972 and 1973.
a/ Quantity used on almonds in 1973 and 1973 total reduced by 738,000 Ib
to adjust for apparent system error; see text.
246
-------
Table 35. USE OF PARATHION IN CALIFORNIA IN 1972, BY CROPS,
APPLICATIONS, QUANTITIES, AND ACRES TREATED
Commodity
Alfalfa
Alfalfa fur seed
Almond
Anise
Apple
Apricot
Artichoke
Asparagus
Avocado
Barley
Beans, dry edible
Beans, green or forage
Beans for seed
Beet
Berries
Boysenberry
Broccoli
Brussels Sprouts
Cabbage
Cantaloupe
Carrot
Cattle lot
Cauliflower
Celery
Cherries/sweet
Chinese cabbage
Citrus
Clover for seed
Corn/field
Corn/sweet
Cotton
County or city parks
Cucumber or pickle
Deciduous fruit crops
Eggplant
Endive
Escarole
Fallow (open ground)
Flowers
Foliage
Garlic
Grapefruit
Grape
Grasses/field
Honeydew melon
Leek
Lemon
Lettuce/head
Lettuce/leaf
Applications
762
26
946
2
23
330
1,197
3
5
31
579
42
1
145
1
1
117
190
205
12
92
1
219
1,005
25
4
176
1
45
45
1,579
13
1
1
2
1
18
37
2
41
42
131
1
1
2
120
5,259
111
Pounds
22,750.66
891.86
87,125.86
4.35
474.32
20,234.65
59,719.59
187.50
230.00
1,100.42
27,374.78
1.122.56
15.24
4,087.71
6.49
5.00
1,480.44
3,865.67
1,762.94
575.12
2,452,39
2.28
2,268.67
8,375.55
767.10
3.50
13,721.63
148.47
4,949.58
9,970.83
90,188.18
79.21
714.06
200.00
0.06
6.00
3.39
818.76
939.77
302.23
1,036.71
2,893.88
14,475.03
138.17
47.38
4.61
7,738.15
79,298.56
822.90
Acres
67,005.20
1,960.00
56,341.56
8.00
347.50
14,505.75
125,272.20
75.00
144.00
2,905.00
39,437.20
1,521.00
20.00
9,442.68
7.00
10.00
2,790.60
6,320.50
3,243.53
1,234.00
3,950.45
6.00
4,144.70
16,176.43
570.50
7.00
5,242.86
80.00
4,619.00
4,568.00
138,256.00
442.00
80.00
12.50
10.00
6.00
479.00
188.25
285.10
1,357.64
518.50
5,936.00
148.00
80.00
18.00
3,352.66
143,022.99
1,797.28
247
-------
Table 35.* (Continued)
Commodity Application!
Melons
Nectarine
Monagricultural areas
Nuraery atock
Data
Okra
Olive
Onion/dry
Onlon/green/spr Ing/shallot
Orange
Orchard
Ornamental!
Ornamental bedding planta
Other agencies
Parsley
Paature/rangeland
Peach
Pear
Pea
Pepper /bell
Plun
Potato
Prune
Pumpkin
Radlah
Residential control
Rice
Safflower
School district
Sorghum
Spinach
Squash, summer
Squash, winter
Strawberry
Sugar beets
Tangelo
Tangerine
Tomatillo/husk tomato
Tomato
Turf
Turnip
University of California
Vector control
Walnut
Water areas
Watermelon
Wheat
Total
20
848
86
3
6
4
130
434
14
1,892
1
23
6
1
48
2,018
75
102
28
632
127
411
28
11
1,047
2
36
283
36
3
25
1,379
5
4
1
1,467
42
5
40
1
13
13
24,943
Pounds
882.34
34,638.86
1,215.85
65.30
303.09
24.59
30,120.72
10,505.22
383.23
160,377.37
15.36
72.61
13.92
66.99
0.03
764.00
115,217.86
10.358.27
379.61
315.15
25,781.16
6,413.46
42,035.64
910.93
84.98
0.49
37,089.58
14.15
10.39
6,414.95
4,136.89
713.84
36.02
248.27
48,317.65
968.74
174.68
2.40
54,824.06
4,657,58
49.75
50.38
19,502.16
2,304.36
166.37
653.56
406.00
1,097,091.02
Acres
1,658.00
16,818.24
12,870.00
62.00
230.00
38.00
2,753.73
16,689.57
590.00
52,854.95
58.00
161.50
20.00
12.00
8,118.50
63,054.65
4,440.60
638.00
672.63
11,580.05
9,218.23
23,587.33
1,351.00
149.00
160,493.20
54.00
1,884.50
8,280.60
1,240.00
110.00
438.00
107,933.88
67.00
291.00
4.00
85,433.63
5,365.14
71.00
1,472.50
200.00
1,158.00
1,043.00
1,271,111.01
'California Department of Agriculture, Pesticide Use Report 1972.
248
-------
Tabla 36? USE OF PA8ATHIOH IK CALIFORMIA IV 1973, BY CROPS,
APPLICATIONS, QUANTITIES, AXD ACHES TREATED
Cownodity
Alfalfa
Alfalfa fur aaad
Almond
Anita
Appla
Apricot
Artichoke
Avocado
Barlay
Baana, dry adibla
Baant, graan or foraga
Baana for aaad
Baat
Barriaa
Broccoli
Bruaaala aprouta
Cabbaga
Cantaloupa
Carrot
Cauliflovar
Calary
Charriaa/avaat
Chinaaa cabbaga
Citrua
Cola cropa
Conifar
Corn/fiald
Corn/a waat
Cotton
County or city parka
Cucunbar or pickla
Daciduoua fruit cropa
Applicattona
593
141
753
2
17
257
1,260
5
41
731
3
1
428
1
113
104
186
1
68
134
923
16
13
79
4
1
42
23
1,866
10
1
Daciduoua ornanantal traaa 1
Fallow (opan ground)
Flowara
Poliaga
Carlic
Crain
Crapa fruit
Crapa
Lanon
L«teuca/laad
Uttuca/laaf
Malona
Muatard
Mactarina
Nonagricultural araaa
Muraary atock
Data
Olive
15
92
1
37
2
50
160
140
4,723
61
17
I
743
27
4
1
186
Pounda
17,438.41
5,676.99
820,076.97
10.50
356.13
20.545.64
49,345.86
290.00
3,541.15
25,977.89
83.14
45.90
16,050.15
4.14
1.844.81
1,730.76
2.061.55
8.88
1,266.47
1,705.68
8,338.25
1.169.79
36.41
12,609.15
13.26
0.08
10,929.58
894.18
107.117.83
87.79
397.02
15.74
10.50
16.900.93
300.29
0.64
1,642.56
174.67
3,017.74
14,683.10
24,787.06
89,729.12
272.47
517.60
4.95
23,236.60
297.42
167.33
66.63
8,863.74
Acraa
48.943.00
10,017.00
42,126.24
21,00
252.50
13,286.00
70.363.60
142.00
9.816.00
45,711.20
141.00
50.00
31,719.40
7.00
2,837.84
2,949.50
3,203.60
20.00
2,983.72
2.625.50
14.915.76
286.50
109.00
3,509.30
49.00
5.00
4.560.00
2,372.00
175,081.44
178.00
9.00
7.00
673.00
488.75
32.00
2,726.50
116.00
616.30
7,817.50
4,099.60
153,259.37
609.68
1,141.00
11.00
14.065.13
589.00
59.75
150.00
3,872.49
€49
-------
Table 36.* (Continued)
Commodity Applications
Onion/dry
Onlon/green/spring/shallot
Orange
Orchard
Ornamentals
Ornamental bedding plants
Other agencies
Pasture/rangeland
Peach
Pear
Pea
Pepper /bell
Pimento
Plum
Potato
Prune
Pumpkin
Radish
Residential control
Rice
Rutabaga
Safflower
Salsify fur .seed
School district
Soil (fumigation only)
Sorghum
Sorghum fur seed
Spinach
Squash/ summer
Squash, winter
Strawberry
Structural control
Sudangrass
Sugar beets
Sunflower seed
Sweet potato
Tangelo
Tangerine
Tomato
Turf
Turnip
University of California
Vectur Control
Walnut
Water Areas
Watermelon
Wheat
Total
401
11
2,206
1
3
3
15
1,904
64
202
37
1
588
76
421
10
8
1,453
1
16
1
5
62
1
187
17
1
36
3
1,779
3
67
2
1
1,514
71
2
72
1
5
30
25,361
Pounds
11,761.03
92.46
194,061.11
98.00
5.12
24.00
11,753.39
2,086.59
112,936.23
6,795.70
774.99
1,113.73
69.59
21,962.58
2,068.47
35,670.73
276.17
147.16
5.40
29,104.95
9.89
14,674.06
3.50
33.22
757.64
2,368.37
0.12
2,040.11
573.03
30.53
463.54
0.90
35.16
70,502.40
493.29
2,784.45
43.75
60.00
89,928.84
7,564.36
21.34
142.55
26,445.43
6,400.90
0.01
369.33
1,084.96
1,951,982.53
Acres
16,160.25
119.00
65,776.52
56.00
12.00
12.00
1,707.00
63,493.38
5,471.50
817.25
1,794.25
75.00
10,596.13
3,438.00
20,463.25
456.00
250.00
217,010.70
16.00
2,965.00
2.00
209.00
4,147.00
98.50
4,112.34
525.00
100.00
842.00
96.00
143,517.78
575.00
2,889.00
30.00
20.00
113,610.50
8,541.00
37.00
2,368.50
2.00
600.00
2,241.00
1,373,878.02
California Department of Agriculture, Pesticide Use report 1973.
250
-------
Regarding the California Department of Agriculture's reported
figure of 820,077 Ib, of parathion used on the State's almond crops
in 1973, available figures for the three proceeding years show that
parathion uses on almonds were considerably lower: 1970, 70,000 Ibs;
1971, 11,000 Ib; 1972, 87,000 Ib; (see Table 34). Based on an analysis
of past level of use and the number of acres treated in 1973, Midwest
Research Institute believes there to be an error in the reported 1973
figure for parathion use in California and has accordingly revised the
figure (See Table 34).*'
At the present time, no other state in the union records or
publishes pesticide use data in comparable detail. Limitations of time
and resources did not permit development of estimates on the uses of
parathion by crops and states beyond the detail provided in Table 34.
Summary - In 1972, parathion was used in the United States on the following
major crops (listed in decreasing order of volume of use): cotton, sorghum
and small grains; deciduous fruit and nut crops; vegetable crops, corn;
citrus fruits; tobacco; and numerous other crops, each accounting for a
relatively small share of the total use.
By geographic regions, the use pattern of parathion in 1972 was as
follows (regions listed in decreasing order of volume of use): West South
Central (Oklahoma and Texas); Southwest (California, Arizona, Hawaii,
New Mexico, and Nevada); Southeast; West North Central states;East South
Central states; Northwest; Northeast.
Slightly more than 10% of the total quantity of parathion used in the
U.S. in 1972 was in California, on almost 100 different crops.
I/ In a personal communication, the California Department of Agriculture
agreed that the reported figure of 820,077 Ib was most likely erroneous.
The agency did not account for the discrepancy.
251
-------
PART III. MINIECONOMIC REVIEW
CONTENTS
Page
Introduction 254
Cotton 256
Efficacy Against Pest Infestation 256
Cost Effectiveness Of Pest Control 257
Sorghum 257
Efficacy Against Sorghum Midge Infestation 258
Cost Effectiveness of Sorghum Midge Control 258
Efficacy Against Greenbug Infestation 259
Cost Effectiveness of Greenbug Control ... 261
Wheat 262
Efficacy Against Pest Infestation 262
Cost Effectiveness of Pest Control 262
Peanuts 263
Efficacy Against Pest Infestation 263
Cost Effectiveness of Pest Control 263
Corn 264
Efficacy Against Pest Infestation 264
Cost Effectiveness of Pest Control 264
252
-------
CONTENTS (Continued)
Page
Potatoes 265
Efficacy Against Wireworm Infestation 265
Cost Effectiveness of Wireworm Control 265
Potato Aphid Control 266
Leafhopper Control 266
Lima Beans 266
Peas 267
Strawberries 267
References 269
253
-------
This section contains a general assessment of the efficacy and cost
effectiveness of parathion. Data on the production of parathion in the
United States as well as an analysis of its use patterns at the regional
level and by major crop are found in Part II of this report.
Introduction
The efficacy and cost effectiveness of a specific pesticide should
be measurable in terms of the increased yield or improved quality of a
treated crop which would result in a greater income or lower cost than
would be achieved if the pesticide had not been used. Thus, one should
be able to pick an isolated test plot of a selected crop, treat it with
a pesticide, and compare its yield with that of a nearby untreated test
plot. The difference in yield should be the increase due to the use of
the pesticide. The increased income (i.e., the yield multiplied by the
selling price of the commodity) less the additional cost (i.e., the pesti-
cide, its application and the harvesting of the increased yield) is the
economic benefit due to the use of the pesticide.
Unfortunately, this method has many limitations. The data derived is
incomplete and should be looked on with caution. Midwest Research Institute's
review of the literature and EPA registration files revealed that experimental
tests comparing crops treated with specific pesticides to the same crop without
treatment are conducted by many of the state agricultural experimental stations.
Only a few of these however, have attempted to measure increased yield and
most of this effort has been directed toward just a few crops such as cotton,
potatoes, and sorghum. Most other crop tests measure the amount of reduction
in pest levels which cannot be directly related to yield.
Even the test plot yield data are marginally reliable, since these
tests are conducted under actual field conditions that may never be
duplicated again and are often not representative of actual field use.
Thus, yield is affected by rainfall, fertilizer use, severe weather con-
ditions, soil type, region of the country, pesticide infestation levels
and the rate, frequency and method of pesticide application.
Because of these factors, yield tests at different locations and
in different years will show a wide variance ranging from a yield de-
cline to significant increases. For example, in a year of heavy pest
infestation, frequent pesticidal use can result in a high yield increase
because the crop from the untreated test plot is practically destroyed.
Conversely, in a year of light infestation, the yield increase will be
slight.
254
-------
Thus, the use of test plot yield data is at best qualitative and is
used for order-of-magnitude economic cost and benefit determination.
The use of market price to estimate the value received by the pro-
ducer also has its limitations. If the use of the pesticide increases
the yield of a crop and the national production is increased, then the
market price should decline. According to J. C. Headley and J. N. Lewis
(1967),— a 1% increase in quantity marketed has at times resulted in a
greater than 1% decrease in price. Thus, the marginal revenue from the
increased yield would be a better measure of value received.
A third limitation to the quantification of the economic costs and
benefits is the limited availability of data on the quantities of the
pesticide used by crop or pest, the acres treated, and the number of ap-
plications. In most cases the amount of parathion used on each crop or
each pest is not available.
As a result of these limitations an overall economic benefit by crop
or pest cannot be determined. This review presents a range of the po-
tential economic benefits derived from the use of parathion for control
of a specific pest on a specific crop. This economic benefit or loss is
measured in dollars per acre for the highest and lowest yield developed
from experimental tests conducted by the pesticide producers and the
state agricultural experimental stations. The high and low yield in-
creases are multiplied by the price of the crop and reduced by the cost
of the parathion applied to generate the range of economic benefits in
dollars per acre*
Efficacy and yield changes due to the use of parathion have been
reported on several crops and pests. This report summarizes the results
of these tests which include the bollworm, boll weevil, and tobacco bud-
worm on cotton; the sorghum midge and greenbug on sorghum; the greenbug
on wheat; the southern corn rootworm on peanuts; the Pacific wireworm,
potato aphid and potato leafhoppers on potatoes; the European corn borer
and western corn rootworm on corn; the lygus lesperus on lima beans; the
tarnished plant bug on strawberries; and the pea aphid on peas.
I/ Headley, J. C., and J. N. Lewis, The Pesticide Problem; An Economic
Approach to Public Policy, Resources for the Future, Inc., pp. 39-40,
(1967).
255
-------
Cotton
Parathion is registered for a wide variety of cotton insects. The
tobacco budworm, bollworm, boll weevil, aphids, fleahoppers, leaf hoppers,
cabbage loopers, spider mites, and thrips are major cotton pests treated
with parathion. Application rates vary from 0.25 to 1.0 Ib/acre, depend-
ing upon the type of insect. The number of applications depends upon
the degree of infestation. Repeated applications are recommended for the
bollworm, budworm, and boll weevil until adequate control is achieved.
Efficacy Against Pest Infestation - Data is available on the efficacy of
parathion for control of the budworm, bollworm, and boll weevil— the three
major cotton pests—'from tests conducted in Texas.
Adkisson et al. (1966)!/ compared a wide variety of insecticides
for control of bollworm larvae near College Station, Texas in 1965. The
use of parathion resulted in a 70% kill after 48 hr when applied at 0.5
Ib/acre.
Adkisson et al. (1967)^.' conducted similar tests in 1966 and reported
an 85% kill of bollworm larvae 48 hr after parathion was applied at 0.5
Ib/acre. Farathion was also less effective against the budworm with an
83% kill at 0.75 Ib/acre after 48 hr compared to a 97% kill for 0.75
Ib/acre of methyl parathion. Against adult boll weevils, 0.25 Ib/acre of
parathion resulted in a 97% kill after 48 hr compared to 100% for methyl
parathion at the same rate.
Wolfenbarger (1973)^7 found that tobacco budworms from a susceptible
strain were 2.45 times more resistant to parathion than to methyl para-
thion during tests conducted in Brownsville, Texas in 1970.
I/ Adkisson, Perry L., and S. J. Nemec, "Comparative Effectiveness of
Certain Insecticides for Killing Bollworms and Tobacco Budworms,"
Publication B-1048, Texas Agr. Exp. Sta. (1966).
2j Adkisson, Perry L., and S. J. Nemec, "Insecticides for Controlling
the Bollworm, Tobacco Budworm, and Boll Weevil," MP-837, Texas Agr.
Exp. Sta. (1967).
3f Wolfenbarger, D. A., "Tobacco Budworm: Cross Resistance to Insecti-
cides in Resistant Strains and in a Susceptible Strain," J. Econ.
Entomol., 66:292-294 (1973).
256
-------
Cost Effectiveness of Pest Control - Information was found on .only one
test relating yield changes to parathion usage. Host (1974)-' summarized
tests conducted between 1956 and 1973 at Stoneville, Mississippi. The re-
sults of one test in 1956 showed a 253 Ib/acre gain over an untreated check
when nine applications of parathion at 0.5 Ib/acre were made.
The 1972 price received by farmers for cotton was 14.0c/lb for lint.
Additional income from cottonseed of 4.2c/lb and government price supports
of 12.5c/lb brought the total income to 40.7c/lb (Agricultural Statistics,
1973).-' Parathion costs averaged $l/lb in 1972, while application costs
averaged $.50 per treatment (Chambers et al., 1974).3'
Using the above cost and price data, the additional income would
amount to $102.98/acre. Subtracting the cost of parathion at $9.00/acre
would result in an economic benefit of $93.98/acre when parathion was used
to control boll weevils, bollworms, and tobacco budworms.
Sorghum
Parathion is registered for control of aphids, greenbugs, spider
mites, sorghum webvorms, and sorghum midges on sorghum. Of these, sorghum
midge and the greenbug are the two insects having the greatest effect on
yield.
I/ Bost, W. M., Director, "Cooperative Extension Service Mississippi
State University, Mississippi State Mississippi, Summary of Test
Results at Stoneville and Verona, Mississippi, and Costs of Pesti-
cides," personal letter to Mr. David F. Hahlen (1974).
|/ U.S. Department of Agriculture, Agricultural Statistics 1973.
3_/ Chambers, William, and Daniel Millel1, Fal'wland Industries, Kansas
City, Missouri, conversation (1974).
257
-------
Efficacy Against Sorghum Midge Infestation - In the early 1960's the
sorghum midge temporarily caused serious crop losses. .However, early
uniform planting has restricted damage from this Insect to Isolated late
planted fields (Gate et al., 1973).17 Huddleston et al. (1972)2/
reported on tests of insecticides for control of the midge and concluded
that parathion gave superior control of midge population with two
applications of 0.5 Ib/acre.
Yields from tests conducted at Plainview, Texas Increased from 22 to
330 Ib/acre over an untreated check as the rate and number of applications
increased. However, increasing the rate to 1.0 Ib/acre for two applica-
tions reduced the increase to 198 Ib/acre. In another test conducted in
Texas in 1961, one application of 0.5 Ib parathion per acre reduced yields
from the untreated check by 230 bushels per acre. The authors attributed
this to the application being made at late bloom.
Gate et al. (1971)J/ evaluated several insecticides for control of
the midge in Lubbock County, Texas in 1969. Parathion was applied at 0.5
Ib/acre and controls measured for two and three applications. The first
application was made when 50% of the grain heads were out of the boot.
The results showed a 63% control with two applications and 55% control
with three applications. Yields compared to an untreated check Increased
236 Ib/acre with two applications but declined 313 Ib/acre with three
applications.
Cost Effectiveness of Sorghum Midge Control - The tests of Cate et al.
(1973) and Huddleston et al. (1972) contain the only data found that
compared yields of parathion treated sorghum plots against an untreated
check. The results of these experiments showed yield changes ranging from
a loss of 313 Ib/acre to an increase of 330 Ib/acre.
JL/ Cate, J. R., Jr., D. 6. Bottrell, and 6. L. Teetes, "Management of the
Greenbug on Grain Sorghum. I. Testing Foliar Treatments of In-
secticides Against Greenbugs and Corn Leaf Aphids," J. Econ. Entomol.
66:945-951 (1973)
21 Huddleston, E. W., D. Ashdown, B. Maunder, C. R. Ward, G. Wilde, and
C. E. Forehand, "Biology and Control of the Sorghum Midge. I.
Chemical and Cultural Control Studies in West Texas," J. Econ.
Entomol., 65:851-855 (1972).
3/ Cate, J. R., Jr., and D. G. Bottrell, "Field Evaluation of Insecticide
Treatments for Control of the Sorghum Midge," PR-2866, pp. 13-15,
Research on Grain Sorghum Insects and Spider Mites in Texas, Texas
Agr. Exp. Sta. (1971).
258
-------
The price of sorghum averaged $2.25/cwt in 1972.Agricultural.
Statistics 1973 and the cost of parathion was $l/lb (Chambers and Miller)
cost, the economic benefits would range from a loss of $10.04/acre to a
gain of $4.93/acre for control of the sorghum midge.
These tests are summarized in Table 37.
Table 37. Results of Parathion Application Sorghum Midge
Additional
Pate
1961
1964
1969
Application
Rate
(Ib Al/acre)
0.5
0.5
1.0
0.5
1.0
0.5
0.5
No.
1
1
1
2
2
2
3
Yield
Increase*
(lb/acre)
(224)
22
154
330
198
236
(313)
income*
$2.25/cwt
($/acre)
(5.04)
0.50
3.47
7.43
4.45
5.31
(7.04)
Application
cost at
AI $l/lb +
treatment at
$ . 50/application
1.00
1.00
1.50
2.00
3.00
2.00
3.00
Economic
benefit*
f$/acre) Source
(5.54)
0
2.47
6.43
2.45
4.31
(8.54)
Data in parentheses indicates decreases in yield, income and economic
benefit.
aj Huddleston et al., op. clt. (1972).
b/ Gate et al., op. cit. (1971).
Efficacy Against Greenbug Infestation - Although there are numerous
Insects affecting sorghum, perhaps the greenbug causes the greatest
damage. Prior to 1968 the greenbug had been found mostly in small grains
such as wheat, barley, and oats. However, in,1968 a new biotype emerged and
began infesting sorghum. Ward et al. (1970)- noted that, in 1968, 7.3
million acres became infested resulting in a production loss estimated at
$20 million. Gate et al. (1979) reported that the Grain Sorghum Producers
Board estimated that $14 million was spent for control of grain sorghum pests
in 1970 compared with only $100,000 spent prior to 1968.
a/
b/
I/ Ward, C. R., E. W. Huddleston, D. Ashdown, J. C. Owens, and K. L.
Polk, "Greenbug Control on Grain Sorghum and the Effects of Tested
Insecticides on Other Insects," J. Econ. Entomol., 63:1929-1934
(1970). "
259
-------
Parathlon gives satisfactory control of greenbugs on sorghum.
Daniels (1971)1/ conducted two tests at Bushland, Texas in 1969 and
achieved a 79% reduction of greenbugs for 29 days in one test and an
897. reduction for 25 days in the other test. The first test consisted
of 0.5 Ib/acre of parathion and the second was at a 0.25 Ib/acre rate.
Yield increases were 112 and 42 Ib/acre respectively.
Gate et al. (1973) conducted several experiments for insecticidal
control of the sorghum greenbug in Lubbock County Texas in 1968, 1969
and 1970. Results showed greenbug control ranging from 657. to 977.
7 days after application of 0.5 Ib/acre parathion. Seasonal control
of greater than 90% was reported in some of the tests. Yield changes
from the untreated check varied from increases of 32 to 1,083 Ib/acre.
Ward et al. (1970) also showed significant reduction of greenbugs in
tests at Lubbock and New Deal, Texas in 1968. Yield increases varied
widely from a low of 9 Ib/acre to a high of 497 Ib/acre. Similar
results were found by DePew (1971)!/ and Harvey et al. (1970)!/.
Parathion appears to be phytotoxic to certain types of sorghum.
Although DePew (.1971) reported no evidence of phytotoxicity, Meisch
et al. (1970)i/ evaluated various insecticides for phytotoxicity to
six varieties of sorghum and found severe leaf damage and significant
yield loss in one variety, but medium to low damage on the other vari-
eties. Yields on the other varieties varied from a loss of 385 Ib/acre
compared to an untreated check to a gain of 408 Ib/acre.
\J Daniels, N. E., "Insecticidal Greenbug Control in Grain Sorghum,"
PR-2868, pp. 16-20, Research on Grain Sorghum Insects and Spider
Mites in Texas, Texas Agr. Exp. Sta. (1971).
2/ DePew, L. J., "Evaluation of Foliar and Soil Treatments for Greenbug
Control on Sorghum," J. Econ. Entomol.. 64:169-172 (1971).
37 Harvey, T. L., and H. L. Hackerott, "Chemical Control of a Greenbug
on Sorghum and Infestation Effects on Yields," J. Econ. Entomol.,
63:1536-1539 (1970).
4/ Meisch, N. V., George L. Teetes, N. M. Randolph, and A. J. Bockholt,
"Phytotoxic Effects of Insecticides on Six Varieties of Grain
Sorghum," J. Econ. Entomol.. 63:1516-1517 (1970).
260
-------
Cost Effectiveness of Greenbue Control - The results of several tests
in Texas and Kansas show that yield changes varied from a loss of 458
Ib of sorghum per acre to a gain of 1,083 Ib/acre when parathion was
used to control the greenbug.
The price of sorghum averaged $2.25/cwt in 1972 (Agricultural
Statistics 1973); the cost of parathion was $1.00/lb (Chambers and
Miller 1974), the cost of application is $.50. At these prices and
costs the economic benefits would range from a loss of $11.81/acre to
a gain of $23.77/acre from the use of parathion to control the greenbug.
These tests ace summarized in Table 38.
Table 38. Results of Parathion Application on Sorghum Greenbug
Pate
1968
1969
1969
1968
1969
1970
1969
1968
1969
Application
Rate
(Ib Al/acre)
0.5
0.5
0.5
1.0
1.0
1.0
1.0
1.0
1.0
0.5
0.5
0.5
0.5
0.1
0.25
0.5
0.5
0.25
0.25
0.5
No.
1
1
1
2
2
2
2
2
2
1
1
1
1
1
1
1
1
1
1
1
Yield
increase*
(Ib/acre)
497
93
9
(117)
(385)
(458)
(345)
385
408
32
770
47
1,083
1,083
783
1,023
84
439
42
112
Additional
income*
$2.25/cwt
($/acre)
11.18
2.09
0.20
(2.63)
(8.66)
(10*31)
(7.76)
8.66
8.82
0.72
17.33
1.06
24.37
24.37
17.62
23.02
1.89
9.88
0.95
2.52
Application
cost at
Al $l/lb +
treatment at
$ . SO/application
1.00
1.00
1.00
3.00
3.00
3.00
3.00
3.00
3.00
1.00
1.00
1.00
1.00
0.60
0.75
1.00
1.00
0.75
0.75
1.00
Economic
benefit*
($/acre) Source
10.18 a/
1.09
(.80)
(3.63) b/
(9.66)
(11.31)
(8.76)
5.66
5.82
0.72 c/
16.33
0.06
23.37
23.77
16.87
22.02
0.89 d/
9.13 a/
0.20
1.52
* Data in parentheses indicate decreases in yield, income, and economic
benefit.
a/ Ward et al., op. cit. (1970).
b/ Meisch et al., op. clt. (1970).
c/ Gate et al., op. cit. (1973).
d/ Harvey et al., op. cit. (1970).
e/ Depew, OP. clt. (1971).
f/ Daniels, op. clt. (1971).
261
-------
Wheat
The greenbug has been regarded as the most destructive of the aphids
infecting small grains since its introduction into North America in the
19th Century.
Efficacy Against Pest Infestation - As a result of a heavy infestation
of greenbugs in Texas in 1961, Daniels (1962)=' evaluated several
insecticides for their control on wheat. These tests at Bushland, Texas
in 1961 resulted in satisfactory control with parathion. In four experi-
ments averages of 88 to 92% reduction of greenbugs were achieved. Tields
increased between 4.0 and 10.8 bushels/acre respectively.
Ward et al. (1972)-' screened various insecticides at Clovis, New
Mexico in 1969 and reported a 98% reduction in greenbugs after 14 days
with parathion. Yields increased by 575 Ib/acre or 9.57 bushels/acre.
3ost Effectiveness of Pest Control - Yield increases based upon the three
rests reported above varied from 4.0 to 10.8 bushels/acre. At a price of
?1.67/bushel for wheat in 1972 (Agricultural Statistics 1973) and an
ipplication cost of $.50 per treatment, a cost of $1.00/lb for parathion
(Chambers and Miller, 1974), the economic benefit would range from $5.68
:o $17.04/acre from control of the greenbug on wheat.
These are summarized in Table 39.
I/ Daniels, N. E., "Insecticidal Control of the Greenbug,11 Progress
Report 2247, Texas Agr. Exp. Sta. (1962).
2j Ward, C. R., J. Owens, D. Ashdown, E. Huddleston, and W. Turner,
"Greenbug Control on Wheat in 1967-1969." J. Econ. Entomol.. 65:
764-767 (1972).
262
-------
Table 39. Results of Parathion Application on Wheat Greenbug
Application
rate
(Ib Al/acre)
0,
0.
0.
1968
0.5
0.5
Yield
Increase
(bu/acre)
4.0
8.0
10.8
9.89
9.57
Addition
income at
$1.67/bu
($/acre)
6.68
13.36
18.04
16.52
15.98
Application
cost at
AI $l/lb +
$.50/application
1.00
1.00
1.00
1.00
1.00
Economic
benefit
($/acre) Source
5.68
12.36
17.04
15.62
14.98
a/
b/
a/ Daniels, op. cit. (1962).
jb/ Ward et al., op. cit (1972).
Peanuts
Efficacy Against Pest Infestation - Parathion is recommended for control of
the southern corn rootworm on peanuts. Smith (1971)^' evaluated several
insecticides for control of the rootworm in Virginia In 1965, 1966 and 1967.
In the 1965 tests, parathion at 2.0 Ib/acre greatly reduced the amount of
damaged fruit from the untreated checks in two experiments. The third
experiment showed a higher rate of fruit damage than the check. In two
tests in 1967, parathlon-damaged fruit was reduced over 80% in one test
but was about the same as the untreated check in the second experiment.
Yield increases in the latter test were 1.1 Ib/plot or 200 Ib/acre.
The author could not explain the lack of control by parathion since typical
application tests have showed the adult rootworm to be highly susceptible
to parathion.
Coat Effectiveness Of Pest Control - The price of peanuts averaged 14.5c/lb
in 1972 (Agricultural Statistics 1973); the cost of parathion was $1.00/lb
(Chambers and Miller, 1974).The cost of application was $.50 per treat-
emtn. At these prices and costs the economic benefits for the above test
amounted to a gain of $26.50/acre.
I/ Smith, J. C., "Field Evaluation of Candidate Insecticides for Control
of the Southern Corn Rootworm on Peanuts in Virginia," J. Econ.
Entomol.. 64:280-283 (1971).
263
-------
Corn
Parathion is registered to control the European corn borer and
Western corn rootworm, pests significantly affecting corn yields.
Efficacy Against Pest Infestation - Munson et al. (1970)- evaluated
several insecticides for control of these pests in 1964 and 1965 at
selected locations in Iowa. At Sanborn, Iowa in 1964, parathion at 1.0
Ib/acre gave significant reductions in corn borer cavities and signifi-
cantly lower net root ratings for corn rootworm control. Yields
increased 113 and 97 bushels/acre over an untreated check for two plots
with parathion applied at different dates. The lower yield increase
occurred on the later date.
An experiment at Hamburg, Iowa in 1965 also showed significant
reductions in net root ratings and corn borer cavities over the untreated.
Yields, however, increased 10 and 5 bushels/acre over the untreated check
for applications at different dates. The author concluded that one
application of parathion can effectively control these pests.
Cost Effectiveness Of Pest Control - The price of corn averaged $1.20/bushel
in 1972 (Agricultural Statistics 1973); the cost of parathion was $l/lb
(Chambers and Miller,1974). The cost of application was $.50 per treatment.
At these prices and costs the economic benefits ranged from $4.95 to
$143.27/acre.
These results are summarized in Table 40.
Table 40. Results of Parathion Application on Corn Insect Pests
Application Yield
rate increase
Date (Ib Al/acre) (bu/acre)
1964 1.0 113
1.0 97
1965 1.0 10
1965 1.0 5
Additional Application
income at cost at
$1.29/bu AI $l/lb +
($/acre) $.50 Application
144.77
125.13
12.90
6.45
Economic
benefit
($/acre) Source
1.50
1.50
1.50
1.50
143.27
123.63
11.40
4.95
a/ Munson et al., op. cit. (1970).
I/ Munson, R. E., T. A. Brindley, D. C. Peters, and W. G. Lovely, "Control
of Both the European Corn Borer and Western Corn Rootworms with One
Application of Insecticide," J. Econ. Entomol.. 63:385-390 (1970).
264
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Potatoes
Efficacy Against Wireworm Infestation. - Parathion is recommended.for
control of the Pacific wireworm in the Northwest. Onsager (1969)-'
conducted experiments in 1965, 1966 and 1967 to evaluate insecticides
for control of the wireworm in Eastern Washington. Parathion effectively
controlled the wireworm as measured by a reduction in culls over an untreated
check. Culls were reduced between 78 and 95% in the three tests. However,
there appears to be no relation between yield and wireworm control since
yields varied from a loss of 3,900 Ib/acre to a gain of 4,400 Ib/acre.
Cost Effectiveness of Wireworm Control - The price received for potatoes
amounted to $2.55/cwt in 1972 (Agricultural Statistics 1973). The cost
of parathion was $l/lb (Chambers and Miller, 1974). The cost of application
was $.50 per treatment. At these prices and cost, the economic benefits
vary from a loss of $103.45 to a gain of $108.70/acre from the use of
parathion to control the wireworm.
These results are summarized in Table 41.
Table 41. Results of Parathion Application for Wireworm Control.
Additional Application
Application Yield* income at* cost at Economic
rate increase $2.55/cwt AI $l/lb + benefit*
Date (Ib Al/acre) (cwt/acre) ($/acre) at $A50/appllcation ($/acre) Source
1965 3.5 (39) (99.45) 4.00 (103.45) a_/
1966 4.0 2 5.10 4.50 9.60
1967 3.0 44 112.20 3.50 108.70
* Data in parentheses indicate decreases in yield, income and economic
benefit.
a/ Onsager, op. cit. (1969).
if Onsager, J. A., "Nonpersistent Insecticides for Control of Pacific
Coast Wireworm," J. Econ. Entomol.. 62:1065-1067 (1969).
265
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Potato Aphid Control - The results of a test reported in American
Cyanamid Pesticide Petition 19-' showed that a 15% parathion wettable
powder applied at a rate of 1 lb/100 gal. (~0.15 Ib/acre) in six
applications to potatoes for control of the potato aphid in New York
yielded an average of AOO bu/acre compared to an untreated check
yield of 340 bu/acre. This is an increase of 60 bushel for 3,600
Ib/acre which results in an economic benefit of $87.90/acre.
Leafhopper Control - In the same petition parathion (15% wettable powder)
was tested for control of the potato leafhopper in Ohio in 1950. The
insecticide was applied three times at a rate of 1 lb/100 gal. (~0.15
Ib/acre) resulting in a yield of 733 bushels/acre compared to an un-
treated check which yielded 402 bushels. The application of 0.45 Ib of
parathion produced a 331 bushel (19,860 Ib) yield increase resulting in
an economic benefit of $504.48/acre.
Lima Beans - The lygus hesperus is a significant pest affecting yields
of lima beans. Bushing et al. (1974)2' evaluated insecticides for
control of this pest at Davis, California, between 1969 and 1971 and
concluded that parathion applied at about the period of first bloom
increased yields significantly. The results of one test showed a
yield increase of 2,305 Ib/acre with the application of parathion.
It had to be applied three times at 0.5 Ib/acre because populations
rebounded to new highs very quickly after each application.
The price of lima beans was $208.00/ton in 1972 Agricultural
Statistics 1973; the costs of parathion was $l/lb (Chambers and Miller,
1974; the cost of application was $.50 per treatment. Using these prices
and costs the additional income from this test which yielded 2,305 Ib/acre
would be $239.72/acre. Subtracting the cost of parathion of $236.22/acre.
I/ American Cyanamid Company, Pesticide Petition No. 19, Malathion -
Summary of Data, EPA Registration Files.
2j Bushing, R. W., and V. E. Burton, "Partial Pest Management Programs
on Dry Large Lima Beans in California: Regulation of L_. hesperus,"
J. Econ. Entomol.. 67:259-261 (1974).
266
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Peas
One test result was available from the EPA files regarding parathion
use on peas to control the pea aphid. American Cyanamid Pesticide Petition
252^' reported that the yield of peas when treated with 40 Ib/acre of 1%
parathion dust in a Maryland test in 1951 was 29.5 Ib/plot. A comparable
untreated check yielded 20.1 Ib for an increase of 9.4 Ib.
In 1972 peas sold for an average of $112/ton and yields were 1.36
tons/acre (Agricultural Statistics 1973). Using the yeild increase of
44.8% from the above test and the price of $112/ton this would result in
yield increase of 0.61 tons or $68.42/acre. At a cost of parathion of
$l/lb (Chambers and Miller, 1974) and application cost of $.50 per
treatment, the resultant economic benefit would be $67.52/acre.
Strawberries
Schaefers et al. (1972)2/ evaluated parathion for control of the
tarnished plant bug on strawberries and concluded that two applications
of parathion at 0.5 Ib/acre appeared to provide satisfactory reduction
in injury, but the advantages of such a program was not evident. These
results are summarized in Table 42.
Table 42. Results of Parathion Application on Strawberry/Tarnished Plant Bug.
Date
1971
Application
rate
s (Ib Al/acre)
0.5
0.5
check
0.5
check
No.
2
1
—
1
—
Number
of
berries
8,065
8,019
8,652
2,721
2,132
Injury
(%)
24
34
55
35
71
Increased
yield
(%)
31
21
—
36
—
Source
a/
a_/ Schaefers, op cit. (1972).
The prices received for strawberries in 1972 averaged $24/cwt and
yields averaged 105 cwt/acre (Agricultural Statistics 1973). The yield
increases from the above tests ranged from 21% to 36% over the untreated
berries. At an income of $2,520 Ib/acre of berries, the additional income.
if American Cyanamid Company, Pesticide Petition No. 252, Malathion -
Summary of Data, EPA Registration Files.
2J Schaefers, G. A., "Insecticidal Evaluations for Reduction of Tarnished
Plant Bug Injury in Strawberries," J. Econ. Entomol.. 65:1156-1160.
(1972).
267
-------
from parathion use at the above yield increases would range from $529.20
to $907.20/acre. Subtracting the parathion costs of $l/lb and the
application cost of $.50 per treatment, the economic benefit would range
from $527.70 to $905.70 acre.
268
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References
Adkisson, Perry L., and S. J. Nemec, "Comparative Effectiveness of
Certain Insecticides for Killing Bollworms and Tobacco Budworms,"
Publication B-1048, Texas Agr. Exp. Sta. (1966).
Adkisson, Perry L., and S. J. Nemec, "Insecticides for Controlling the
Bo11worm, Tobacco Budworm, and Boll Weevil," MP-837, Texas Agr. Exp.
Sta. (1967).
Agricultural Statistics, 1973, U.S. Department of Agriculture (1973).
American Cyanamid Company, Pesticide Petition No. 19, Malathion -
Summary of Data, EPA Registration Files.
American Cyanamid Company, Pesticide Petition No. 252, Malathion -
Summary of Data, EPA Registration Files.
Bost, W. M., Director, "Cooperative Extension Service Mississippi State
University, Mississippi State Mississippi, Summary of Test Results at
Stoneville and Verona, Mississippi, and Costs of Pesticides," persona^
letter to Mr. David F. Hahlen (1974).
Bushing, R. W., and V. E. Burton, "Partial Pest Management Programs on
Dry Large Lima Beans in California: Regulation of L. hesperus,"
J. Econ. Entomol.. 67:259-261 (1974).
Gate, J. R., Jr., and D. 6. Bottrell, "Field Evaluation of Insecticide
Treatments for Control of the Sorghum Midge," PR-2866, pp. 13-15,
Research on Grain Sorghum Insects and Spider Mites in Texas, Texas
Agr. Exp. Sta. (1971).
Gate, J. R., Jr., D. G. Bottrell, and G. L. Teetes, "Management of the
Greenbug on Grain Sorghum. I. Testing Foliar Treatments of In-
secticides Against Greenbugs and Corn Leaf Aphids," J. Econ. Entomol.,
66:945-951 (1973).
Chambers, William, and Daniel Miller, Farmland Industries, Kansas City,
Missouri, conversation (1974).
Daniels, N. E., "Insecticidal Greenbug Control in Grain Sorghum," PR-
2868, pp. 16-20, Research on Grain Sorghum Insects and Spider Mites
in Texas, Texas Agr. Exp. Sta. (1971).
Daniels, N. E., "Insecticidal Control of the Greenbug," Progress Report
2247, Texas Agr. Exp. Sta. (1962).
269
-------
DePew, L. J., "Evaluation of Foliar and Soil Treatments for Greenbug
Control on Sorghum," J. Econ. Entomol.. 64:169-172 (1971).
Harvey, T. L., and H. L. Hackeratt, "Chemical Control of a Greenbug on
Sorghum and Infestation Effects on Yields," J. Econ. Entomol.. 63:
1536-1539 (1970).
Headley, J. C., and J. N. Lewis, the Pesticide Problem; An Economic
Approach to Public Policy. Resources for the Future, Inc., pp. 39-40
(1967).
Huddleston, E. W., D. Ashdown, B. Maunder, C. R. Ward, G. Wilde, and C. E.
Forehand, "Biology and Control of the Sorghum Midge. I. Chemical and
Cultural Control Studies in West Texas," J. Econ. Entomol.. 65:851-855
(1972).
Meisch, N. V., George L. Teetes, N. M. Randolph, and A. J. Bockholt,
"Phytotoxic Effects of Insecticides on Six Varieties of Grain Sorghum,"
J. Econ. Entomol.. 63:1516-1517 (1970).
Munson, R. E., T. A. Brindley, D. C. Peters, and W. G. Lovely, "Control
of Both the European Corn Borer and Western Corn Rootworms With One
Application of Insecticide," J. Econ. Entomol.. 63:385-390 (1970).
Onsager, J. A., "Nonpersistent Insecticides for Control of Pacific Coast
Wireworm," J. Econ. Entomol.. 62:1065-1067 (1969).
Plapp, F. W., Jr., "Insect Resistance in Heliothis; Tolerance in Larvae
of H. virescens as Compared With H. zea to Organophosphate Insecticides,"
J. Econ. Entomol., 64:999-10002 (1971).
Schaefers, G. A., "Insecticidal Evaluations for Reduction of Tarnished
Plant Bug Injury in Strawberries," J. Econ. Entomol., 65:1156-1160
(1972).
Smith, J. C., "Field Evaluation of Candidate Insecticides for Control of
The Southern Corn Rootworm on Peanuts in Virginia," J. Econ. Entomol.,
64:280-283 (1971).
U.S. Department of Agriculture, Agricultural Statistics 1973.
U.S. Environmental Protection Agency, EPA Compendium of Registered
Pesticides, Vol. Ill, (1973).
U.S. Tariff Commission, Synthetic Organic Chemicals, U.S. Production and
Sales, 1972, TC Publication 681 (1973).
Ward, C. R., E. W. Huddleston, D. Ashdown, J. C. Owens, and K. L. Polk,
"Greenbug Control on Grain Sorghum and the Effects of Tested Insecti-
cides on Other Insects," J. Econ. Entomol.. 63:1929-1934 (1970).
270
-------
Ward, C. R., J. Owens, D. Ashdovm, E. Huddleston, and W. Turner, "Green-
bug Control on Wheat in 1967-1969," J. Econ. Entomol., 65:764-767 (1972)
Wolfenbarger, D. A., "Tobacco Budworm: Cross Resistance to Insecticides
in Resistant Strains and in a Susceptible Strain," J. Econ. Entomol.,
66:292-294 (1973).
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