E X T O X N E T
Extension Toxicology Network
A Pesticide Information Project of Cooperative Extension Offices of
Cornell University, Michigan State University, Oregon State University, and
University of California at Davis. Major support and funding was provided
by the USDA/Extension Service/National Agricultural Pesticide Impact
Assessment Program.
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Pesticide
Information
Profile
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Acephate
Publication Date: 9/95
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TRADE OR OTHER NAMES
Acephate is found in a variety of commercial insecticides. Trade
names for products containing acephate include Orthene, Asataf,
Pillarthene, Kitron, Aimthane, Ortran, Ortho 12420, Ortril, Chrevron RE
12420, and Orthene 755 (8, 9).
REGULATORY STATUS
Acephate is considered a general use insecticide and is used on
many crops inside and outside the U.S. (6). In Canada, maximum residue
limits (MRL) have not been established under the Canadian Food and Drug
Act and Regulations for acephate on any crop, and therefore only
negligible residues (< 0.1 mg/kg) are permitted on any produce. MRLs
have been established for acephate's transformation product,
methamidophos, at 1.0 mg/kg for lettuce and peppers, and 0.5 mg/kg for
tomatoes (10).
Products containing acephate must bear the signal word "Caution" on
their label (3). Check with specific state regulations for local
restrictions which may apply.
INTRODUCTION
Acephate is an organophosphate foliar spray insecticide of moderate
persistence with residual systemic activity of about 10-15 days at the
recommended use rate. It is used for control of a wide range of biting
and sucking insects, especially aphids, including resistant species, in
fruit, vegetables (e.g. potatoes and sugar beets), vine, and hop
cultivation and in horticulture (e.g. on roses and chrysanthemums grown
outdoors) (1). It also controls leaf miners, lepidopterous larvae,
sawflies and thrips in the previously stated crops as well as turf, mint
and forestry (6). It is considered non-phytotoxic on many crop plants
(2). Although, a marginal leaf-burn has occurred on Red Delicious
apples (6). Acephate and its primary metabolite, methamidophos, are
toxic to Heliothis spp. that are considered resistant to other
organophosphate insecticides (10).
Acephate emits toxic fumes of phosphorus, nitrogen, and sulfur
oxides when heated to decomposition. Symptoms of exposure to acephate
include a slight irritation of eyes and skin. Acephate comes in soluble
powder, pressurized spray and granular formulations (2).
TOXICOLOGICAL EFFECTS
ACUTE TOXICITY
The amount of acephate that is lethal to one-half (50%) of
experimental animals fed the material is referred to as its acute oral
lethal dose fifty, or LD50. The acute oral toxicity of acephate to
mammals is medium (LD50 = 500-5,000 mg/kg) to high (LD50 = 50-500
mg/kg), and acute toxicity from inhalation is medium (LC50 = 2-20 mg/l)
(7). The acute dermal LD50 for rabbits is 2,000 mg/kg (11); no
irritation or sensitization was observed in skin tests on guinea-pigs
(2). The effect of 900 mg/kg on cholinesterase inhibition in rats was
not as severe as parathion at 15 mg/kg. Atropine sulfate is an
effective antidote (12).
The acute oral LD50 for technical grade acephate in female rats is
866 mg/kg; 945 mg/kg for male rats; 361 mg/kg for mice; 350 mg/kg for
mallard ducks; 852 mg/kg for chickens; and 140 mg/kg for ringneck
pheasants (2).
The oral LDLo (Lethal Dose Low - lowest dose of a substance other
than LD50 introduced by any route other than inhalation, over any given
period of time in one or more divided portions and reported to have
caused death in humans or animals) for dogs is 681 mg/kg (8).
The lethal concentration fifty, or LC50, is that concentration of a
chemical in air or water that kills half of the experimental animals
exposed to it for a set period of time. The 96 hour LC50 for rainbow
trout is >1,000 mg/l; 2,050 mg/l for bluegill fish; 1,725 mg/l for
largemouth black bass; 2,230 mg/l for channel catfish; and 9550 mg/l for
goldfish (2). The toxicity of acephate to rainbow trout increased with
increasing temperature (14).
CHRONIC TOXICITY
In 2-year feeding trials, dogs exhibited depression of
cholinesterase at 100 mg/kg diet (maximum dose level) of acephate but no
other significant effects; rats showed depression of cholinesterase but
no effect on weight gain or pathological effect at 30 mg/kg diet (2).
Another feeding study noted that rats did not produce pathological
changes over a 90-day period when fed up to 300 mg/kg body weight of
acephate (1).
Acephate has a negligible chronic toxicity to fish (14).
Reproductive Effects
Acephate is considered a fetotoxin (can poison the fetus) and there
is some evidence of hormonal effects (7).
Teratogenic Effects
No effects were observed in 2-year feeding trials on dogs (2).
Mutagenic Effects
No effects were observed in 2-year feeding trials on dogs (2).
Carcinogenic Effects
No effects were observed in 2-year feeding trials in dogs (2).
Organ Toxicity
Exposure effects of acephate in humans can include: cardiac
responses (bradycardia/tachycardia, heart block), central nervous system
impairment, eye problems (miosis/mydriasis, loss of accommodation,
ocular pain, sensation of retrobulbar pressure, tearing, dark or blurred
vision, conjunctiva hyperemia, cataracts), gastrointestinal problems
(abdominal cramps, heart burn, hyperperistalsis), respiratory effects
(apnea, dyspnea, hypopnea, atelectasis, bronchoconstriction,
bronchopharyngeal secretion, chest tightness, productive cough,
rales/ronchi, wheezing, pulmonary edema, laryngeal spasms, rhinorrhea,
oronasal frothing) and death due to respiratory failure (15).
Fate in Humans and Animals
Exposure to acephate can result in alkyl phophates in urine (15).
ECOLOGICAL EFFECTS
Effects on Birds
Acephate is considered moderately toxic to upland game birds. The
LD50 for acephate in mallard ducks is 350 mg/kg; 140 mg/kg in pheasants;
> 5,000 ppm for the mallard and 1,280 ppm for the bobwhite quail (3).
Acephate may affect behavior and breeding success (7).
Effects on Aquatic Organisms
The compound is considered relatively non-toxic to fish with an
LC50 for goldfish of 9,550 mg/l and rainbow trout >1,000 mg/l over 96
hours (1). Another study noted that the LC50 was >1,000 ppm for both
the rainbow trout and the bluegill (3).
Acephate did not increase "coughing" (interruption of normal
ventilating cycle, with a more rapid expansion and contraction of the
buccal and opercular cavities, which serves the purpose of clearing the
gills of accumulated debris) frequency of rainbow trout (14).
In laboratory studies, the cholinesterase activity in the
erythrocytes, gills, and serum of rainbow trout was reduced within 3
hours of exposure to acephate. With methamidophos, the extent of brain
and liver AChE inhibition in carp was proportional to the insecticide
concentration and exposure time. Smaller fish started dying when the
AChE inhibition was 40 to 50%, but very large fingerlings survived an
inhibition of more than 80% (14).
In field studies, however, subsequent to aerial spraying of
acephate to control spruce budworm, no significant depression of brain
AChE activity of brook trout and salmon in streams near the target area
occurred; but, there was a significant depression of brain AChE activity
in suckers, which returned to normal by the eighth day (14).
Effects on Other Animals (Nontarget species)
Acephate is considered toxic to bees (1). The LC50 for bees is 1.2
ug/bee (3).
In studies examining the residual toxicity of insecticides on
beneficial species in citrus, it was found that acephate had the longest
residual activity toward Aphytis melinus, DeBach, and that mortality
with dimethoate treatment occurred for a shorter period of time than
with acephate treatment. This same study showed that residues of
acephate caused greater mortalities over a longer period of time to A.
melinus than other materials tested (13).
In some cases, there is no effect on fecundity of the beneficial,
but survival of the offspring is affected. For example, fecundity of
Diaeretiella rapae was not reduced by treatment of Myzus persicae host
mummies with acephate, but acephate significantly affected survival for
the first day after emergence (13).
In studies of insecticides commonly used in cotton, acephate was
shown to be very toxic to adult Microplitis croceipes parasitoids, and
caused 100% mortality at the lowest recommended field rates (13).
ENVIRONMENTAL FATE
Breakdown of Chemical in Soil and Groundwater
Acephate dissipates rapidly with half-lives of <3 and 6 days in
aerobic and anaerobic soils, respectively. The major metabolite was CO2
in both soil types. TLC and soil column studies indicate acephate is
mobile in most soils but that aged residues (excluding acephate and its
degradate methamidophos) are immobile in sandy loam soil. Most of the
applied acephate and degradate methamidophos degrade to immobile
compounds in 20 days (4). Methamidophos and carbon dioxide were
identified as the major soil metabolites (9).
Breakdown of Chemical in Surface Water
No information was currently available.
Breakdown of Chemical in Vegetation
Acephate is quickly absorbed, translocated, and transformed in pine
seedlings and cotton plants. The chemical was metabolized via cleavage
of the amide bond to form methamidophos and an unknown, but
insecticidally active compound, which were identified in the roots,
stems, and leaves. Methamidophos was also found in cotton leaves
following a single application of acephate. Four additional degradation
products were formed - two of which were tentatively identified as O, S-
dimethyphosphorothioate and S-methyl acetylphosphoramidothioate. The
amount of methamidophos and the four products represented about 9% and
5% of the applied amount, respectively (9).
In studies on tobacco leaves, citrus fruit, greenhouse tomatoes,
and celery and lettuce, half-life disappearance of residues ranged from
1 to 15 days, depending on the crop species and the part of the plant
analyzed. This same study showed residues of both acephate and
methamidophos on carrots and potatoes even though no direct spraying of
the underground portion of these crops occurred. Carrots contained much
higher residues (up to 5.2 mg/kg) than potatoes (up to 3.6 mg/kg). In
contrast to carrots, potatoes and the fruit bearing vegetables studied,
the amount of rainfall occurring was directly proportional to the
disappearance of both acephate and methamidophos residues on lettuce and
celery. The level of residues on the eight crops studied on day 3 after
application generally reflected the weight to volume ratios of the crops
except where translocation appeared to give higher residues than would
be expected. In carrots, potatoes, peppers and tomatoes, residues on
day 7 were higher than on day 3 and day 14, thus suggesting absorption
and translocation from foliage to root, tuber or fruit. Methamidophos
was identified in the eight crops studied, at high levels on peppers,
but at very low levels on lettuce and celery (10).
Acephate is rapidly absorbed into the leaf tissue of cotton plants
when applied foliarly, with nearly 40% of the applied acephate present
in the internal extract and 25% remaining on the leaf surface 24 hours
after application. The unrecovered acephate probably was translocated
from the leaves or bound in unextractable form in the leaf tissue. The
low vapor pressure of acephate indicates that loss due to volatilization
would be negligible. Translocation of acephate into the fruiting body
of the cotton plant following foliar application is not sufficient to be
toxic to cotton insect pests. Little to no degradation of acephate to
methamidophos occurred on the leaf surface. Methamidophos was more
persistent in plant tissue than acephate (i.e. acephate was degrading to
methamidophos faster than methamidophos was degrading to another
compound) (11).
PHYSICAL PROPERTIES AND GUIDELINES
Exposure Guidelines:
| ADI: | Until 1987, the temporary acceptable daily intake (ADI) for man was 0.005 mg/kg (2) |
| H-t1/2: | at 40 degrees C and pH 9: 60 hours, at 40 degrees C and pH 3: 710 hours (9) |
| KH: | 5.2 x 10 to the minus 13 atm x m3/mol at 20-24 degrees C (9) |
Physical Properties:
| Appearance: | Colorless to white solid (9) |
| CAS No.: | 30560-19-1 (5) |
| RTECS (Registry of Toxic Effects of Chemical Substances Number): | TB4760000 (8, 9) |
| Chemical name: | O, S-dimethyl acetylphos-phoramidothioate (IUPAC) (1, 3), O, S-dimethyl acetic phosphoramidothioate, (7) N-[methoxy (methylthio)phosphinoyl] acetamide (2, 9) |
| Chemical Class/Use: | organophosphate/systemic insecticide (3) |
| Specific gravity: | 1.35 (5) |
| Specific density: | 1.35 at 20 - 24 degrees C (2, 9) |
| Solubility in water: | readily soluble in water (79 g/100 ml at 20 degrees C) (1). 650 g/l at 20 degrees C (2) |
| Solubility in other solvents: | In acetone 15.1, ethyl acetate 3.5, benzene 1.6, hexane 0.01 (all in g/100 ml at 20 degrees C) (1) ethanol < 50 g/l at 20 degrees C (2, 9) |
| Melting point: | 93 degrees C (198-199 degrees F) (1, 5), technical grade acephate (purity 80 - 90%) is 82 - 89 degrees C (2), 72 - 80 degrees C (12), 64 - 68 degrees C for impure (9) |
| Molecular weight: | 183.18 (8) |
| Molecular Formula: | C4H10NO3P5 (8) |
| Boiling point: | decomposes on distillation (1) |
| Decomposition temperature: | at 40 degrees C, 50% decomposition occurs in 60 hours at pH 9 and in 710 hours at pH 3 (1) |
| Flashpoint: | low volatility, but some of the minor degradation products are volatile (12) |
| Vapor pressure: | 2.3 x 10 to the minus 6 mbar at 24 degrees C (1), 0.226 mPa (24 degrees C) (2), 1.7 x 10 to the minus 6 mmHg at 24 degrees C (9) |
| log Koc: | 0.48 (9) |
| log Kow: | -1.87 (9) |
BASIC MANUFACTURER
Valent USA
1333 North California Blvd.
Suite 600
P. O. Box 8025
Walnut Creek, CA 94596-8025
Telephone: 510-256-2700
Emergency: 800-457-2022
Review by Basic Manufacturer:
Comments solicited: March, 1994
Comments received:
REFERENCES
The Agrochemicals Handbook. 1983. The Royal Society of
Chemistry, The University, Nottingham, England.
Worthing, C. R. (ed.) 1987. The Pesticide Manual: A World
Compendium. Eighth edition. Published by The British Crop Protection
Council.
Farm Chemicals Handbook. 1994. Meister Publishing Co.
Willoughby, OH.
Thomson, W. T. 1989. Agricultural Chemicals. Book 1:
Insecticides. Thomson Publications, Fresno, CA.
OHS Database. Occupational Health Services, Inc. 1993 (August)
MSDS for Acephate. OHS Inc., Secaucus, NJ.
Thomson, W. T. Agricultural Chemicals. Book 1: Insecticides.
1992. Thomson Publications, Fresno, CA.
Briggs, S. A. 1992. Basic Guide to Pesticides: Their
Characteristics and Hazards. Hemisphere Publishing Corp. Washington,
Philadelphia, London.
Fairchild, E. J. (ed.) PhD. Agricultural Chemicals and
Pesticides: A Subfile fo the Registry of Toxic Effects of Chemical
Substances. 1977. Published by U.S. Department of Health, Education,
and Welfare, Public Health Service, Center for Disease Control, National
Institute for Occupational Safety and Health.
Montgomery, J. H. (ed.). Agrochemicals Desk Reference. 1993.
Environmental Data. Published by Lewis Publishers, Chelsea, MI.
Frank, R., G. Ritcy, H.E. Braun and F.L. McEwen. 1984.
Disappearance of Acephate Residue from Beans, Carrots, Celery, Lettuce,
Peppers, Potatoes, Strawberries and Tomatoes. J. Econ. Ent. 77:5 1110-
1115.
Bouchard, D. C. and T. L. Lavy. 1982. Fate of Acephate in the
Cotton Plant. J. Econ. Ent. 75:5 921-923.
Spencer, E. Y. 1981. Guide to the Chemicals Used in Crop
Protection. 7th edition. Publication 1093. Research Branch.
Agriculture Canada.
Elzen, G. W. 1989. Sublethal Effects of Pesticides on Beneficial
Parasitoids. In: Pesticides and Non-target Invertebrates. Ed. by Paul
C. Jepson. Intercept Ltd. Dorset, England. pp 129-150.
Morty, A. S. 1986. Toxicity of Pesticides to Fish. Volume II.
CRC Press. Boca Raton, FL.
Hallenbeck, W. H. and K. M. Cunningham-Burns. 1985. Pesticides
and Human Health. Springer-Verlag. New York, Berlin, Heidelberg and
Tokyo.
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are for convenience only; no endorsement of products is intended, nor is
criticism of unnamed products implied. Most of this information is historical
in nature and may no longer be applicable.
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